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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Effects Of Clinically Relevant Acute Hypercapnic And Metabolic Acidosis On The Cardiovascular System: An Experimental Porcine Study
Effects of clinically relevant acute hypercapnic and metabolic acidosis on the cardiovascular system: an experimental porcine study Stengl et al.; licensee BioMed Central Ltd.2013 Hypercapnic acidosis (HCA) that accompanies lung-protective ventilation may be considered permissive (a tolerable side effect), or it may be therapeutic by itself. Cardiovascular effects may contribute to, or limit, the potential therapeutic impact of HCA; therefore, a complex physiological study was performed in healthy pigs to evaluate the systemic and organ-specific circulatory effects of HCA, and to compare them with those of metabolic (eucapnic) acidosis (MAC). In anesthetized, mechanically ventilated and instrumented pigs, HCA was induced by increasing the inspired fraction of CO2 (n = 8) and MAC (n = 8) by the infusion of HCl, to reach an arterial plasma pH of 7.1. In the control group (n = 8), the normal plasma pH was maintained throughout the experiment. Hemodynamic parameters, including regional organ hemodynamics, blood gases, and electrocardiograms, were measured in vivo. Subsequently, isometric contractions and membrane potentials were recorded in vitro in the right ventricular trabeculae. HCA affected both the pulmonary (increase in mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance (PVR)) and systemic (increase in mean arterial pressure (MAP), decrease in systemic vascular resistance (SVR)) circulations. Although the renal perfusion remained unaffected by any type of acidosis, HCA increased carotid, portal, and, hence, total liver blood flow. MAC influenced the pulmonary circulation only (increase in MPAP and PVR). Both MAC and HCA reduced the stroke volume, which was compensated for by an increase in heart rate to maintain (MAC), or even increase (HCA), Continue reading >>
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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 >>
Acidosis - Causes And Effects
Acidosis - A medical condition in which the acid-base balance in the blood plasma is disturbed in the direction of excess acidity, the pH falling below 7.35. Over acidity, which can become a dangerous condition that weakens all body systems, is very common today. It gives rise to an internal environment conducive to disease, as opposed to a pH-balanced environment which allows normal body function necessary for the body to resist disease. A healthy body maintains adequate alkaline reserves to meet emergency demands. When excess acids (acidosis) must be neutralized, our alkaline reserves are depleted, leaving the body in a weakened condition. Every day we wage our own private war against molds, yeasts, bacteria, viruses and fungi. By using antibiotics as the first line of defense we have encouraged the development of more powerful deadly bugs and bacteria. Our immune systems are becoming weaker and over-taxed in this war. Louis Pasteur declared the germ theory of disease that states germs are the cause of disease. But note Dr. Pasteur's dying words: "The germ is nothing, the inner terrain is everything". The concept of acid alkaline imbalance as the cause of disease is not new. In 1933 a New York doctor named William Howard Hay published a ground-breaking book, A New Health Era in which he maintains that all disease is caused by autotoxication (or "self-poisoning") due to acidosis in the body. Now we depart from health in just the proportion to which we have allowed our alkalis to be dissipated by introduction of acid-forming food in too great amount... It may seem strange to say that all disease is the same thing, no matter what its myriad modes of expression, but it is verily so. More recently, in his remarkable book Alkalize or Die , Dr. Theodore A. Baroody says esse 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 >>
Acidosis - An Overview | Sciencedirect Topics
Acidosis is an important prognostic factor in survival from respiratory failure during COPD exacerbation, and thus early correction of acidosis is an essential goal of therapy. Katherine Ahn Jin, in Comprehensive Pediatric Hospital Medicine , 2007 Acidosis is defined as an abnormal clinical process that causes a net gain in hydrogen ions (H+) in the extracellular fluid. Metabolic acidosis occurs when there is an accumulation of H+ or a loss of bicarbonate ions (HCO3) and is reflected by a decrease in plasma HCO3 (<22 mEq/L). Respiratory acidosis occurs when there is an accumulation of carbon dioxide (CO2) and is reflected by an increase in the arterial partial pressure of carbon dioxide (Pco2 >40 mm Hg). Clinically, acid-base scenarios can involve a primary acidosis or alkalosis with or without compensation, or a mixed acid-base disorder. The pH reflects the net effect of these processes (Fig. 27-1). The term acidemia is defined as an abnormal decrease in blood pH (<7.37). Sharma S. Prabhakar M.D., M.B.A., F.A.C.P., F.A.S.N., in Medical Secrets (Fifth Edition) , 2012 What is the conceptual difference between an AG and a non-AG metabolic acidosis? An AG acidosis is caused by the addition of a nonvolatile acid to the ECF. Examples include diabetic ketoacidosis, lactic acidosis, and uremic acidosis. A non-AG acidosis commonly (but not exclusively) represents a loss of . Examples include lower GI losses from diarrhea and urinary losses due to renal tubular acidosis (RTA). Therefore, when approaching a patient with an AG acidosis, one should look for the source and identity of the acid gained. By contrast, when evaluating a patient with a non-AG acidosis, one should begin by looking for the source of the Mario G. Bianchetti, Alberto Bettinelli, in Comprehensive Pediatric Ne Continue reading >>
