Himmayat Mhatre

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Polylactic acid, also known as poly(lactic acid) poly, lactic, acid or polylactide (PLA), is a thermoplastic polyester with backbone formula (C3H4O2)n or [–C(CH3)HC(=O)O–]n, formally obtained by condensation of lactic acid C(CH3)(OH)HCOOH with loss of water (hence its name). It can also be prepared by ring-opening polymerization of lactide [–C(CH3)HC(=O)O–]2, the cyclic dimer of the basic repeating unit.

PLA has become a popular material due to it being economically produced from renewable resources. In 2021, PLA had the highest consumption volume of any bioplastic of the world,[3] although it is still not a commodity polymer. Its widespread application has been hindered by numerous physical and processing shortcomings.[4] PLA is the most widely used plastic filament material in 3D printing. Its low melting point, high strength, low thermal expansion, good layer adhesion, and high heat resistance when annealed make it an ideal material for this purpose. Without annealing, however, PLA has the lowest heat resistance of the common 3D printing plastics.

Although the name "polylactic acid" is widely used, it does not comply with IUPAC standard nomenclature, which is "poly(lactic acid)".[5] The name "polylactic acid" is potentially ambiguous or confusing, because PLA is not a polyacid (polyelectrolyte), but rather a polyester.[6]

The monomer is typically made from fermented plant starch such as from corn, cassava, sugarcane or sugar beet pulp.

Several industrial routes afford usable (i.e. high molecular weight) PLA. Two main monomers are used: lactic acid, and the cyclic di-ester, lactide. The most common route to PLA is the ring-opening polymerization of lactide with various metal catalysts (typically tin octoate) in solution or as a suspension. The metal-catalyzed reaction tends to cause racemization of the PLA, reducing its stereoregularity compared to the starting material (usually corn starch).[7]

The direct condensation of lactic acid monomers can also be used to produce PLA. This process needs to be carried out at less than 200 °C; above that temperature, the entropically favored lactide monomer is generated. This reaction generates one equivalent of water for every condensation (esterification) step. The condensation reaction is reversible and subject to equilibrium, so removal of water is required to generate high molecular weight species. Water removal by application of a vacuum or by azeotropic distillation is required to drive the reaction toward polycondensation. Molecular weights of 130 kDa can be obtained this way. Even higher molecular weights can be attained by carefully crystallizing the crude polymer from the melt. Carboxylic acid and alcohol end groups are thus concentrated in the amorphous region of the solid polymer, and so they can react. Molecular weights of 128–152 kDa are obtainable thus.[7]

Another method devised is by contacting lactic acid with a zeolite. This condensation reaction is a one-step process, and runs about 100 °C lower in temperature.[8][9]

Due to the chiral nature of lactic acid, several distinct forms of polylactide exist: poly-L-lactide (PLLA) is the product resulting from polymerization of L,L-lactide (also known as L-lactide). Progress in biotechnology has resulted in the development of commercial production of the D enantiomer form.[10]

Polymerization of a racemic mixture of L- and D-lactides usually leads to the synthesis of poly-DL-lactide (PDLLA), which is amorphous. Use of stereospecific catalysts can lead to heterotactic PLA which has been found to show crystallinity. The degree of crystallinity, and hence many important properties, is largely controlled by the ratio of D to L enantiomers used, and to a lesser extent on the type of catalyst used. Apart from lactic acid and lactide, lactic acid O-carboxyanhydride ("lac-OCA"), a five-membered cyclic compound has been used academically as well. This compound is more reactive than lactide, because its polymerization is driven by the loss of one equivalent of carbon dioxide per equivalent of lactic acid. Water is not a co-product.[11]

The direct biosynthesis of PLA, in a manner similar to production of poly(hydroxyalkanoate)s, has been reported.[12]

PLA polymers range from amorphous glassy polymer to semi-crystalline and highly crystalline polymer with a glass transition 60–65 °C, a melting temperature 130-180 °C, and a Young's modulus 2.7–16 GPa.[13][14][15] Heat-resistant PLA can withstand temperatures of 110 °C.[16] The basic mechanical properties of PLA are between those of polystyrene and PET.[13] The melting temperature of PLLA can be increased by 40–50 °C and its heat deflection temperature can be increased from approximately 60 °C to up to 190 °C by physically blending the polymer with PDLA (poly-D-lactide). PDLA and PLLA form a highly regular stereocomplex with increased crystallinity. The temperature stability is maximised when a 1:1 blend is used, but even at lower concentrations of 3–10% of PDLA, there is still a substantial improvement. In the latter case, PDLA acts as a nucleating agent, thereby increasing the crystallization rate.[17] Biodegradation of PDLA is slower than for PLA due to the higher crystallinity of PDLA[citation needed]. The flexural modulus of PLA is higher than polystyrene and PLA has good heat sealability.

