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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The behavior of a model for the partial depletion of adenine nucleotides in the perfused rat heart has been compared for ischemic and high coronary flow anoxic conditions. The accumulation of noradrenaline in the interstitial fluid greatly activates adenylate cyclase ultimately resulting in the degradation of 11.02 micronmol/g dry wt of ATP to adenosine, inosine, and hypoxanthine in 30 min. The high coronary flow rate during anoxic perfusion promotes washout of the noradrenaline from the interstitial fluid so that the hormone accumulates to only one fifth of its highest level in ischemia. This results in only slight activation of adenylate cyclase and in insignificant degradation of ATP in 2 min. The behavior of the model has been examined for two aerobic conditions--a transition from light to heavy work (2 min) and a transition from substrate-free to glucose perfusion (12 min), In both cases adenylate cyclase was not activated above its basal activity, and insignificant depletion of adenine nucleotides is predicted by the model.
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PMID:Computer simulation of ischemic rat heart purine metabolism. II. Model behavior. 1 61

The total activities of sucrase, trehalase, amino-peptidase, and gamma-glutamyltransferase in the isolated brush border of the entire small bowel are reduced to 35, 55, 33, and 21 per cent, respectively, of control values (p less than 0.001) 2 hours after a 45 minute occlusion of the superior mesenteric artery. Since brush border proteins are also reduced by ischemia to 42 per cent of control, enzymatic activity when expressed as U/mg protein is significantly reduced only in the case of gamma-glutamyltransferase, to 48 per cent of control.
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PMID:Intestinal brush border enzymes after short-term mesenteric ischemia. 1 65

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

Regional cerebral blood flow (rCBF) was measured in normotensive rate (NTR) and spontaneously hypertensive rats (SHR), in a lightly anesthetized state and with control of PaCO2 by artificial ventilation. Without carotid artery ligation, NTR and SHR showed almost identical rCBF values and distribution, despite significantly elevated levels of blood pressure in SHR. Bilateral carotid artery ligation, however, caused much more pronounced decreases of rCBF (ischemia) in SHR than NTR, in regions supplied by the carotid artery. The reduction of rCBF in SHR was rather homogenous and symmetrical. Mechanisms causing the differences between NTR and SHR are discussed.
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PMID:Effect of carotid artery ligation on regional cerebral blood flow in normotensive and spontaneously hypertensive rats. 1 64

A computer technique for determination of the distribution of adenine nucleotides among compartmented, protonated, and metal-chelated species has been developed for the perfused rat heart. This procedure requires knowledge of tissue levels of creatine, creatine phosphate, ATP, ADP, and AMP and the glycolytic and respiration rates. The method is applicable to any physiological state of the organ and has been applied to transient behavior in aerobic, anoxic, and ischemic hearts. The results suggest that ADP uptake and ATP export by mitochondria are normally linked and equal in rate during aerobic metabolism or short-term anoxia but become separate and unequal during ischemia, so that mitochondrial adenine nucleotides, primarily AMP, accumulate.
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PMID:Distribution of adenine nucleotides in the perfused rat heart. 1 1

The author studies only the usual investigations required for watching E.C.C. during the operatory period and directly afterwards. During E.C.C., one must essentially oversee the flow (2,4l/m2 or 70 ml/kg), the arterial pressure (70 torrs) essential factor for myocardiac injection, the C.V.P., where excess is factor of cerebral oedema, the peripheric vascular resistances (P.V.R.) which inform on the level of vasomotoricity. Control of pulmonary capillary pressure (P.C.P.), which is under E.C.C. the reflection of the left ventricular pressure (L.V.P.) is also a capital element of this watching (any elevation of L.V.P. is factor of sub-endocardiac ischemia and of acute pulmonary edema). In post E.C.C., the same parameters will be watched. A cardiac output equal or inferior to 2 l/m2 involve an immediate treatment. The C.V.P. allows adaptation of blood quantity. Calcul of V.P.R. sets treatment of low cardiac output. C.P.C. control allows evaluation of left ventricular efficacity. These datas must be completed by calcul of subendocardiac viability by studying the arterial pressure curves which inform on oxygen supply and demand, and by the contractility index measure (aortic output speed and measure of systolic interval).
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PMID:[Hemodynamic parameters which should be watched during and immediately after extracorporeal circulation]. 1 25

Hypothermic protection of myocardia during E.C.C. has been estimated on a 35 dogs experimental series and on a clinical series of 700 acquired cardiopathies of adult, including 400 valvular replacements and 300 aorto-coronary by-pass. Experimental results have been estimated by biochemic and morphologic controls done on myocardic samples took up by drillbiopsy. The biochemical study includes among others a dosing of the high-energy phosphorus compounds (P.C. and A.T.P.). Morphological study was done by optic and electronic microscopy. Results made clear the superiority of the hypothermic ischemia at 10 degrees C on the continued perfusion at 32 degrees C with fibrillative heart. An hypothermic protection method with successively cold perfusion of the coronary system and a heart immersion in a salted solution at 4 degrees C has been utilized during valvular and coronary surgery on human in 700 cases. The total mortality was of 5,8 p. 100. The rate of post-operative infarcts was 2,4 p. 100. Incidence of intra-ventricular conduction troubles has been 1,1 p. 100. There was no relation between mortality and morbidity of myocardic origin and the lasting of the ischemic clamp, which were of 21 mn up to 165 mn. The low incidence of complications of myocardic origin is due to the hypothermic protection of the myocardia.
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PMID:[Protection of the myocardium by hypothermia during extracorporeal circulation. Experimental and clinical study]. 1 26

