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

In twenty dogs, anticoagulated with heparin 300 units/kg, the right cortical sensory evoked response (CSER) to contralateral median nerve stimulation was suppressed during 60 min ischemia induced by periodic infusion of 50 to 100 microliter increments of air via the right internal carotid artery. The post-ischemic recovery of the CSER was followed an additional 60 min in 19 of these animals divided into 2 groups. Ten dogs were subjected to glass-wool filtration of their blood by extracorporeal shunting from femoral artery to femoral vein for one hr prior to infusing air. Nine dogs did not receive glass-wool filtration. Post-ischemic recovery of CSER amplitude, a quantifiable electrophysiologic index of neuronal function, was significantly greater in the filtered group than in the non-filtered group. 14C-antipyrine autoradiographic blood flow studies were performed in 3 dogs. One was studied at the end of a 60 min ischemic CSER suppression period and showed severe flow disruption by air embolism. Two dogs, one from each group, were studied at the conclusion of the 60 min recovery period. In the filtered animal, cortical blood flow exceeded the threshold for CSER maintenance while cortical flow rates in the unfiltered animal fell below this threshold. The enhanced postischemic neuronal recovery in the filtered group as indicated by the CSER in attributed to the preservation of injury zone nutrient blood flow that is supported by collateral circulation.
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PMID:Extracorporeal glass-wool filtration of whole blood enhances post-ischemic recovery of the cortical sensory evoked response. 3 63

Complete global ischemia was produced in 39 dogs by temporary ligation of the aorta. Prior to the ischemic episode, pentobarbital (30 to 45 mg per kilogram of body weight) was administered to 19 of these dogs. The neurological effects of cerebral ischemia episodes lasting 8, 9, or 10 minutes were compared in dogs treated with pentobarbital and those not treated. At 48 hours following the ischemic episode most of the dogs made ischemic for 8 minutes were normal, whereas most animals made ischemic for 10 minutes were dead or comatose. The 9-minute ischemic period resulted in a relatively even distribution of normal and damaged dogs. There were no differences between treated and untreated dogs. Cerebral blood flow, cerebral metabolic rate for oxygen, and various cerebral metabolites were measured in dogs surviving 48 hours. Again, there were no differences between treated and undertreated dogs. We conclude that barbiturates provide no protection in this model of complete global ischemia. This conclusion supports the hypothesis that the likely mechanism of barbiturate protection in models of incomplete ischemia or hypoxia is based on cerebral metabolic depression; such a mechanism would not be expected to be effective in complete global ischemia.
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PMID:No barbiturate protection in a dog model of complete cerebral ischemia. 3 25

Aggressive treatment with H(2) receptor blocking agents and/or antacids has been advocated as effective prophylaxis against and treatment for "stress ulcer," based on the logical but infrequently tested assumption that the severity of the disease is critically determined by the concentration of intraluminal acid. The present study investigated this assumption in a model which employed topical acid, topical bile acid and mucosal ischemia to induce ulcerogenesis. With vascularized, chambered ex vivo wedges of canine proximal gastric wall, groups of animals were studied during three sequential periods using topical test solutions (TS) containing either 0 mM, 100 mM or 160 mM HCI. During period 1, mucosae were exposed to TS alone; during period 2, either to TS containing 1 mM sodium taurocholate (TC) or to TS and concomitant vasopressin infusion (VP); and during period 3, to TS + TC + VP. Parameters evaluated included net H(+) flux ( big up tri, openH(+)), aminopyrine clearance (AC), a measure of mucosal blood flow, net TC flux ( big up tri, openTC) and the lesion index, graded 0-5. The data indicate that in nonischemic mucosa exposed to constant [TC], AC was significantly increased, big up tri, openH(+) ("back-diffusion") increased as a linear function of [H(+)] and no lesions were observed. Under the same circumstances in ischemic mucosa, big up tri, openH(+) increased as linear function of [H(+)]. As a consequence, lesion severity was also a linear function of [H(+)]. big up tri, openTC was enhanced at low pH but bore no relation to the degree of mucosal damage induced. Assuming applicability of the model, these studies provide support for the use of H(2) receptor blocking agents and/or antacids to prevent or ameliorate "stress ulcer" disease.
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PMID:Influence of hydrogen ion concentration on bile acid induced acute gastric mucosal ulcerogenesis. 3 49