Several technologies such as annealing,[18][19][20] adding nucleating agents, forming composites with fibers or nano-particles,[21][22][23] chain extending[24][25] and introducing crosslink structures have been used to enhance the mechanical properties of PLA polymers. Polylactic acid can be processed like most thermoplastics into fiber (for example, using conventional melt spinning processes) and film. PLA has similar mechanical properties to PETE polymer, but has a significantly lower maximum continuous use temperature.[26]

Racemic PLA and pure PLLA have low glass transition temperatures, making them undesirable because of low strength and melting point. A stereocomplex of PDLA and PLLA has a higher glass transition temperature, lending it more mechanical strength.[27]

The high surface energy of PLA results in good printability, making it widely used in 3D printing. The tensile strength for 3D printed PLA was previously determined.[28]

PLA is soluble in a range of organic solvents.[29] Ethyl acetate is widely used because of its ease of access and low risk. It is useful in 3D printers for cleaning the extruder heads and for removing PLA supports.

Other safe solvents include propylene carbonate, which is safer than ethyl acetate but is difficult to purchase commercially. Pyridine can be used, but it has a distinct fish odor and is less safe than ethyl acetate. PLA is also soluble in hot benzene, tetrahydrofuran, and dioxane.[30]

PLA objects can be fabricated by 3D printing, casting, injection moulding, extrusion, machining, and solvent welding.

PLA is used as a feedstock material in desktop fused filament fabrication by 3D printers, such as RepRap printers.[31][32]

PLA can be solvent welded using dichloromethane.[33] Acetone also softens the surface of PLA, making it sticky without dissolving it, for welding to another PLA surface.[34]

PLA-printed solids can be encased in plaster-like moulding materials, then burned out in a furnace, so that the resulting void can be filled with molten metal. This is known as "lost PLA casting", a type of investment casting.[35]

PLA is used in a large variety of consumer products such as disposable tableware, cutlery, housings for kitchen appliances and electronics such as laptops and handheld devices, and microwavable trays. (However, PLA is not suitable for microwavable containers because of its low glass transition temperature.) It is used for compost bags, food packaging and loose-fill packaging material that is cast, injection molded, or spun.[36] In the form of a film, it shrinks upon heating, allowing it to be used in shrink tunnels. In the form of fibers, it is used for monofilament fishing line and netting. In the form of nonwoven fabrics, it is used for upholstery, disposable garments, awnings, feminine hygiene products, and diapers.

PLA has applications in engineering plastics, where the stereocomplex is blended with a rubber-like polymer such as ABS. Such blends have good form stability and visual transparency, making them useful in low-end packaging applications.

PLA is used for automotive parts such as floor mats, panels, and covers. Its heat resistance and durability are inferior to the widely used polypropylene (PP), but its properties are improved by means such as capping of the end groups to reduce hydrolysis.[36]

In the form of fibers, PLA is used for monofilament fishing line and netting for vegetation and weed prevention. It is used for sandbags, planting pots, binding tape and ropes .[36]

PLA can degrade into innocuous lactic acid, making it suitable for use as medical implants in the form of anchors, screws, plates, pins, rods, and mesh.[36] Depending on the type used, it breaks down inside the body within 6 months to 2 years. This gradual degradation is desirable for a support structure, because it gradually transfers the load to the body (e.g., to the bone) as that area heals. The strength characteristics of PLA and PLLA implants are well documented.[37]

Thanks to its bio-compatibility and biodegradability, PLA found interest as a polymeric scaffold for drug delivery purposes.

The composite blend of poly(L-lactide-co-D,L-lactide) (PLDLLA) with tricalcium phosphate (TCP) is used as PLDLLA/TCP scaffolds for bone engineering.[38][39]

Poly-L-lactic acid (PLLA) is the main ingredient in Sculptra, a facial volume enhancer used for treating lipoatrophy of the cheeks.

