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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of increased acidity and of lactate at acid pH values on the ultrastruct of normal dog myocardium were investigated using a simple in vitro system. Thin tissue slices incubated in isotonic, phosphate-buffered sodium chloride at pH 6.5, 6.8, or 7.0 developed within 10 minutes electron-dense mitochondrial inclusions resembling those seen in dog heart muscle after 40 or more minutes of ischemia. Mitochondria of tissue incubated in a comparable medium incorporating 3000 mu g. of lactate per ml. showed similar electron-dense inclusions, together with marked swelling. These results indicate that lowered tissue pH alone is not responsible for the mitochondrial changes typical of ischemic heart muscle. Since an earlier study has shown that marked mitochondrial swelling without dense granule formation can be produced by incubation of tissue in lactate at physiologic pH, it seems likely that the swelling of mitochondria in ischemic myocardium is due to the accumulation of lactate anions, whereas the development of the mitochondrial inclusions is associated with decreased pH.
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PMID:Mitochondrial changes in dog myocardium induced by lowered pH in vitro. 23 54

To test the hypothesis that O2 chemoreception in the carotid body (CB) is mediated by cellular acidosis, we simultaneously measured responses of the chemosensory and intracellular pH (pHi) to agents that are known to change pHi and studied the effects of hypoxia and ischemia on these variables in the cat CB. The CB was perfused and superfused in vitro with a modified Tyrode's solution at 36.0 +/- 0.5 degrees C with or without CO2-HCO3- (pH 7.40) and equilibrated at a given PO2. Chemosensory discharges were recorded from the whole carotid sinus nerve. To measure pHi changes, the CB was loaded with the pH-sensitive indicator 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein, and the fluorescence (excitation 420-490 nm, emission greater than 515 nm) was detected by an intensified charged coupled device camera with an epifluorescence macroscope. Boluses of Tyrode's solution (0.5 ml, free of CO2-HCO3-) containing sodium acetate or NH4Cl prolonged perfusion of acid Tyrode's solution (pH 7.20-6.50), and boluses of Tyrode's solution with CO2-HCO3- were used. A decrease of fluorescence indicated pHi turning acid, and an increase of fluorescence indicated a change in alkaline pHi. Chemosensory activity varied inversely with the fluorescence change after application of these agents. Interruption of perfusate flow or application of hypoxic perfusate resulted in large increases in chemosensory discharge without any change in the fluorescence. The results indicated that chemosensory responses to brief ischemia and hypoxia were not mediated by a fall of pHi of CB cells, whereas those to CO2 and extracellular acidity were associated with decreases in pHi.
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PMID:Intracellular pH and oxygen chemoreception in the cat carotid body in vitro. 162 81

The influence of the proximal selective vagotomy (PSV) on the origin and the extent of experimental gastric ulcer were investigated in rats. The lesions of the gastric mucosa were caused in three groups: by stress through swimming-test, by application of phenylbutazone, and by ischemia (ligature of the left gastric and the right gastroepiploic vessels). The PSV practised a protective influence on the pharmacodynamic etiology, however, not on the stress ulcer. The areas of the ischemic gastric ulcers were larger on an average of 40% after PSV than in the control animals. The difference was not statistically significant. In case the PSV caused besides hyposecretion and hypo-acidity even passive hyperemia caused in the denervated part of the stomach then these did not produce any sufficient defence against the origin of stress ulcers and ischemic lesions.
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PMID:[The effect of proximal selective vagotomy on experimental gastric mucosal lesions in the rat]. 222 3

Virtually all patients who are under the physiologic stress of an intensive care unit (ICU) are vulnerable to stress-related mucosal damage and ulceration. Although clinically significant hemorrhage from stress ulceration occurs in only 5-20 percent of patients in the ICU, the associated mortality is greater than 50 percent. The pathophysiologic mechanisms of stress ulcer are not well understood; however, a number of risk factors such as intraluminal gastric acidity and mucosal ischemia have been implicated. To prevent the development of stress ulcers and subsequent complications, it is important to identify and correct these underlying risk factors. Improving mucosal blood flow (i.e., fluid resuscitation and low-dose dopamine) and providing adequate nutritional support are invaluable adjuncts in minimizing the risk of stress ulcer formation. The use of pharmacologic prophylaxis controls the gastric acidity and prevents the formation of stress ulcers. The potential for drug-induced adverse effects and drug-drug interactions are of particular concern in the care of critically ill patients. Multiple organ system dysfunction or failure, malnutrition, fluid and electrolyte abnormalities, as well as the use of multiple pharmacologic agents predispose these patients to alterations in drug pharmacokinetics, drug-induced adverse effects and drug-drug interactions. These changes may alter the pharmacodynamic response to therapy and must be considered when designing drug dosage regimens for critically ill patients.
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PMID:Pathophysiologic changes in the critically ill patient: risk factors for ulceration and altered drug metabolism. 227 Jun 97

