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

The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure-volume relationship. Thus, the elevation of left ventricular end-diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.
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PMID:Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia. 108 86

An acute circulatory renal failure (ARF) was induced in 18 rabbits by temporary ischemia of the remaining kidney 8 days after unilateral nephrectomy and subcuteaneous autotransplantation of renomedullary tissue.--Mortality in the postischemic course was 50% in treated animals but 100% in the control group (n = 18) without autotransplantation. In the postischemic period plasma urea concentration was significantly lower (p smaller than 0.005) in the surviving transplanted animals and excretion of sodium and water significantly higher (p smaller than 0.005) as compared with the control group. Plasma renin values which were significantly lower than thos of the control(p smaller than 0.005) had decreased significantly even as compared with the initial values. These results indicate that hormonal substances are produced in interstitial cells of renomedullary autotransplants exerting a distinct protective effect against experimental acute renal failure. Decreased plasma renin activity may point to an inhibition of circulating and/or intrarenal renin by lipids originating from the transplants. Changes in sodium and water excretion indicate effects of circulating prostaglandins
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PMID:Experimental oliguric acute renal failure: protective effects of renomedullary autotransplants. 109 74

The subendocardial to subepicardial gradient in the severity of ischemia following acute coronary occlusion is described. The effects of mild, moderate, and severe ischemia on cell structure and function are compared in summary form, and special attention is given to the effects of severe ischemia on myocardial cells. The characteristics of reversible and irreversible ischemic injury are defined in biologic terms. The failure of cell volume regulation in cells which have entered an irreversible state of ischemic injury is demonstrated by the use of free-hand slices in vitro. Irreversibility is associated with structural defects in the plasma membrane and is reflected in an increased slice inulin-diffusible space, increased slice H2O and Na+ content, and failure of the tissue to maintain the high K+ and Mg2+ levels characteristic of normal left ventricular myocardium. Defective cell membrane function is an early feature of irreversible ischemic injury and may be a primary event in the genesis of the irreversible state.
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PMID:Ischemic tissue injury. 118 Mar 31

This study was intended to define the early early electrolyte and water abnormalities of ischemic myocardium in the intact anesthetized dog. We have defined the appropriate circumstances for using 52Cr-ethyelendiamineletraacetate as an extracellular marker during ischemia and have discerned no change in this space at a time when tissue water increments were observed, by 15 min of ischemia. Calculated on the basis of cell dry weight, the cell sodium increment exceeded potassium loss in this early period of ischemia. This is consistent with the view that interference with energy metabolism reduces the pumping of sodium from the cell. The enhanced entry of sodium is associated with a gain of water, initiating events that effect irreversibility.
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PMID:Myocardial cell electrolytes and water during acute ischemia. 120 75

In 34 anesthetized, open-chest dogs aortic blood pressure was kept at 35-40 mmHg for 3 h to determine if maldistribution of coronary blood flow (CBF) could contribute to the irreversibility of hemorrhagic shock. Six dogs were pretreated with phenoxybenzamine (PBZ) and 11 dogs (3 with PBZ) received hypertonic mannitol infusions in late hemorrhage. Changes of heart rate, cardiac output, and peripheral resistance were similar to those described by others. In untreated dogs total and left ventricular CBF fell, as did coronary vascular resistance. However, minimal coronary resistance after transient ischemia rose progressively and the ratio of subendocardial:subepicardial flow fell, as did the percentage of diastolic coronary flow. Mannitol infusion returned CBF and steady-state and minimal postischemic coronary resistance to control values and also returned to normal the increased myocardial water content found in late hemorrhage. Phenoxybenzamine delayed but did not prevent the rise of coronary vascular resistance or decreased subendocardial flow. These studies suggest that there may be subendocardial ischemia, possibly due to myocardial edema, in hemorrhagic shock.
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PMID:Intramyocardial distribution of blood flow in hemorrhagic shock in anesthetized dogs. 125 9

Twenty-four dogs underwent in vivo left pulmonary hilar occlusion with the lung continuously expanded at 10 centimeters or 25 centimeters of water pressure to determine the period of pulmonary ischemia that may be tolerated before consistent pulmonary edema and congestion develop after lung revascularization. Consistent and prolonged pulmonary edema and congestion that caused death of the dog occurred in at least one-half of the dogs when the period of hilar occlusion was extended beyond six hours. Elevation of the left pulmonary artery pressure was only a rough measurement of the severity of the anoxic pulmonary injury. Expansion of the lung at 10 centimeters of water continuous pressure was more beneficial than was expansion at 25 centimeters of pressure. Cyclic ventilation with slight negative-expiratory pressure provided less support to the lung than did continuous expansion at either pressure tested. Intial decreases in both ventilation and perfusion isotope uptake and the percentage of the total volume of oxygen uptake per minute by the ischemic lung returned to near normal levels in three weeks in dogs that survived. Lung expansion during periods of ischemia appears to prevent alveolar collapse and to facilitate oxygenation.
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PMID:Evaluation of pulmonary function in the ischemic expanded canine lung. 125 71