PLLA is used to stimulate collagen synthesis in fibroblasts via foreign body reaction in the presence of macrophages. Macrophages act as a stimulant in secretion of cytokines and mediators such as TGF-β, which stimulate the fibroblast to secrete collagen into the surrounding tissue. Therefore, PLLA has potential applications in the dermatological studies.[40][41]

PLLA is under investigation as a scaffold that can generate a small amount of electric current via the piezoelectric effect that stimulates the growth of mechanically robust cartilage in multiple animal models.[42]

PLA is degraded abiotically by three mechanisms:[44]

The hydrolytic reaction is: − COO + H 2 O ⟶ − COOH + − OH − {\displaystyle {\ce {-COO + H2O -> - COOH + -OH-}}}

The degradation rate is very slow in ambient temperatures. A 2017 study found that at 25 °C (77 °F) in seawater, PLA showed no loss of mass over a year, but the study did not measure breakdown of the polymer chains or water absorption.[45] As a result, it degrades poorly in landfills and household composts, but is effectively digested in hotter industrial composts, usually degrading best at temperatures of over 60 °C (140 °F).[46]

Pure PLA foams are selectively hydrolysed in Dulbecco's modified Eagle's medium (DMEM) supplemented with fetal bovine serum (FBS) (a solution mimicking body fluid). After 30 days of submersion in DMEM+FBS, a PLLA scaffold lost about 20% of its weight.[47]

PLA samples of various molecular weights were degraded into methyl lactate (a green solvent) by using a metal complex catalyst.[48][49][50]

PLA can also be degraded by some bacteria, such as Amycolatopsis and Saccharothrix. A purified protease from Amycolatopsis sp., PLA depolymerase, can also degrade PLA. Enzymes such as pronase and most effectively proteinase K from Tritirachium album degrade PLA.[51]

Four possible end-of-life scenarios are the most common:

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There is aTRACT

Understanding what alcohol is and how it works in the body is important to a pharmacological point of view. There is no simple cause, but a complicated interaction of factors that lead to the development of this disease. The reduction of synaptic transmission in the human nervous system is what causes the psychophysiological and pharmacodynamic action of alcohol to be fundamentally depressed. It is known that excessive alcohol consumption can cause problems in the brain and central nervous system, which can affect memory and intellectual functions.

If alcohol continues to be consumed, it will cause alcoholic hepatitis, a condition in which the metabolism of alcohol causes a large alcoholic fat liver, which ends in inflammation of the liver. Alcohol has also been related to myocardial alterations; It has been found in healthy experimental animals that both the speed of contraction of the heart muscle and its maximum tension decrease in the presence of alcohol, as a consequence, the force of each contraction and the increase in pressure in the left ventricle are less, losing effectiveness of the heart muscle. heart like bomb

Drug addiction, Excitability, Alcoholism, Neuroscience, Cirrhosis are some of the topics covered.

TheTRACT

It's important to understand what alcohol is and how it works in the body.

There is a complex interaction of factors that lead to this serious drug dependent illness. The reduction of the synaptic transmission in the human nervous system is what causes the psycho-physiological and drug-dynamic action of alcohol. It's well known that excessive drinking of alcohol causes a chronic and acute problem of the brain, which can cause disorders in the central nervous system, as well as alterations in the memory and intellectual functions. The metabolism of alcohol will cause an alcoholic-fat liver bigger in size and cause inflammation of the liver.

If the person continues to drink, they will develop alcoholic hepatitis, a disease that can cause damage to the body's organs. Alcohol has also been related to changes in the myocardium and it has been seen in healthy animals that the speed of contraction of the cardiac muscle as well as the maximum tension achieved by that contraction decrease in the presence of alcohol, and therefore, the strength of each contraction and the increase of pressure in the left ventricle are less and the hert cannot act as a pump.

Drug-addiction, Excitability, Alcoholism, Neuroscience, Cirrhosis, and other related topics.

One of the best-known definitions of alcoholism is the one established by the WHO Expert Committee in 1954. According to it:

Its origin and development are due to a complicated interaction of factors.

Individuals who tend to become alcoholics are those who react physiologically to alcoholic beverages in a certain way, who find in it an experience of calm and relaxation, who possess certain personality traits that prevent them from coping successfully with states of mind. pressure, anxiety and frustration, or those who belong to cultures in which a certain amount of guilt and confusion is caused around the behavior of the drinker.