This study tries to specify the tolerance limit of heart to ischemia and has three parts. In the first one, the author considers the heart resistance in normothermy related to the circulatory arrest type, the anesthetic technique, existence or not or a ventricular fibrillation. Everybody is tody in agreement to admit that 35 to 45 minutes are the security limit of the cardiogenous circulatory stop. In the second part, conditions of cardiac tolerance to ischemia in hypothermy are foreseen. The security margin is here large, provided a nonagressive realization of the cooling. Lastly, the author reports the looseness of the biochimic, histochemic or histologic criteriums which permit an appreciation of the heart functional capacity, appreciation which still persist to be essentially clinical.
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PMID:[Changes in myocardial tolerance to ischemia as a function of circulatory arrest mechanisms]. 1 29

This article presents an analysis of acute gastroduodenal mucosal lesions (AGML) based on a review of current literature and the personal experience of the authors. The pathology of AGML involes two distinct types of lesions, namely, superficial erosions confined to the acid-secreting gastric mucosa and presenting as erosive hemorrhagic gastritis, and acute ulcers that occur in the alkaline gastric mucosa and duodenum. The etiology of these two lesions is very likely different. Acut gastroduodenal ulcers, best known as stress ulcers, are probably "peptic" lesions, whereas erosive hemorrhagic gastritis appears to be due to pathologic back diffusion of hydrogen ions caused by a breakdown of the gastric mucosal barrier as a result of endogenous factors, such as gastric mucosal ischemia, and sometimes exogenous factors, such as alcohol, urea, and acetylsalicylic acid. Catecholamine hypersecretion resulting from severe stress, such as occurs in hypovolemia, sepsis, and hypercapnea, contributes to ischemia of the gastric mucosa by producing splanchnic vasoconstriction. The key to the diagnosis of AGML is early endoscopy in all cases of upper gastrointestinal bleeding. Therapy for AGML should begin with a trial of medical measures directed at restoring effective perfusion of tissues and removing hydrogen ions from the stomach by gastric washing. Medical therapy is effective in 80% of patients with erosive hemorrhagic gastritis, but surgical treatment is usually required in acute gastroduodenal ulcer. When surgery is necessary for either type of lesion, vagotomy with hemigastrectomy appears to be the most effective operation. The personal experience of the authors has involved 36 patients with AGML who were treated in three periods between 1968 and 1976. The mortality rate of patients with AGML has been reduced from 50% in the first 2 years to zero in the last 2 years by the use of emergency endoscopy for diagnosis, appropriate medical therapy, properly timed and executed surgery, and, most recently, selective angiography.
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PMID:Progress in the treatment of acute gastroduodenal mucosal lesions (AGML). 1 30

This study tests the hypothesis that postischemic myocardial depression can be reduced by providing an initial reperfusate pH which is appropriate for myocardial temperature (i.e., metabolic systems function optimally when pH is kept slightly alkaline to the neutral point, which changes with temperature in concordance with the pK of water). Ten dogs underwent 1 hour of ischemic arrest with topical hypothermia (intramyocardial temperature 16+/-2 degrees C). The initial reperfusate (500 cc of blood from the extracorporeal circuit) was infused (100 cc/minute) into the proximal aorta just before removing the cross-clamp. Reperfusate pH was kept at 7.4 in five dogs (control) and raised to 7.8 with THAM [tris (hydroxymethyl) aminomethane] in five dogs. Measurements 30 minutes after reperfusion showed that raising reperfusate pH to 7.8 resulted in (1) higher subendocardial blood flows (109+/-20 vs 61 cc+/-8 cc/100 gm/minute), (2) redistribution of postischemic blood flow toward the subendocardium (endocardial/epicardial flow 1.25+/-0.1 vs 1.0+/-0.03), (3) higher left ventricular oxygen uptakes (0.046 vs 0.033 cc/100 gm/beat), (4) better postischemic left ventricular compliance (56+/-3% more compliant), and (5) improved left ventricular performance (88+/-7% recovery vs only 57+/-3% recovery at pH 7.4). Postischemic edema (2% water gain) was unchanged by pH modification. We conclude that initial reperfusion with the appropriate pH provides an optimal milieu for restoration of cellular metabolism, counteracts the acidosis of ischemia, and improves postischemic left ventricular blood flow, distribution, oxygen uptake, compliance, and performance.
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PMID:Studies on myocardial reperfusion injury. I. Favorable modification by adjusting reperfusate pH. 1 28


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