Effects Of Acidosis On Rat Muscle Metabolism And Performance During Heavy Exercise.
Effects of acidosis on rat muscle metabolism and performance during heavy exercise. Am J Physiol. 1985 Mar;248(3 Pt 1):C337-47. The metabolism and performance of a perfused rat hindquarter preparation was examined during heavy exercise in three conditions: control (C), metabolic acidosis (MA, decreased bicarbonate concentration), and respiratory acidosis (RA, increased CO2 tension). A one-pass system was used to perfuse the hindquarters for 30 min at rest and 20 min during tetanic stimulation via the sciatic nerve. The isometric tension generated by the gastrocnemius-plantaris-soleus muscle group was recorded, and biopsies were taken pre- and postperfusion. Initial isometric tensions were similar in all conditions, but the rate of tension decay was largest in acidosis; the 5-min tensions for C, MA, and RA were 1,835 +/- 63, 1,534 +/- 63, and 1,434 +/- 73 g, respectively. O2 uptake in C was greater than in MA and RA (23.4 +/- 1.3 vs. 17.0 +/- 1.4 and 16.5 +/- 2.3 mumol X min-1), paralleling the tension findings. Hindquarter lactate release was greatest in C, least in MA, and intermediate in RA. Acidosis resulted in less muscle glycogen utilization and lactate accumulation than during control. Muscle creatine phosphate utilization and ATP levels were unaffected by acidosis. Acidosis decreased the muscle's ability to generate isometric tension and depressed both aerobic and anaerobic metabolism. During stimulation in this model lactate left the muscle mainly as a function of the production rate, although a low plasma bicarbonate concentration at pH 7.15 depressed muscle lactate release. Continue reading >>
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Effects Of Metabolic And Respiratory Acidosis On Bone.
1. Curr Opin Nephrol Hypertens. 1993 Jul;2(4):588-96. Effects of metabolic and respiratory acidosis on bone. (1)University of Rochester School of Medicine and Dentistry, Strong Memorial Hospital, NY 14642. Acidosis had long been thought to influence the bone mineral; however, there was little direct evidence to support this impression. When neonatal mouse calvariae are cultured for 3 hours in medium with a reduced bicarbonate concentration, amodel of acute metabolic acidosis, there is net calcium efflux from bone inaddition to a net influx of protons into bone lessening the magnitude of theacidosis. The protons appear to exchange for sodium and potassium on the bonesurface. In these acute experiments, the calcium efflux appears to be due tomobilization of carbonated apatite through an alteration in the physicochemicaldriving forces for bone accretion and dissolution. In more chronic cultures(greater than 48 hours) metabolic acidosis induces calcium efflux by stimulating osteoclastic bone resorption and inhibiting osteoblastic bone formation. Whencalvariae are cultured acutely in medium with an elevated partial pressure ofcarbon dioxide, a model of respiratory acidosis, there is also calcium efflux,but at the same decrement in pH the magnitude is far less than that observedduring metabolic acidosis. There does not appear to be any measurable influx ofprotons into bone, and during chronic cultures there is no measurable calciumefflux. Thus, acidosis influences the bone mineral; however, for the samedecrement in pH there is a marked difference in the response of bone to models ofmetabolic and respiratory acidosis. Continue reading >>
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Merck And The Merck Manuals
Acidosis is caused by an overproduction of acid in the blood or an excessive loss of bicarbonate from the blood (metabolic acidosis) or by a buildup of carbon dioxide in the blood that results from poor lung function or depressed breathing (respiratory acidosis). If an increase in acid overwhelms the body's acid-base control systems, the blood will become acidic. As blood pH drops (becomes more acidic), the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing (respiratory compensation). Breathing faster and deeper increases the amount of carbon dioxide exhaled. The kidneys also try to compensate by excreting more acid in the urine. However, both mechanisms can be overwhelmed if the body continues to produce too much acid, leading to severe acidosis and eventually heart problems and coma. The acidity or alkalinity of any solution, including blood, is indicated on the pH scale. Metabolic acidosis develops when the amount of acid in the body is increased through ingestion of a substance that is, or can be broken