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Query: UMLS:C0002063 (alkalosis)
 2,286 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Contractile performance of ischemic feline myocardium was evaluated under conditions of selective changes in perfusate in pH and pCO2. A substantial increase in myocardial performance was noted when the pCO2 was lowered at constant pH, and depression of performance was noted when the pCO2 was increased at constant pH. Perfusate acidosis at constant pCO2 resulted in depression of performance and decreased performance only after 20 min of exposure. Alkalosis did not increase performance and decreased performance transiently during mild ischemia. These studies suggest that performance of myocardium during ischemia is closely related to tissue pCO2 and is minimally related to the level of extracellular pH.
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PMID:Effects of pH and pCO2 on performance of ischemic myocardium. 0 32

The purpose of this study was to examine the magnitude of the influence of coronary arterial pH (pHa) on myocardial oxygen uptake (MV 02). In order to isolate and control the recognized determinants of MV02, a perfused heart preparation was developed which permitted control of heart rate and pressure and flow work. A perfusion system was used which allowed independent regulation of O2 N2 and CO2 flow to a membrane lung and precise control of coronary blood flow. Myocardial oxygen delivery (Ca02 x flow) could be held constant (+/- 1%) during 4 hours of perfusion. Catheter decompression of both ventricles prevented any external pressure or flow work. Blood temperature was maintained at 37.27 +/- 0.07degrees C. Perfusing blood pH was related initially to spontaneous heart rate in five dogs: pulse = 82 pH - 487. In 12 subsequent animals heart rate was fixed. MV02 was directly and significantly related to coronary arterial pH in all animals studied: MVO2% = 109 pH - 143 (r = 0.823). An increase in pHa of 0.1 will increase MV02 by 10.9%. This study isolates pH as a determinant of myocardial oxygen uptake and indicates that progressive alkalosis induces increased myocardial oxygen uptake. This must be recognized in the treatment of patients with compromised myocardial function and rerional areas of ischemia.
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PMID:The influence of coronary arterial pH on myocardial oxygen demand. 1 52

Intracellular acidosis may depress myocardial function and metabolism during ischemia. In the present study, the function and metabolism of a globally ischemic, isovolumic cat left ventricle preparation, perfused with oxygenated Krebs-Ringer biocarbonate solution, was examined. Addition of tris(hydroxymethyl)-aminomethane (Tris) (15 mM) to the perfusate at physiologic pH and PCO2 increased performance during ischemia to a greater extent and for a longer period than low PCO2 )15 mmHg), alkalotic (pH, 7.8) perfusate and a control sucrose perfusate. Under nonischemic conditions the inotropic effect of Tris was only briefly greater than sucrose perfusate. The inotropic effect of Tris during ischemia did not appear to depend on changes in coronary flow, oxygen consumption, sodium concentration, perfusate osmolality, or catecholamine release. During ischemia, lactate production was unchanged with Tris, but increased with low PCO2-alkalosis. Tissue levels of ATP and creatine phosphate for control ischemic hearts did not differ from Tris-perfused or low PCO2-alkalosis hearts. Thus, Tris appears to exert an inotropic effect that is more prominent in ischemic than nonischemic myocardium. The results are consistent with the possibility that Tris acts as an intracellular buffer to increase the efficiency of energy production and/or utilization during ischemia.
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PMID:Effect of tris(hydroxymethyl)aminomethane on ischemic myocardium. 68 84

Isolated working rat hearts were made ischemic for 5, 10, and 30 minutes respectively. After the ischemic period, all hearts were perfused in a retrograde nonworking way for 30 minutes. During the 5 first minutes of ischemia, there was a marked fall of cardiac output and coronary flow. A significant release of GOT was seen and this was more marked after longer periods of ischemia. Addition of adrenaline to the perfusate increased the enzyme release. Pacing at 400/minute, high preload, high afterload, acidosis, or alkalosis did not alter enzyme release. Glycogen, ATP and CrP levels were depressed at the end of the ischemic period, but were seen to be rising again during the retrograde perfusion. This study indicates that myocardial tissue may release enzymes without being irreversibly damaged.
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PMID:Myocardial enzyme release from ischemic isolated perfused working rat heart. 120 85

This article attempts correlating changes in cellular energy metabolism, acid-base alterations, and ion homeostasis in ischemia and other conditions. It is emphasized that loss of ion homeostasis, with thermodynamically downhill fluxes of K+, Ca2+, Na+, Cl-, and H+, occurs because energy production fails and (or) ion conductances are increased. In ischemia, energy failure is the leading event but, in hypoglycemia, activation of ion conductances is what precipitates energy failure. The initial event is a rise in K+ e, at least in part caused by activation of K+ conductances modulated by Ca2+ or ATP/ADP ratio. Secondarily, this leads to release of excitatory amino acids and massive activation of unspecific cation (and anion) conductances. Production of H+ occurs in states characterized by energy failure (ischemia and hypoxia) or by alkalosis (hypocapnia and ammonia accumulation). H+ equilibrates between intra- and extra-cellular fluid via nonionic diffusion of lactic acid, and transmembrane fluxes of H+ or HCO3- via ion channels. Since the relationship between lactate and either pHi or pHe is linear, there are no abrupt pH shifts explaining why hyperglycemia worsens ischemic damage. The reversible insults seem to induce a sustained stimulation of H+ extrusion from cells giving rise to intracellular alkalosis and extracellular acidosis.
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PMID:Coupling among changes in energy metabolism, acid-base homeostasis, and ion fluxes in ischemia. 128 29