When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s processes produce acid. Your lungs and kidneys can usually compensate for slight pH imbalances, but problems with these organs can lead to excess acid accumulating in your body. The acidity of your blood is measured by determining its pH. A lower pH means that your blood is more acidic, while a higher pH means that your blood is more basic. The pH of your blood should be around 7.4. According to the American Association for Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight, these numerical differences can be serious. Acidosis can lead to numerous health issues, and it can even be life-threatening. There are two types of acidosis, each with various causes. The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, depending on the primary cause of your acidosis. Respiratory acidosis Respiratory acidosis occurs when too much CO2 builds up in the body. Normally, the lungs remove CO2 while you breathe. However, sometimes your body can’t get rid of enough CO2. This may happen due to: chronic airway conditions, like asthma injury to the chest obesity, which can make breathing difficult sedative misuse deformed chest structure Metabolic acidosis Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t eliminate enough acid or when they get rid of too much base. There are three major forms of metabolic acidosis: Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your body lacks enough insulin, keton Continue reading >>
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 >>
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 >>
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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Acute Effects Of Acidosis On Protein And Amino Acid Metabolism In Perfused Rat Liver
Acute effects of acidosis on protein and amino acid metabolism in perfused rat liver 1Department of Physiology, Charles University Prague, Hradec Krlov, Czech Republic 2Department of Pharmacology, Charles University Prague, Hradec Krlov, Czech Republic 3University Hospital Motol, Prague, Czech Republic Correspondence: Dr Milan Holeek, Department of Physiology, Charles University Medical Faculty, imkova 870, 500 38 Hradec Krlov, Czech Republic. Tel.:/Fax: +420 49 5518190; E-mail: [email protected] Received 2003 Feb 5; Accepted 2003 Aug 1. Copyright 2003 Blackwell Publishing Ltd This article has been cited by other articles in PMC. Acidosis is frequently associated with protein wasting and derangements in amino acid metabolism. As its effect on protein metabolism is significantly modulated by other abnormal metabolic conditions caused by specific illnesses, it is difficult to separate out the effects on protein metabolism solely due to acidosis. The aim of the present study was to evaluate, using a model of isolated perfused rat liver, the direct response of hepatic tissue to acidosis. We have compared hepatic response to perfusion with a solution of pH 7.2 and 7.4 (controls). Parameters of protein and amino acid metabolism were measured using both recirculation and single-pass technique with 4,5-[3H]leucine, [114C]leucine and [114C]ketoisocaproate (ketoleucine) as tracers and on the basis of difference of amino acid levels in perfusion solution at the beginning and end of perfusion. In liver perfused with a solution of pH 7.2, we observed higher rates of proteolysis, protein synthesis, amino acid utilization and urea production. Furthermore, the liver perfused with a solution of pH 7.2 released a higher amount of proteins to perfusate than the liver perfused with a s 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 >>
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 >>
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 >>
Effects Of Acute Alkalosis And Acidosis On Performance: A Meta-analysis.
Sports Med. 2011 Oct 1;41(10):801-14. doi: 10.2165/11591440-000000000-00000. Effects of acute alkalosis and acidosis on performance: a meta-analysis. Physiology, Australian Institute of Sport, Canberra, ACT, Australia. [email protected] Ingestion of agents that modify blood buffering action may affect high-intensity performance. Here we present a meta-analysis of the effects of acute ingestion of three such agents - sodium bicarbonate, sodium citrate and ammonium chloride - on performance and related physiological variables (blood bicarbonate, pH and lactate). A literature search yielded 59 useable studies with 188 observations of performance effects. To perform the mixed-model meta-analysis, all performance effects were converted into a percentage change in mean power and were weighted using standard errors derived from exact p-values, confidence limits (CLs) or estimated errors of measurement. The fixed effects in the meta-analytic model included the number of performance-test bouts (linear), test duration (log linear), blinding (yes/no), competitive status (athlete/nonathlete) and sex (male/female). Dose expressed as buffering mmoL/kg/body mass (BM) was included as a strictly proportional linear effect interacted with all effects except blinding. Probabilistic inferences were derived with reference to thresholds for small and moderate effects on performance of 0.5% and 1.5%, respectively. Publication bias was reduced by excluding study estimates with a standard error >2.7%. The remaining 38 studies and 137 estimates for sodium bicarbonate produced a possibly moderate performance enhancement of 1.7% (90% CL 2.0%) with a typical dose of 3.5 mmoL/kg/BM (0.3 g/kg/BM) in a single 1-minute sprint, following blinded consumption by male athletes. In the 16 studies and 4 Continue reading >>
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