down (metabolized) to, an acid—such as wood alcohol (methanol), antifreeze (ethylene glycol), or large doses of aspirin (acetylsalicylic acid). Metabolic acidosis can also occur as a result of abnormal metabolism. The body produces excess acid in the advanced stages of shock and in poorly controlled type 1 diabetes mellitus (diabetic ketoacidosis). Even the production of normal amounts of acid may lead to acidosis when the kidneys are not functioning normally and are therefore not able to excrete sufficient amounts of acid in the urine. Major Causes of Metabolic Acidosis Diabetic ketoacidosis (buildup of ketoacids) Drugs and substances such as acetazolamide, alcohols, and aspirin Lactic acidosis (buildup of lactic acid Continue reading >>
What Is Acidosis? Acidosis Causes & Treatment | High Alkaline Diet
DEFINITION: Acidosis is an increased acidity in the blood and other body tissue. Acidosis is said to occur when arterial pH falls below 7.35. The pH level of our blood affects every cell in our body. Chronic acidosis corrodes body tissue, and if left unchecked, will interrupt all cellular activities and functions. HIGH ACID-FORMING FOODS and DIETS all lead to ACIDOSIS. Living a fast-paced daily lifestyle, such as eating on the run, will lead people to face constant symptoms of indigestion and growing endangerment of over-acidification (Acidosis) of the body cells, which will interrupt cellular activities and functions. It is a major root of sickness and disease. Having our cells constantly exposed to an acidic environment leads to acidosis and then chronic acidosis and, finally, various forms of disease such as cancer and many more! Studies have shown that an acidic, anaerobic (which is also the lack of oxygen) body environment encourages the breeding of fungus, mold, bacteria, and viruses. As a result, our inner biological terrain shifts from a healthy oxygenated, alkaline environment to an unhealthy acidic one (acidic pH scale). This forces the body to constantly deplete its cellular energy to neutralize and detoxify these acids before they can act as poisons in and around the cells, ultimately changing the environment of each cell and finally compromising its immune system, leaving it vulnerable to the ravages of disease to take a foothold in the body. When our body pH becomes overly acidic, it starts to set up defense mechanisms to keep the damaging acids from entering the vital organs. Modern Day Athletes and Acid-Forming Foods Unfortunately, Modern Day Athletes and/or Non-Athletes have been raised in a fast food environment that is more concerned about convenienc Continue reading >>
Effects Of Acidosis On Brain Capillary Endothelial Cells And Cholinergic Neurons: Relevance To Vascular Dementia And Alzheimer's Disease.
Effects of acidosis on brain capillary endothelial cells and cholinergic neurons: relevance to vascular dementia and Alzheimer's disease. Laboratory of Experimental Alzheimer's Research, Department of General Psychiatry, Innsbruck Medical University, Austria. Alzheimer's disease is a progressive brain disorder which is neuropathologically characterized by an increased number of beta-amyloid plaques, tau pathology and synapse loss. Recent research suggests that vascular pathology may be also important for the development and progression of Alzheimer's disease. It is still unknown whether there is a relation between damage of brain capillary endothelial cells (BCEC) and subsequent cholinergic cell death. The aim of this study was to examine the effects of acidosis on cell death of BCEC and cholinergic neurons in an organotypic brain slice model. We show that BCEC were heavily damaged in medium at pH<6.6. Cholinergic neurons incubated in medium pH 6.0 degenerated within 2-3 days and were not rescued by nerve growth factor (NGF). Lactate did not affect the survival of BCEC or cholinergic neurons. Both BCEC and cholinergic cells were not affected at pH 7.4, 7.0 or 6.6. It is concluded that both endothelial cells and cholinergic neurons have a high capacity to compensate for pH changes. At a certain pH, however, the vascular and neuronal cells show the same vulnerability, indicating that a low pH is deleterious for the cerebral microenvironment. Future studies are necessary to explore whether temporary pH changes could be responsible for cerebrovascular damage and cholinergic cell death. Acidosis may play an important role in the development of vascular dementia and Alzheimer's disease. Continue reading >>
Respiratory Acidosis: Causes, Symptoms, And Treatment