We measured rat brain cortex PO2 (PtO2) with gold microelectrodes (tip diameter 5--10 micron) for up to 2 hours after 16 min of transient global brain ischemia with and without thiopental 90 mg/kg infused iv over 60 min beginning at 5 min postischemia. Seventeen rats were immobilized and mechanically ventilated on 1% halothane in oxygen with continuous monitoring of PtO2, ECG, end-expiratory CO2, rectal temperature, and arterial blood pressure. Global ischemia was induced by trimethaphan hypotension to an MAP of about 50 torr and a neck tourniquet inflated to 1500 torr. Postischemia, nine control rats (11 PtO2 measurements) were untreated and eight rats (8 PtO2 measurements) received thiopental 90 mg/kg. Preischemia, PtO2 values in both groups ranged from less than 5--70 torr with values of greatest frequency between 10 and 15 torr. Postischemia, PtO2 in control rats peaked at 45 +/- 8 (SEM) torr at 20 min. In thiopental treated rats, peak PtO2 was 24 +/- 6 torr at 10 min postischemia. Relative frequency histograms of PtO2 revealed that PtO2 in thiopental treated rats was lower (p less than 0.05) between 15 and 30 min postischemia. The magnitude of the decrease in PtO2 between 105 and 120 min postischemia appeared to correlate directly with the absolute preischemic value (i.e., the higher the preischemic PtO2, the greater the decrease in PtO2 postischemia). These results suggest that thiopental administered in large doses in early postischemia does not improve brain oxygenation secondary to a reduction in brain oxygen consumption. The relevance of the correlation between the magnitude of the fall in PtO2 postischemia and the magnitude of the preischemic value is discussed.
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PMID:Postischemic brain oxygenation with barbiturate therapy in rats. 3 43

70 rats were subjected to tourniquet ischemia of a hind limb for a period of two and three hours. 12 rats served as controls. After release of the 3 hours tourniquets 20 rats were treated either with Ringer's solution or with hydroxyethyl starch. Kidney function and morphology, systolic blood pressure, hematocrit, serum electrolytes, creatinine and urea were studied as different times of recirculation. 1. Reduction in renal function was only observed after releasing the tourniquets. 2. The extent of reduction in renal function depended on the time of ischemia and time of recirculation. 3 hours of tourniquet with two hours of recirculation led to the largest extent of reduction in renal function and renal parenchymal lesions. 3. If the infusion of HES was applied at the beginning of recirculation, reduction in renal function was prevented, as well as parenchymal lesions. Ringer's infusion, however, did not improve kidney function to a normal range.
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PMID:[Animal experimental studies on partial kidney function after temporary tourniquet ischemia with and without blood substitute therapy]. 3 60

Of the orchiopexies performed for abdominal undescended testicles 85 per cent have resulted in satisfactory testicular growth and position. Three-fourths of these cases were in boys with the prune belly syndrome. We are satisfied with our recent experience using the Fowler-Stephens procedure to salvage intra-abdominal undescended testicles. An analysis of the failures in 5 testes early in this series, resulting in partial atrophy, has helped us to avoid technical errors through attention to the following details: 1) preservation of a broad pedicle of peritoneum overlying the mobilized vas, 2) avoidance of any dissection of the spermatic cord and 3) high ligation of the spermatic vessels well above the point of confluence of the vas and spermatic vessels. Although the Fowler-Stephens procedure has some risk of testicular ischemia and atrophy we believe it to be the preferred way to gain mobility on a short tethering gonadal vascular pedicle.
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PMID:Management of the abdominal undescended testicle. 3 53