There is as yet no adequate animal mode for human myocardial ischemia. The commonly utilized technique of coronary arterial ligation in large animals may induce regional ischemia but introduces variables that make it difficult to compare studies in different laboratories. A model of global ischemia in an isolated perfused rat heart that offers a rapid, inexpensive means for producing graded, controlled, stable state and reproducible ischemia is described. The technique has been utilized with success to study the hemodynamic and metabolic effects of ischemia and to evaluate pharmacologic interventions designed to protect the ischemic myocardium. Propranolol has been shown to improve bioenergetics and reduce anaerobic glycolysis by a depression of the hemodynamic response of ischemic myocardium. Methylprednisolone appears to exert its primary effect by direct coronary vasodilation, increasing resting or control flow and providing an enhanced reserve when ischemia is imposed. Mannitol improves cardiac performance by reducing the increased myocardial cell water content induced by hypoxia or anoxia.
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PMID:Metabolic evaluation of agents designed to protect the ischemic myocardium and to reduce infarct size. 125 90

The effects of six hours of ischemia and six hours of perfusion with 10 per cent dextrose and water solution, Sacks' solution and Intralipid on the endothelium of common femoral arteries in dogs were examined by light and by scanning electron microscopy and compared with normal arteries. Arteries that were ischemic or perfused with 10 per cent dextrose and water solution or Sacks' solution showed a flattening of the normal linear convolutions and extensive crater formation, with fragmentation and even complete loss of endothelial cells in many areas. The more severe changes occurred in perfused vessels. Fibrin and platelets covered the luminal surface in many areas in which there was extensive injury to the endothelium. Light microscopy revealed thickening of the internal elastic membrane and intimal fibrosis. Results of biopsies performed two weeks after perfusion showed slight, although incomplete, improvement in the structure of the endothelium. Arteries perfused with Intralipid had thickening of the intima with a proliferation of plump cells orientd linearly over the surface but with an absence of craters. Results of present studies confirm the observations of other investigators that injury to endothelial cells may be produced by ischemia and that perfusion with various solutions may produce an even more severe alteration in structure of the endothelial cell which does not return to normal within two weeks. The origin of new endothelial cells is not demonstrated by this study.
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PMID:Arterial endothelial changes after ischemia and perfusion. 126 12

The acidic fibroblast growth factor (aFGF) in rat cerebrospinal fluid (CSF) increased 1000 times in the 2 hr period after food intake, or intraperitoneal (IP) or intracerebroventricular (ICV) glucose infusion. It diffused into the brain parenchyma and was taken up into neurons in the hypothalamus, hippocampus, etc.... aFGF is produced in the ependymal cells and released into CSF in response to increased glucose. ICV application of aFGF dose dependently inhibits, and anti-aFGF antibody facilitates food intake. IP injection of glucose 2 hr before a task that combined acquisition with passive avoidance significantly increased retention of avoidance by mice tested 24 hr later. In a Morris water maze task, IP glucose injection 2 hr before a first trial block reduced time to find and climb onto a platform hidden just below the water surface. These facilitation by glucose of affective and spatial memory were abolished by pretreatment with anti-aFGF antibody applied ICV. Continuous ICV infusion of aFGF into rats also significantly increased the reliability of passive avoidance for several days. The memory facilitation by aFGF was significantly attenuated by CA1 neuron death in the hippocampus caused by 5 min ischemia of the brain, in gerbils. After food intake, centrally-released aFGF reaches the hippocampus and facilitates memory, while peripherally released cholecystokinin reaches the endings of the afferent vagal nerves in the portal vein and changes the vagal nerve activity, which modulates hippocampal activity, to lead to memory facilitation. This, however, is blocked by vagotomy below the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological significance of brain acidic fibroblast growth factor. 128 50

Cortical mouse astrocytes in culture were impaled with two-channel microelectrodes. These mouse astrocytes have the same responses to different K+ concentrations, ouabain, and glutamate as cultured rat astrocytes, with the exception that a large barium-sensitive K+ conductance clamps the membrane potential at the K+ equilibrium potential. Glycolytic and mitochondrial inhibitors have little effect on the mouse astrocytes. Total blockade of energy metabolism leads to an irreversible, calcium-dependent depolarization, but only if applied for longer than 45 min. Increasing the extracellular K+ concentration to 60 mM increases the intracellular K+ concentration by 43 mM and the bicarbonate concentration by 22 mM and leads to a concomitant fast swelling. Together with the 20 mM increase in Cl- concentration reported in the literature this is a good indication for a Boyle- and Conway-mediated K(+)-anion influx with water. This influx is accomplished by the depolarization-induced opening of Cl- channels as reported in the literature. In conclusion, ischemia-like conditions have little direct, immediate impact on astrocytes. In contrast, ischemia-induced release of substances from neurones, such as K+, produces an immediate and fast response.
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PMID:Coupling of metabolism and electrical activity in cortical astrocytes. 129 68


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