Respiratory acidosis develops when air exhaled out of the lungs does not adequately exchange the carbon dioxide formed in the body for the inhaled oxygen in air. There are many conditions or situations that may lead to this. One of the conditions that can reduce the ability to adequately exhale carbon dioxide (CO2) is chronic obstructive pulmonary disease or COPD. CO2 that is not exhaled can shift the normal balance of acids and bases in the body toward acidic. The CO2 mixes with water in the body to form carbonic acid. With chronic respiratory acidosis, the body partially makes up for the retained CO2 and maintains acid-base balance near normal. The body's main response is an increase in excretion of carbonic acid and retention of bicarbonate base in the kidneys. Medical treatment for chronic respiratory acidosis is mainly treatment of the underlying illness which has hindered breathing. Treatment may also be applied to improve breathing directly. Respiratory acidosis can also be acute rather than chronic, developing suddenly from respiratory failure. Emergency medical treatment is required for acute respiratory acidosis to: Regain healthful respiration Restore acid-base balance Treat the causes of the respiratory failure Here are some key points about respiratory acidosis. More detail and supporting information is in the main article. Respiratory acidosis develops when decreased breathing fails to get rid of CO2 formed in the body adequately The pH of blood, as a measure of acid-base balance, is maintained near normal in chronic respiratory acidosis by compensating responses in the body mainly in the kidney Acute respiratory acidosis requires emergency treatment Tipping acid-base balance to acidosis When acid levels in the body are in balance with the base levels in t Continue reading >>
For acidosis referring to acidity of the urine, see renal tubular acidosis. "Acidemia" redirects here. It is not to be confused with Academia. Acidosis is a process causing increased acidity in the blood and other body tissues (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma. The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH. Acidosis is said to occur when arterial pH falls below 7.35 (except in the fetus – see below), while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes. The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g., healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage. Signs and symptoms General symptoms of acidosis. These usually accompany symptoms of another primary defect (respiratory or metabolic). Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen i Continue reading >>
Effects Of Metabolic Acidosis On Viability Of Cells Exposed To Anoxia.
1. Am J Physiol. 1985 Jul;249(1 Pt 1):C149-59. Effects of metabolic acidosis on viability of cells exposed to anoxia. The effects of metabolic acidosis were examined in isolated rat hepatocytes undersubstrate-free oxygenated or anoxic conditions. Lowering extracellular pH to 6.6 under aerobic conditions had no deleterious effects on the cells as determined bytrypan blue exclusion, lactate dehydrogenase (LDH) release, cellular K+ and Ca2+ content, and ability to increase ATP levels after nutrients and adenosine wereadded to media. Cytosolic pH was measured in aerobic cells at varyingextracellular pH using 6-carboxyfluorescein. By using values for cytosolic pHobtained in this manner together with 5,5-dimethyl[2-14C]oxazolidine-2,4-dione(DMO) distribution data, a method was derived for determining intramitochondrial pH. The pH gradient across the mitochondrial membrane was found not to changewith a decrease in extracellular pH from 7.4 to 6.9. At pH 6.9 hepatocytes wereprotected against anoxic injury as compared with cells incubated at pH 7.5 or6.6. This protection was manifested by a decrease in vital dye uptake and LDHrelease, maintenance of higher cellular K+ content, less stimulation ofrespiration with succinate, improved recovery of ATP levels after return to anoxygenated nutrient environment, and maintenance of normal cellular Ca2+ content after reoxygenation. Recovery of cellular ATP content was independent of ATPlevels, total adenine nucleotide pool, and energy charge ratio at the end of the anoxic period. Measurement of cytoplasmic pH in anaerobic cells by [14C]DMOdistribution showed progressive cellular acidification with lowering ofextracellular pH. The protective effects observed at pH 6.9 are not unique tohepatocytes since isolated renal cortical tubules expo Continue reading >>
Effects Of Acidosis And Alkalosis On Hypoxic Pulmonary Vasoconstriction In Dogs.
Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs. Laboratory of Cardiovascular and Respiratory Physiology, Erasme University Hospital, Brussels, Belgium. Am J Physiol. 1990 Feb;258(2 Pt 2):H347-53. We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2. Continue reading >>
The Effects Of Extracellular Acidosis On Neurons And Glia In Vitro.
1. J Cereb Blood Flow Metab. 1989 Aug;9(4):471-7. The effects of extracellular acidosis on neurons and glia in vitro. Goldman SA(1), Pulsinelli WA, Clarke WY, Kraig RP, Plum F. (1)Department of Neurology, Cornell University Medical College, New York 10021. Cerebral lactic acid, a product of ischemic anaerobic glycolysis, may directlycontribute to ischemic brain damage in vivo. In this study we evaluated theeffects of extracellular acid exposure on 7-day-old cultures of embryonic ratforebrain. Mixed neuronal and glial cultures were exposed to either lactic orhydrochloric acid to compare the toxicities of relatively permeable andimpermeable acids. Neurons were relatively resistant to extra-cellular HClacidosis, often surviving 10-min exposures to pH 3.8. In the same cultures,immunochemically defined astrocytes survived 10-min HCl exposures to a maximumacidity of pH 4.2. Similarly, axonal bundles defasciculated in HCl-titrated mediabelow pH 4.4, although their constituent fibers often survived pH 3.8. Cell deathoccurred at higher pH in cultures subjected to lactic acidosis than in thoseexposed to HCl. Over half of forebrain neurons and glia subjected for 10 min tolactic acidification failed to survive exposure to pH 4.9. Longer 1-h lactic acidincubations resulted in cell death below pH 5.2. The potent cytotoxicity oflactic acid may be a direct result of the relatively rapid transfer of itsneutral protonated form across cell membranes. This process would rapidly depleteintracellular buffer stores, resulting in unchecked cytosolic acidification.Neuronal and glial death from extracellular acidosis may therefore be a function of both the degree and the rapidity of intracellular acidification. Continue reading >>
5.4 Metabolic Acidosis - Metabolic Effects
5.4 Metabolic Acidosis - Metabolic Effects A metabolic acidosis can cause significant physiological effects, particularly affecting the respiratory and cardiovascular systems. Hyperventilation ( Kussmaul respirations ) - this is the compensatory response Shift of oxyhaemoglobin dissociation curve (ODC) to the right Decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) Sympathetic overactivity (incl tachycardia, vasoconstriction,decreased arrhythmia threshold) Resistance to the effects of catecholamines Increased bone resorption (chronic acidosis only) Shift of K+ out of cells causing hyperkalaemia 5.4.2 Some Effects have Opposing Actions. The cardiac stimulatory effects of sympathetic activity and release of catecholamines usually counteract the direct myocardial depression while plasma pH remains above 7.2. At systemic pH values less than this, the direct depression of contractility usually predominates. The direct vasodilatation is offset by the indirect sympathetically mediated vasoconstriction and cardiac stimulation during a mild acidosis. The venoconstriction shifts blood centrally and this causes pulmonary congestion. Pulmonary artery pressure usually rises during acidosis. The shift of the oxygen dissociation curve to the right due to the acidosis occurs rapidly. After 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Acidosis is commonly said to cause hyperkalaemia by a shift of potassium out of cells. The effect on potassium levels is extremely variable and indirect effects due to the type of acidosis present are much more important. For example hyperkalaemia is due to renal failure in uraemic acidosis rather than the acidosis. Significant potassium loss du Continue reading >>
Effects Of Acidosis On Ventricular Muscle From Adult And Neonatal Rats.