Deep hypothermic circulatory arrest facilitates repair of congenital cardiac anomalies in infants. It is known empirically that hypothermia protects against central nervous system (CNS) ischemic damage. The Q10O2 is only 2.2 for brain and thus a decrease in metabolic rate does not fully account for protective effects of hypothermia. Since enthalpy of dissociation of H2O is high (approximately 7 kcal/mole), its pH is temperature dependent (7.0 at 25 degrees C, 7.4 at 20 degrees C) and hypothermia may in part protect by its influence on hydrogen ion concentration. A manifestation of CNS susceptibility to ischemia is an obstruction of the microcirculation [no-reflow lesion (NRL)] demonstrated by infusion of carbon black into the cerebral circulation after a period of circulatory arrest. White lesions (NRL) against a gray background on cut section of brain increase in size with increasing time of arrest. The effect of anoxia versus circulatory arrest, brain temperature, and extracellular brain pH on NRL was studied in 45 mongrel dogs, subjected to varying periods of N2-induced anoxia on cardiopulmonary bypass (CPB) at 37 degrees C or 20 degrees C. In some studies jugular venous pH was adjusted by infusion of NaHCO3 or HCl. Control groups included normothermic CPB without anoxic and normothermic CPB, anoxia, and equimolar NaCl infusion. NRL was quantified by planimetry of photographs of cut sections of brain. These results confirm that NRL is abated by hypothermia and suggest that (1) NRL is a function of anoxia and not arrested circulation since perfusion with N2 at 37 degrees C does not protect the brain (i.e., NRL is not solely related to "critical reopening pressure") and (2) NRL is in part a function of extracellular pH.
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PMID:Cerebral anoxia: effect of deep hypothermia and pH. 3 7

A new model of transient, bilateral hemispheric ischemia in the unanesthetized rat is described. During ether anesthesia the rat's vertebral arteries were electrocauterized through the alar foramina of the first cervical vertebra and reversible clasps placed loosely around the common carotid arteries. Twenty-four hr later, the awake rats were restrained and the carotid clasps tightened to produce 4-vessel occlusion. The carotid clasps were removed after 10, 20 or 30 min of 4-vessel occlusion and the animals killed by perfusion fixation 72 hr later. Rats which convulsed during the ischemic or post-ischemic period were excluded from further study. All rats subjected to 20 or 30 min of 4-vessel occlusion demonstrated ischemic neuronal damage. The H1 and paramedian hippocampus, striatum and layers 3, 5 and 6 of the posterior neocortex were the regions most frequently damaged. The advantages of this model are the ease of preparation of large numbers of animals, a high rate of predictable ischemic neuronal damage, a low incidence of seizures and the absence of anesthesia.
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PMID:A new model of bilateral hemispheric ischemia in the unanesthetized rat. 3 14

Cerebral ischemia was produced by a combination of vascular occlusion and mild systemic hypotension in 2 groups of rabbits. Arterial blood pressure, arterial pH, arterial blood gases, blood glucose and PCV were monitored and recorded before, during and for 3 hours after reperfusion. Return of EEG activity, vasomotor control, spontaneous ventilation and corneal reflex were also recorded. At 4, 8, 12, 24 and 48 hours after reperfusion, the rabbits' neurologic status was assessed according to an arbitrary scale based on motor function. The 2 groups differed in return of reflexes and motor function. Eighty percent of the rabbits ischemic for 20 minutes and 75% of the rabbits ischemic for 30 minutes survived. The graduated response of motor function to cerebral ischemia is attributed to the ventilatory and circulatory support given the rabbits for the first 3 hours after reperfusion. The graduate response of motor function to ischemia supports the suggestion that motor function can be used as an index of neurologic damage.
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PMID:Survival of rabbits after prolonged cerebral ischemia. 3 15

The intestinal mucosa of the rat was examined by light and electron microscopy 15, 30, 60 and 120 min after complete ligation of the vessel arcades of the proximal jejunum. The characteristic sign of ischemic damage to the small intestinal mucosa and the reason for epithelial shedding is the appearance of membrane enclosed cytoplasmic blebs which arise at the cell base of the enterocytes and detach the epithelium from the basement membrane. This process begins at the tip of the villi before the enterocytes display signs of irreversible damage and progress to the base of the villi with continuation of the ischemia.
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PMID:The mechanism of epithelial shedding after ischemic damage to the small intestinal mucosa. A light and electron microscopic investigation. 3 41


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