Alcohol is formed by a molecule with two carbon atoms and a hydroxyl group (OH) attached to one of the two carbons, whose structure is highly soluble in water (hydrophilicity), and insoluble in fats (lipophobic) (Sánchez-Tutret, 1997); it diffuses easily through biological membranes, allowing for wide and easy dispersal in the body. Breath analysis is possible due to the high permeability of the lung.

Alcohol has a direct effect on behavior because it can cross the blood-brain barrier and even interfere with nerve action.

When alcohol is ingested, it produces biochemical changes until it is converted into a substance called acetaldehyde, which passes into the blood and becomes inert compounds; once the alcohol has been metabolized into acetaldehyde, it produces the intoxication picture; some theorists maintain that it acts on brain neurotransmitters to produce tetraisoquinolines that interfere with neuronal functioning. The available data on its cerebral action speaks of non-specific modes of action. The action of other depressants is the same as well.

Another recognized effect is the alteration of aldosterone metabolism, which produces retention of sodium, potassium and chlorine; The powerful effect of alcohol on urine output occurs, in part, as a result of the effect of the posterior pituitary on antidiuretic hormone (Souza and Machorro, 1988).

The majority of alcohol remains in the body until it leaves the body and enters the water and CO2. From 1 to 15% can be eliminated through the breathed air and from 1 to 5% through urine.

The sedative properties of alcohol cause it to have an anesthetic effect on the body on some areas of the brain, decreasing its activity; and like all sedative-hypnotic drugs, it acts to promote synaptic inhibition, produced by the transmitter called gamma-aminobutyric acid (the same happens with amphetamines and barbiturates).

The anesthetic effect is carried out mainly through an inhibitory action on the NMDA receptors of the glutamate neurotransmitter, which has an excitatory power in the brain (Collinbridge and Lester cited by Sánchez-Tutret, 1997), producing modifications in the neuronal mechanism of pain. hippocampus and cortex, which could constitute neurochemical correlates of memory and be the basis of its anesthetic effects (Sanchez-Tutret, 1997).

The importance of the study is due to the fact that a drug that modifies the neurotransmitters in the brain will affect the behavior of the individual.

Several laboratories have been able to show that the postsynaptic molecule associated with the gyptian receptor is related to other postsynaptic molecule in many gyptians. The molecule has a special affinity for the drug.

A single complex mechanism called a complex is formed by a special affinity of one of the related genes to bind to barbiturates and other drugs. The inhibition of nerve impulses in the postsynaptic cell can be achieved by a drug molecule binding to the GABA receptor complex.

One of the theories about the effects of alcohol on nerve cells is related to the previous chemical description. It is difficult for many authors to clarify since there are many actions and effects that alcohol has on the nervous system.

There is no consensus about the mechanisms of action of alcohol, since it seems that it acts in the brain without the mediation of specific receptors.

The basis of the effect of alcohol is poorly understood. Current research suggests that the primary interaction is an altered function in the membranes, which leads to alterations in the neurotransmitter mechanisms.

In mouse studies, the action of TRH on sleep is shown to decrease, but cholinergic blockers don't block it. The results show that the cholinergic system of the brain is affected by both TRH and ethanol.

The most common theories about the action of alcohol on the central nervous system have been summarized.

When alcohol concentrations are within the pharmacological limits, it is known to prevent the release of oxytocin, vasopressin, and possibly other hypothalamic peptides.

In both humans and animals, the effects of the two hormones on behavioral aspects are apparent.

When administered intracerebrally or systemically, attention has focused on the effects on memory and learning.

The data would be consistent with the fact that there are fibers in the brain that are related to neural mechanisms of learning, memory, and other higher forms of behavior.

Alcohol has a major influence on the nervous system and both tolerance and dependence are dependent on it. It is similar to general anesthetics in that it has a depressed psychophysiological action.

It acts on the neurone membrane thanks to its high conjugate solubility.

There is a discussion about whether alcohol causes depression by reducing synaptic transmission or by blocking excitability.

Some researchers admit that alcohol in high doses can affect the brain's electrical activity, while in low amounts it can be stimulatory.

