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

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

An in vitro model of myocardial ischemia has been established with primary monolayer cultures of postnatal rat myocardial cells. Ischemic conditions were simulated in vitro by subjecting the myocardial cell cultures to various levels of oxygen and glucose deprivation. The experimental protocol consisted of treatment with 20% or 0% O2 and 1000, 500 or 0 mg glucose per 1 of medium for 4 or 24 hr. Control cultures were treated with 20% O2 and 1000 mg glucose. After the ischemic treatments, cultures of beating muscle (M) cells were evaluated for signs of injury, i.e. leakage of cytoplasmic enzymes into the culture medium. Differences were found in leakage of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) from the cultures that were exposed to partial ischemia of glucose deprivation and from those cultures that were exposed to total ischemia of oxygen and glucose deprivation. Glucose deprivation along resulted in a slight-to-moderate loss of LDH and CPK from the cells, whereas total ischemia resulted in a significant release of the two cytoplasmic enzymes. When the cultures were allowed to recover after ischemic treatment in complete medium (1000 mg glucose) and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures. Cell viability and total protein content of the ischemic cultures did not differ significantly from controls.
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PMID:Ischemic myocardial injury in cultured heart cells: leakage of cytoplasmic enzymes from injured cells. 68 9

This paper presents the case history of a female patient with systemic lupus erythematosus, in whom pneumatosis intestinalis developed. The lesions disappeared in response to oxygen therapy. Arteriography revealed evidence of mesenteric arteritis. The patient subsequently developed paralytic ileus with lesions of the intestinal wall, probably based on ischemia as a result of this arteritis.
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PMID:Pneumatosis intestinalis in a female patient with systemic lupus erythematosus. 70 7

The present study, which concerns the rate of changes in the cerebral cortex concentrations of phosphocreatine (PCr), ATP, ADP, AMP, lactate and pyruvate during complete ischemia, had the objective of finding out whether or not phenobarbital retards depletion of tissue energy reserves during ischemia. Ischemia was induced for periods of 10 s to 10 min in animals maintained on 70% N2O or given 150 mg.kg-1 of phenobarbital. The results showed that the barbiturate anaesthesia delayed utilization of ATP during the first 2 min. However, after 5 min of ischemia PCr and ATP concentrations, as well as the calculated adenylate energy charge, were identical in animals anaesthetized with nitrous oxide and phenobarbital. Thus, phenobarbital induces a very moderate delay in the depletion of cerebral energy reserves that occurs during complete ischemia. The results obtained after 5-20 s of ischemia allowed calculation of energy (approximately P) utilization according to Lowry et al. (1964). The closed system method gave values for approximately P utilization which were not far from those obtained by CMRo2 measurements. However, with normal values for metabolic rate (70% N2O) valid estimates are obtained only with very short ischemic periods (5-10 s) and, with such short periods, the oxygen content of the tissue may introduce an error.
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PMID:Influence of phenobarbital on changes in the metabolites of the energy reserve of the cerebral cortex following complete ischemia. 71 81

We measured cerebral oxygen extraction, cerebral blood flow(CBF), and cerebral metabolic rate (CMRO2) in comatose patients during the first 60 hours after resuscitation from cardiac arrest. Each patient was studied 2 or 3 times. CBF was determined by a modification of the Kety-Schmidt method using inhaled Xenon133. Over the study period jugular venous oxygen tension and saturation rose, while the oxygen content difference between arterial and jugular venous blood fell, indicating a progressive increase in the ratio of CBF to metabolism CBF and CMRO2 measurements confirmed this. Between 2 and 6 hours after resuscitation both measurements were severely but proportionately depressed to less than 50% of normal. After 6 hours CBF was increased disproportionately to CMRO2 so that a relative hyperemia developed and persisted for the duration of the study. Although regional inhomogeneity of flow and regional ischemia cannot be ruled out, we have found no evidence for global cerebral ischemia between 2 and 60 hours post-resuscitation as an explanation for failure of recovery. In man following cardiac arrest restoration of levels of global cerebral blood flow, which can be considered adequate relative to the depressed metabolic state of the tissue, is achieved within 2 hours of resuscitation.
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PMID:Cerebral blood flow and metabolism in man following cardiac arrest. 74 88

Since sub-endocardial ischemia is the consequence of a discrepancy between the blood demand and supply of oxygen at this level, the study of the myocardial performance by the measurement of the endocardial viability ratio (E.V.R.) is both useful and possible during anesthesia. E.V.R. is the ratio between the oxygen supply and demand of the myocardium. It is equal to the diastolic pressure time index (D.P.T.I.) over the tension time index (T.T.I.). Measurements are made at different times, by means of the arterial pressure and the left atrial pressure, as well as with the Datascope-E.V.R. Computer. During gradual morphine administration (0.5-1-1.5 mg/kg) and if no major surgical stress occurs, E.V.R. remains excellent and stable (1.46 - 1.48 - 1.43). It deteriorates more or less (1.29 - 1.09) during tachycardia or hypertension. Within the hour following the end of extracorporeal circulation, E.V.R. significantly improves (1.04 - 1.06 - 1.09 - 1.23). Although E.V.R. measurement is easy during cardiac surgery, it is impossible to carry out in case of arrhythmia. While morphine anesthesia induces no variation in E.V.R., tachycardia or hypertension require the addition of therapeutic drug. Within one hour following the end of extra-corporeal circulation, E.V.R. measurement shows improved endocardial viability, although the hemodynamic parameters undergo no significant change.
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PMID:Measurement of endocardial viability ratio (E.V.R.) during anesthesia for cardiac surgery. 75 39