Rat gastric mucosal blood flow, hydrochloric acid (HC1) secretion, and morphological changes of parietal cells were studied by light and electron microscopy using histochemical techniques. Mucosal blood flow of restrained rats was remarkably decreased compared with that of control rats, whereas the acetylcholinesterase activity, demonstrated by the method of Karnovsky and Roots, was significantly increased especially near the ulcer. In contrast, the differences in volume, acidity and acid output of gastric juice were not significant between control and restrained rats. Hypersecretion of HC1 induced by a parasympathetic stimulant, bethanechol, was inhibited by blood loss or infusion of cytochalasin B, an actin depolymerizing agent. 14C-aminopyrine accumulation in the primary cultured parietal cells was decreased by the treatment with hypoxia and cytochalasin B. These treatments also prevented the increase of 14C-aminopyrine accumulation induced by bethanechol. Actin filaments were evident in the cytoplasm of the parietal cells, particularly around the intracellular canaliculi and beneath the plasma membrane using the FITC-labeled phalloidin reaction and transmission electron microscopic observations of uranyl acetate block stained preparations following heavy meromyosin decorations. Ultrastructural studies of the parietal cells in restrained rats revealed that intracellular canaliculi were dilated with loss of microvilli. Actin filaments were noted to be disassembled, and granular with focal aggregation of actin filaments. Hypoxic vacuoles were also found in the cytoplasm. Treatments with blood loss and cytochalasin B infusion in the in vivo model, and hypoxia and cytochalasin B in the in vitro model, resulted in the similar changes. These observations indicate that actin filaments in the parietal cells of restrained rats may be depolymerized by ischemia. As the result, HC1 secretion would not be enhanced even if the parasympathetic nerves are excessively stimulated in the gastric mucosa. Thus, disturbances of the gastric mucosal microcirculation are considered to be important in the pathogenesis of the stress-induced gastric ulcer.
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PMID:[Studies on the mechanism of restraint-induced gastric ulcer--with special reference to mucosal ischemia and gastric secretion]. 232 29

Stress-related gastrointestinal bleeding is known to occur in approximately 25 percent of untreated seriously ill patients, but with appropriate prophylaxis is largely preventable. Since the treatment of stress bleeding is generally unsatisfactory and has a high mortality, routine prophylaxis should be instituted for susceptible patients. Multiple mechanisms contribute to stress ulcer formation, the most important of which appear to be mucosal ischemia and the inability to control back-diffused hydrogen. Antacids and histamine2-blocking agents are presently the cornerstone of effective prophylaxis, but because they have been implicated as contributors to nosocomial pneumonias due to bacterial overgrowth in the stomach, investigation is ongoing into such alternative prophylactic agents as sucralfate and prostaglandins that do not alter the normal gastric acidity. This article presents a review of the literature on the development and prevention of stress ulcer disease.
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PMID:Stress ulcers: current understanding of pathogenesis and prophylaxis. 329 57

Excessive cellular acidosis is thought to enhance destruction of brain from ischemia. Protein denaturation may contribute to such injury although the behavior of brain proteins to acidosis is poorly defined. As a first approach to detect acid-induced changes in brain proteins and to characterize buffer content, homogenates were acidified for 20 min (as low as pH 3.1), returned to baseline pH (6.9), and then titrated. Titration curves show a significant (P less than 0.0001) and permanent increase in buffer content compared to controls when pH of acid exposure was 4.5-3.7 or less. Since acidity of pH 4.5 is rarely, if ever, achieved in vivo, protein denaturation from acidity alone is unlikely to account for necrosis of brain from ischemia.
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PMID:Acid-induced changes of brain protein buffering. 359 48

Bacterial contamination of the small bowel in the elderly can occur without any anatomical defect, but the importance and pathogenesis of this phenomenon are debatable. We describe two such patients, both with profound vitamin B12 deficiency. Clinical recovery took place without specific treatment of the bacterial overgrowth. In one patient with pernicious anemia, malabsorption of xylose and fat was corrected after vitamin B12 therapy. In the other gastric acidity was normal, but unsuspected mesenteric ischemia led to gangrene of the bowel. In old age there may be more than one explanation for vitamin B12 deficiency and for bacterial overgrowth. Vitamin B12 deficiency within the intestinal cells may be one common factor leading to malabsorption.
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PMID:Small bowel contamination and vitamin B12 deficiency in the elderly. 376 May 23

We studied the effects of propranolol on degradation of cardiac structural proteins resulting from ischemia induced by 24 h ligation of the coronary artery in dogs. Degradation of myocardial myosin heavy chain, alpha-actinin and troponin-I was used as an indicator of degradation of cardiac structural proteins. In dogs with left circumflex coronary artery ligation, propranolol, given orally in the dose of 10 or 30 mg/kg, significantly reduced degradation of cardiac structural proteins. This can be supported by the facts that treatment with propranolol, 10 or 30 mg/kg, reduced release of cathepsins B, L and D from lysosome to cytosol in the ischemic tissue and that the reduced acidity of the ischemic tissue was improved by treatment with propranolol, 30 mg/kg. In conclusion, propranlol delays the necrotic development of the severely ischemic myocardial tissue as shown by reduced protein degradation.
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PMID:Effects of propranolol on tissue necrosis in experimental myocardial infarction in dogs. 382 60

To investigate ischemic potentiation of thermal cell killing, mammary carcinomas transplanted to the legs or tails of C3H mice were treated with hyperthermia using rubber-lined compression cuffs. During treatment, warm water was circulated through the cuffs under pressure so that blood flow to the contained tumor-bearing limbs was interrupted. Ninety min at 41.5, 42.0, or 42.5 degrees and pressures between 60 and 135 mm Hg destroyed about 50% of tumors but damaged the normal tissues. Damage increased with the degree of compression. Intermittent pressure application was therefore adopted (five 18-min periods at 80 to 90 mm Hg alternating with four periods of 5 min at zero pressure). This favored the normal tissues, a high cure rate being maintained (73%) with damage to normal tissue virtually eliminated. The most satisfactory explanation of these results is a selective heat sensitivity, augmented by ischemia, on the part of tumor blood vessels. The success of intermittent treatment is then attributable to progressive impairment of the blood supply to the tumors, preventing the heat dissipation and relief of conditions such as acidity and nutrient deficiency which would otherwise result from periodic restoration of the circulation.
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PMID:Treatment of mouse mammary tumors using combined hyperthermia and ischemia. 685 Jun 44


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