Although the literature denies the stimulating action of alcohol, it is known that there is a certain euphoric effect, attributed to the liberating effect of social inhibitions, which is associated in turn with the pharmacokinetic phase, in which alcohol levels increase.

Another explanation for why alcohol produces directly stimulating effects, such as euphoria, is that some of its metabolites, such as acetaldehyde (a highly toxic substance that results from the primary oxidation of alcohol and is in turn rapidly oxidized in the liver by dehydrogenated aldehyde ), could be the agent responsible for this supposed stimulation, by causing an activation of the catecholaminergic brain systems.

The small amount of acetaldehyde, which is released from immediate oxidation in the liver and is incorporated into the bloodstream, could act as a monoamine oxidase inhibitor.

The release of dopamine in the nucleus and in the tegmental area has been shown to be related to the stimulating effect of alcohol.

It is difficult to understand the role played by acetaldehyde given the impossibility of differentiating its effects from those produced by alcohol itself during intoxication; however, there is a possibility that the actions of alcohol and acetaldehyde are related. According to some authors, acetaldehyde is more toxic than alcohol and acts as a stimulating substance; high levels of acetaldehydemia cause the same effects as acetaldehyde shock, produced by the administration of disulfiran and alcohol ingestion: headaches, nausea, facial flushing, and tachycardia.

According to the results of various investigations, the brain system of the serotonergic family may be involved in the development of tolerance to drugs.

The elevation of the same rate is accompanied by a decrease in tolerance for alcohol.

According to Littleton, cited by Swonger and Constantine (1985), the central depressive effect of alcohol can be conditioned by its fluidizing action on lipids, the reduction of polyunsaturated phospholipids and the increase in cholesterol; this would directly affect the transmitter systems, particularly on the synapse of the GABAergic system, which would be the last link responsible for the acquisition of tolerance to alcohol.

The authors suggest that physical dependence on alcohol is more related to the lipids than to the proteins, because it is difficult to admit the existence of a specific receptor for alcohol.

Alcohol can be absorbed from the mouth to the rectum, but it can't be absorbed in the small intestine. It is absorbed through the oral mucosa, bloodstream and lungs, because it is volatile. Most of alcohol metabolism takes place in the portal vein of the stomach and the level of retention in the stomach is a factor in absorption.

It is said that the main organ involved in the metabolism of alcohol is the liver, and that it is a rather harmful chemical effect.

A diet rich in alcohol can cause a huge overload for the liver. In this situation, alcohol becomes the main fuel, leaving the liver to metabolize its usual fuel (fats), which in turn leads to a number of disorders, such as theAccumulation of fats that are not oxidation, and the oxidation of ethanol.

It makes a lot of hydrogen.

The high concentration of hydrogen in the blood leads to acidosis, a condition in which the body's cells become acidic. Secondary hyperuremia is caused by hyperlactasidemia, which reduces the excretion of uric acid. Some people develop severe ketoacidosis when the liver releases ketone bodies in excessive quantities. Chronic alcoholism is usually associated with hyperlipidemia because of the fact that the liver eliminates part of the fat in the form of hypoproteins.

The function of the liver is to carry out the metabolism and storage of certain vitamins and minerals, so the interference of alcohol in that function can cause secondary deficiencies. In alcoholic liver disease, the active form of pyrophosphate is also inhibited. The development of alcoholism can be caused by a deficiency in the ATP in the liver.

Most alcoholics reach the state of alcoholic fatty liver, which consists of mild and enlarged livers, due to this reason.

Some alcoholics have problems with the body. If it is not associated with inflammation or necrosis, it can be cured by abstaining from alcohol for 1-2 months.

Hepatocyte necrosis occurs in some patients, when the degree of necrosis and inflammation is severe, which frequently represents a life-threatening risk, if the person continues to drink.

Cirrhosis is an advanced process of fibrosis that is associated with the destruction of the normal lobular architecture. The appearance of scars and hepatocyte necrosis caused these to form. The cirrhotic patient develops hypertension, accompanied by astitis, edema, and the appearance of esophageal varices.

It is not clear why some patients develop cirrhosis at an early age, while others never progress from the fat in their body.

It is known that excessive alcohol consumption can cause problems in the central nervous system.

Alterations in memory and intellectual functions are caused by both acute and chronic forms.

Acute cerebral alcohol syndrome can proceed without permanent brain damage, but chronic cerebral alcoholic syndrome is associated with a specific brain abnormality. The autopsy of people with an advanced degree of alcoholism showed that the gyri on the dorsolateral surface had been atrophyed.