Effects of acidosis on ventricular muscle from adult and neonatal rats. Department of Physiology, University College London, England. We compared the response of ventricular muscle from adult and neonatal rats to hypercapnic acidosis. In adult muscle, acidosis caused an initial rapid fall of developed tension to 30 +/- 5% of control (mean +/- SEM, n = 6). However, tension recovered slowly to a steady state that was 56 +/- 6% of control. In neonatal muscle, acidosis caused a significantly smaller initial fall in tension to 43 +/- 3% (n = 8, p less than 0.05), but the tension then showed a subsequent slower fall to a steady state that was 29 +/- 4% of control, significantly less than in the adult (p less than 0.01). We have attempted to identify the mechanisms underlying these differences in response. In detergent-skinned myofibrils, reducing the pH from 7.0 to 6.5 caused a reduction in the pCa50 of 0.61 units in the adult muscle, but only 0.27 units in the neonatal ventricular muscle. Myofibrillar Ca2+ sensitivity in neonatal ventricular muscle is thus less susceptible to the effects of acidic pH than that of adult muscle. Since intracellular pH decreases rapidly on application of increased external CO2, these results are consistent with the finding that, initially, developed tension in neonatal muscles is less sensitive to the effects of acidosis. Sodium dodecylsulfate gel electrophoresis of myofibrillar preparations from adult and neonatal rats demonstrated differences in thin filament proteins, including troponin I, which may underlie the observed differences in Ca2+ sensitivity. In adult rat ventricular muscles, the slow recovery of tension during acidosis is associated with an increase in the amplitude of the Ca2+ transients to 263 +/- 34% of control (n = 4).(ABSTR Continue reading >>
Physiological Effects Of Hyperchloraemia And Acidosis
Physiological effects of hyperchloraemia and acidosis Chelsea and Westminster NHS Foundation Trust Chelsea and Westminster NHS Foundation Trust BJA: British Journal of Anaesthesia, Volume 101, Issue 2, 1 August 2008, Pages 141150, J. M. Handy, N. Soni; Physiological effects of hyperchloraemia and acidosis, BJA: British Journal of Anaesthesia, Volume 101, Issue 2, 1 August 2008, Pages 141150, The advent of balanced solutions for i.v. fluid resuscitation and replacement is imminent and will affect any specialty involved in fluid management. Part of the background to their introduction has focused on the non-physiological nature of normal saline solution and the developing science about the potential problems of hyperchloraemic acidosis. This review assesses the physiological significance of hyperchloraemic acidosis and of acidosis in general. It aims to differentiate the effects of the causes of acidosis from the physiological consequences of acidosis. It is intended to provide an assessment of the importance of hyperchloraemic acidosis and thereby the likely benefits of balanced solutions. Hyperchloraemic acidosis is increasingly recognized as a clinical entity, a new enemy within, that had gone otherwise unnoticed for decades. Although any associated morbidity may be subtle at present, there is a trend in current evidence to suggest that hyperchloraemic acidosis may have adverse consequences which may be circumvented by the use of balanced solutions. These consequences, both theoretical and clinical, may result from hyperchloraemia, acidosis, or both. There is some evidence of hyperchloraemia causing problems, but at present the clinical relevance is uncertain. The literature does appear to be unified in stating that acidosis results in adverse physiological effects bu Continue reading >>
Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>
The Effects Of Acidosis And Alkalosis On Long Bone Vascular Resistance.
The effects of acidosis and alkalosis on long bone vascular resistance. Mayo Graduate School of Medicine, Rochester, Minnesota. This study used an ex vivo perfusion model to investigate the direct effects of acidosis and alkalosis on the vascular resistance of the canine tibia. Baseline vascular resistance (BVR) and the vascular smooth muscle response to bolus doses of norepinephrine (NE) (0.025-3.2 nmol) and periarterial sympathetic nerve stimulation (NS) (10-25 Hz: 9 V, 2 ms pulses, 10 s) were studied. In Group I, these parameters were measured at normal pH (duration 7.34-7.44) and then during acidosis (pH 7.2-7.33). In Group II, they were measured at normal pH and then during alkalosis (pH 7.47-7.58). In Group III (control), they were measured serially at a normal pH. Alkalosis increased BVR by 56% (p < 0.0001). Acidosis attenuated (18% reduction) and alkalosis enhanced (66% increase) the vasoconstrictor action of NE (p < 0.0001). Acidosis also attenuated (11% reduction) the effect of sympathetic NS (p = 0.012). It is concluded that perfusion pH influences the sensitivity of long bone resistance vessels to circulating NE and sympathetic NS. Thus, local concentration of hydrogen ions may provide bone with a mechanism to autoregulate blood flow. Continue reading >>