Radiation necrosis is a significant complication of surgery for previously irradiated head and neck malignant neoplasms. We used hyperbaric oxygen therapy (HBO) as adjunctive therapy in 52 cases of radiation necrosis. Thirty-nine cases involved the head and neck. Nineteen of 23 cases of osteoradionecrosis of the mandible remain arrested after as much as two years of follow-up. Fifteen of the 16 cases of soft-tissue radionecrosis of the head and neck were successfully managed with HBO therapy as an adjunct to surgery and antibiotics. Fibroblastic proliferation, collagen formation, and capillary budding require at least 20 to 30 mm Hg of wound Po2. This effect can be achieved in wounds that are rendered hypoxic by radiation endarteritis and ischemia with high-dose or hyperbaric oxygenation.
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PMID:Hyperbaric oxygen. A new adjunct in the management of radiation necrosis. 76 Jul 15

This review considers functional repercussions of shock state on the different stages of oxygen transport from alveolus to mitochondria. At the pulmonary level, the decrease in perfusion pressure induces disturbances in the distribition of VA/Q ratio, and therefore leads to aerial hypoxaemia. Prolonged ischemia injures the air-blood barrier and reduces the area of exchange. Decrease in oxygen delivery to the tissue is related to a fall in cardiac output (hemorrhagic and cardiogenic shock) or to a primary disturbance in peripheral circulatory distribution (septic shock) or to a primary disturbance in peripheral circulatory distribution (septic shock). The intervention of compensating factors leads to a redistribution of the regional perfusion and probably to an easier oxygen delivery by haemoglobin. However circulatory inhomogeneity by itself produces a progressive deterioration of microcirculation. Decrease in intracapillary circulation. Decrease in intracapillary circulation and impairment in blood rheologic properties contribute to aggregates formation and intravascular coagulation. The result is a decrease in capillary diffusion capacity and in oxygen intracellular transport. When intracellular PO2 reaches a critical level, the functional exclusion of mitochondria involves a metabolic shift to anaerobiosis. The value of hyperlactacidemia as a sign of oxygen debt is discussed.
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PMID:[Oxygen transport in shock (author's transl)]. 76 77

To reduce myocardial ischemia effectively, mechanical or surgical interventions must achieve either augmentation in coronary blood flow, a reduction in myocardial oxygen demand, or a combination of both. Coronary bypass graft procedures can achieve an immediate augmentation in coronary blood flow distally through the involved vessel and thereby improve myocardial perfusion and oxygen delivery and thus have the potential for reversing myocardial ischemia both acutely and for the long term. Although myocardial revascularization may resolve the ventricular functional alterations associated with acute myocardial ischemia it remains uncertain whether revascularization can reverse ischemic myocardial cellular injury and in what time framework, as related to reversible vs. irreversible ischemic cellular changes. Mechanical circulatory assistance (MCA) using diastolic counterpulsation effectively reduces myocardial ischemia by the physiologic mechanisms of 1) decrease in left ventricular after-load and left ventricular wall tension, 2) improvement is cardiac output by diastolic counterpulsation and 3) augmentation of coronary blood flow by diastolic pressure augmentation. The most effective indication for either MCA or myocardial revascularization is for interruption of myocardial ischemia prior to the development of infarction. Clinical sudies have demonstrated that acute myocardial ischemia can be effectively interrupted by intraaortic balloon pumping (IABP) including reversal of left ventricular dysfunction associated with acute myocardial ischemia. In most instances, cessation of IABP resulted in recurrence of myocardial ischemia indicating the need for urgent revascularization surgery. In the management of medically refractory myocardial ischemia. IABP has been effective in complete suppression of ischemia in 80 percent and resulted in marked improvement in all, allowing safe revascularization surgery with an operative mortality in the range of 5% and perioperative myocardial infarction incidence of 2%. In patients with acute myocardial infarction and cardiogenic shock (AMI-CS), IABP can resolve CS in 75 percent. The combination of IABP and surgery has resulted in survival approaching 45 percent indicative of a significant improvement in salvage in this group of patients where expected mortality approaches 100 percent.
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PMID:Mechanical and surgical interventions for the reduction of myocardial ischemia. 76 16

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
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PMID:Pathological aspects of brain transport phenomena. 78 95


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