The autopsy findings have been consistent in the diagnosis of cortical atrophy in alcoholics and people who have abused alcohol. The symptoms of these alterations of the cerebral cortex are loss of recent memory, confusion, and mental confusion. Scientists found that alcoholics scored closer to brain-injured people on tests of adaptive capacity.

Among the factors proposed as the cause of chronic brain injury in alcoholics are the appearance of areas of hypoxia, due to the slowing of forward flow, microhemorrhages, and areas of edema that appear as a consequence of the loss of plasmatic proteins through the walls of hypoxic capillaries. Some authors suggest that alcoholic brain injury may be related to alcohol-caused impaired brain cell synthesis.

It can be stated from the above.

A state of dementia is caused by the loss of neurons in chronic cerebral alcoholic syndrome. As is known, neurons, like the rest of the nerve cells, do not have the capacity to regenerate; It has been calculated that the human being is born with an average of 100 trillion neurons, which according to some calculations is a much higher amount for the normal functioning of the brain, so this amount allows the loss of a certain number without affecting the functioning brain, in eighty years a person has a loss of 10% of neurons that they had at birth. If there is an accelerated loss of neurons, there is a depletion of reserves, which makes it difficult to adapt.

The mechanism of neuron loss in alcoholics is unknown, but it is known that it occurs.

Its symptoms include fatigue, apathy, loss of interest, depression and sometimes anxiety and agitation. There is a decline in the capacity for abstract reasoning, concentration and retention of recently learned material, as well as a change in personality, which may include petulance.

People don't know what is happening but they know something is wrong.

Wernicke's Syndrome is a pathology associated with alcoholism. The active coenzyme Thiamine is found in many vegetables, but it needs to be phosphorized in the liver to be effective. There is an area of the brain that is irritated by the central gray matter of the brain stem, which is the location of the clinical lesion in Wernicke's Syndrome.

The patient calms down as the midbrain lesion becomes destructive. The midbrain and diencephalon are the location of the lesions when in a coma.

The disease of Korsakoff's Psychosis is characterized by a loss of recent memory, and the patient is unable to retain certain data for a few seconds. He accepts any idea that is suggested to him, he has little capacity for judgement or intuition to recognize the credibility of any suggestion that is made to him, or of any statement made by himself. He tends to fill in the gaps left by his recent memory.

The clinical picture consists of a loss of judgement about what may be true and a great impatience to cover the memory deficit with accounts of feats and facts that are clearly false and absurd.

It is thought that the cause of Korsakoff Syndrome is a deficiency of thiamine. There is no doubt that there is more to it than a deficiency of vitamins. This can be a result of tumors, surgical tumors, mammillary tubercles from encephalitis, and cerebral circulation disorders.

Damage to the central nervous system can be caused by Alcoholic hypoglycemia.

Alcohol metabolism involves the reduction of nicotinamide adenine dinucleotide. The metabolism of alcohol is related to the appearance of a blood sugar problem. The normal mechanism of gluconeogenesis from the amino acids is not functioning when the blood sugar concentration begins to decrease as a consequence of deficient nutrition.

The Fetal Alcohol Syndrome is a condition where children with a set of facial characteristics, short stature and thin complexion, all of which give them a special appearance, are a consequence of alcohol abuse before and after birth. Growth deficiency, typical facial features and damage to the central nervous system are the characteristics of this disease.

It is observed that an improvement in the environment is accompanied by social and functional improvement of these people. A follow-up study carried out among adolescents and adults diagnosed early with Fetal Alcohol Syndrome shows the importance of a stable, consistent and structured home in the development of personality characteristics, which facilitate the optimal use of each child's potential.

Alcohol has been found to decrease the rate of contraction of the heart muscle in healthy animals. The heart becomes less efficient as a pump because the force of each contraction and increase in pressure in the left ventricle are less.

The increase in heart rate is greater if you give alcohol to healthy people before exercising, but the recovery period is longer if you don't. In alcoholics, alcohol decreases the functioning of the left ventricle, increases its diastolic pressure and decreases cardiac contraction.

Studies done on animals and humans show that when alcohol is consumed, the cells of the heart release a number of chemicals. The findings can be seen as a consequence of alcohol's toxic action on the myocardium.