We investigated the effect of 30 degrees C whole body hypothermia on neuronal injury, astroglial reactivity and intracellular pH in rats subjected to 15 min of forebrain ischemia. Experimental groups included: (1) normothermic ischemia (n = 8), ischemia induced under 37 degrees C body temperature, (2) hypothermic ischemia (n = 6), ischemia induced under 30 degrees C body temperature. Cerebral intracellular pH was measured using in vivo 31P NMR spectroscopy over 7 days. Neuronal injury and astrocytic reactivity were evaluated using hematoxylin and eosin staining, and immunoreactivity to glial fibrillary acidic protein, respectively. Normothermic animals revealed significant alkalosis (P less than 0.01) at 48 h after ischemia compared to the pre-ischemic value. No significant intracellular pH change was detected after ischemia in the hypothermic group. Ischemic neuronal injury was prevented in the hypothermic animals, compared to the severe neuronal injury found in the normothermic animals (P less than 0.01). The marked astrocytosis of normothermic animals was significantly inhibited in the hypothermic animals (P less than 0.01). Our data indicate, that hypothermia significantly inhibits neuronal injury as well as post-ischemic alkaloids and astrocytosis, induced by 15 min of forebrain ischemia in the rat.
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PMID:Neuronal damage, glial response and cerebral metabolism after hypothermic forebrain ischemia in the rat. 138 61

The authors investigated early human focal ischemia with phosphorus-31 nuclear magnetic resonance spectroscopy at 1.89 T to characterize the temporal evolution and relationship of brain pH and phosphate energy metabolism. Data from 65 symptomatic patients were prospectively studied; none of the patients had had ischemic stroke in the internal carotid artery territory before. Twenty-eight neurologically normal individuals served as control subjects. Serial ischemic brain pH levels indicated a progression from early acidosis to subacute alkalosis. When acidosis was present there was a significant elevation in the relative signal intensity of inorganic phosphate (Pi) and significant reductions in signal intensities of alpha-adenosine triphosphate (ATP) and gamma-ATP compared with those of control subjects. Ischemic brain pH values directly correlated with the relative signal intensity of phosphocreatine (PCr) and the PCr index and inversely correlated with the signal intensity of Pi. There was a general lack of correlation between either ischemic brain pH or phosphate energy metabolism and the initial clinical stroke severity. The data suggest a link between high-energy phosphate metabolism and brain pH, especially during the period of ischemic brain acidosis, and the authors propose that effective acute stroke therapy should be instituted during this period.
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PMID:Human focal cerebral ischemia: evaluation of brain pH and energy metabolism with P-31 NMR spectroscopy. 141 Mar 69

After surgery for acute arterial occlusion in the lower extremities 59 patients have developed tachypnea, respiratory alkalosis and arterial hypoxemia. These symptoms persisted over the whole postoperative period. In 66% of dead patients pulmonary changes have been observed and only in 34% of patients who died suddenly the lungs were unaffected. Morphological changes in the lungs are most marked in long-standing ischemia and have the signs of the "shock lung" (adult respiratory distress syndrome). Pronounced changes in the respiratory function, acid-base balance, blood gas composition can account for a more severe course of the disease, deteriorate the prognosis, predetermine multiorgan failure in the early postoperative period.
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PMID:[The pulmonary distress syndrome during acute arterial occlusion of the lower extremities]. 141 10

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.
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PMID:[Acid-base disturbances in surgical operation]. 143 18

The goal of this study was to investigate lactate and pH distributions in subacutely and chronically infarcted human brains. Magnetic resonance spectroscopic imaging (MRSI) was used to map spatial distributions of 1H and 31P metabolites in 11 nonhemorrhagic subacute to chronic cerebral infarction patients and 11 controls. All six infarcts containing lactate were alkalotic (pHi = 7.20 +/- 0.04 vs. 7.05 +/- 0.01 contralateral, p less than 0.01). This finding of elevated lactate and alkalosis in chronic infarctions does not support the presence of chronic ischemia; however, it is consistent with the presence of phagocytic cells, gliosis, altered buffering mechanisms, and/or luxury perfusion. Total 1H and 31P metabolites were markedly reduced (about 50% on average) in subacute and chronic brain infarctions (p less than 0.01), and N-acetyl aspartate (NAA) was reduced more (approximately 75%) than other metabolites (p less than 0.01). Because NAA is localized in neurons, selective NAA reduction is consistent with pathological findings of a greater loss of neurons than glial cells in chronic infarctions.
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PMID:Elevated lactate and alkalosis in chronic human brain infarction observed by 1H and 31P MR spectroscopic imaging. 150 41


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