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 >>
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 >>
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 >>
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 >>
Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Adverse Effects Of Metabolic Acidosis
Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) 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 >>
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 >>
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 >>
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 >>
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 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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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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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 >>
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 >>
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 >>