Alcoholic cardiomyopathy is a syndrome of cardiac function in which the disease settles in the heart muscle, and the rest of the cardiovascular system is relatively healthy.

Symptoms of alcoholic cardiomyopathy include arrhythmias or heart failure, decreased exercise tolerance, and palpitations.

Aspiration pneumonitis is one of the most common respiratory problems caused by alcohol consumption.

Likewise, excessive alcohol consumption can cause gastrointestinal problems such as halitosis (mouth), acute and chronic pharyngitis (pharynx), acute and chronic esophagitis, esophageal varices (esophagus), hemorrhagic gastritis and peptic ulcer (stomach and duodenum), pancreatitis. acute (pancreas), fatty infiltration of the liver, alcoholic hepatitis and cirrhosis (liver).

The effects of alcohol depend on how much is concentrated in body fluids or in the blood.

When compared with the total volume of liquid that exists in the body, from 0.05% to 0.10% of its concentration in the blood, a sensation of relaxation, sedation and euphoria is produced due to the disinhibition it produces; for this reason, it is mistakenly considered as a stimulant (Souza and Macharro, 1988). Alcohol is a depressant of the central nervous system, and it disinhibits the individual and then depresses him, according to the CEDA.

When the level of alcohol concentration in the blood oscillates between 0.10% and 0.20%, most drinkers show signs of intoxication, a physical and mental impairment occurs that affects perception and motor performance, muscle coordination deteriorates, judgment is affected, reactions to stimuli are delayed, alterations appear in visual and auditory discrimination, language becomes confused, the person sometimes becomes foolish, scandalous, melancholic or aggressive, there is an exaggerated confidence in the own abilities (hence the risk of accident), antisocial behaviors manifest, or in certain cases the intoxicated individual isolates himself silently. It is important to point out that the same individual can manifest all of this range of behaviors.

Before concentrations greater than 0.20%, the person is seriously sedated, they will not perceive what is happening around them, they will not be able to stand up or remain alert; if the concentration exceeds 0.40%, the individual enters a coma, from then on and up to 0.60% is in danger of death, since respiratory and circulatory functions can stop (Souza and Macharro, 1988; Swonger and Constantine, 1985). It is important to take into account that the body has to eliminate between 5 and 10% of the alcohol through breathing, urine and sweat, since it is the only way to fully absorb the alcohol.

The most sensitive system to alcohol is the central nervous system. Its consumption produces similar effects to other drugs.

Alcohol modifies human behavior at the level of motor coordination, but also at the level of perceptual and cognitive level, and significantly influences the performance of the individual.

Sexual behavior and aggressiveness can be affected by alcohol consumption.

conclusions.

The central nervous system is sensitive to alcohol. There is a dose dependent general depression, which begins with mild sedation and progresses to anesthesia, coma, and even death.

Depression of brain areas responsible for inhibitory mechanisms is what leads to the stimulating properties attributed to alcohol.

Some parts of the brain are released from the brake.

Thought flows freely, but in a disorderly and chaotic way as a consequence of this. The cerebral cortex is affected by blood alcohol levels, resulting in impairment of judgement, and poor attention. Alcohol in the blood causes other cortical regions to be depressed, including blunted sensitivity, aparaxia, and double vision.

A lack of balance can be caused by the brain.

The alcoholic becomes self-assured and assertive when they drink.

Motor skills are almost completely reduced despite increased confidence

Respiratory depression occurs when there is acute poisoning, requiring artificial respiration, anlepatics and caffeine to counteract it.

It helps to suppress pain if alcohol is used as a sedative. In the sexual aspect, alcohol increases libido.

The cardiovascular system is affected in moderate doses and can cause a variety of symptoms.

Alcohol causes irritation of the stomach lining and chronic gastritis by stimulating salivary fluids. Chronic pancreatitis can be worsened by alcohol.

The authors listed the five basic actions of alcohol on the nervous system.

The amount of alcohol in the blood and the duration of alcohol consumption have a direct relationship with each other.

The vision of some drinkers has been altered even during periods of abstinence because of the damages of alcohol.

A person with mild alcohol intoxication has problems driving a vehicle because they have a reduced ability to judge and reason through visual, auditory, and any type of stimuli that are usually encountered by drivers. excessive consumption of alcohol is a factor in many deaths.

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