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

Abdominal aortic aneurysmectomy is being performed with progressively lower operative mortality and morbidity. Three hundred thirty seven patients have had elective aneurysm repair since 1954. Factors affecting mortality and morbidity in the last 108 cases are analyzed. Seventy-four per cent of patients had pre-existing disease, either cardiac, pulmonary, renal, cerebrovascular, diabetes mellitus, or hypertension. Six patients died following operation, a mortality rate of 5.5%. One died of pulmonary and 5 of cardiac causes. No patient died of renal failure or required dialysis. A signficant feature of management is the regimen of fluid therapy using dextrose in lactated Ringer's solution during and after operation to minimize hypotensive and renal complications. No patient developed a wound infection, graft infection, wound dehiscence, stroke, or intestinal ischemia. Serious postoperative complications were largely cardiac or pulmonary. Despite recent liberalization of indications for operation, comparative figures show continued reduction in operative mortality from 17% during 1954-1961, or 7.4% during 1962-1967, to 5.5% in the 1968-1974 era. This declining mortality is related to earlier diagnosis using non-invasive methods (sonogram), simplified operative techniques, improvement in fluid management, innovations in cardiopulmonary therapy, and recognition and proper handling of unusual manifestations of aortic aneurysms.
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PMID:Surgical management of abdominal aortic aneurysms: factors influencing mortality and morbidity--a 20-year experience. 12 60

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

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

Increased extracellular concentrations of glutamate during episodes of cerebral ischemia may be due in part to a positive glutaminergic feedback loop. We evaluated the effect of selective AMPA or NMDA receptor antagonists on hippocampal extracellular concentrations of excitatory amino acids during ischemia and reperfusion. Thirteen New Zealand white rabbits were subjected to 10 min of global cerebral ischemia produced by neck tourniquet inflation (20 psi) combined with systemic hypotension during halothane (1-1.5%) anesthesia. Hippocampal extracellular concentrations of glutamate, aspartate, and glycine were monitored using in vivo microdialysis. NBQX (a selective AMPA receptor antagonist), MK801 (a noncompetitive NMDA receptor antagonist), or 5% dextrose was administered starting 1 h before ischemia. The NBQX group (n = 4) received 5 mg.kg-1 of NBQX intravenously (dissolved in 5% dextrose) over 5 min followed by an infusion of 5 mg.kg-1.h-1. The 5% dextrose group (n = 4) received an equivalent volume of 5% dextrose. The peak concentrations of glutamate, aspartate, and glycine in the early reperfusion period were 5-8-fold, 9-10-fold, and 4-5-fold higher than preischemic values, respectively. There were no significant differences, however, among the three groups in the concentrations of glutamate, aspartate, or glycine at any time during the study. These results do not support the existence of a positive feedback loop for glutamate mediated via AMPA or NMDA autoreceptors in the hippocampus during transient global ischemia or reperfusion.
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PMID:AMPA and NMDA receptor antagonists do not decrease hippocampal glutamate concentrations during transient global ischemia. 135 5

To determine whether cytotoxic brain edema is associated with a decrease in diffusion, it was induced in rats, in the absence of ischemia, with an established model of acute hyponatremic encephalopathy. Cytotoxic brain edema secondary to acute hyponatremia was induced with intraperitoneal injections of 2.5% dextrose in water and subcutaneous injection of arginine-vasopressin. Coronal spin-echo magnetic resonance (MR) images were obtained with and without strong diffusion-sensitizing gradients before and after induction of acute hyponatremia. The apparent diffusion coefficient (ADC) was measured at two coronal section locations. In hyponatremic rats, the brain ADC was significantly reduced (P = .0153 and .0001) and was positively correlated with increased total brain water content (P = .0011). Plots of ADC versus total brain water showed a statistically significant inverse linear relationship between ADC and increasing brain water at the anterior coronal section location. The results indicate that the ADC may be a sensitive indicator of cytotoxic brain edema and thus may enable quantitative evaluation of such edema with diffusion-weighted MR imaging.
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PMID:Cytotoxic brain edema: assessment with diffusion-weighted MR imaging. 143 45

Retinal vessel changes were experimentally investigated by a combination of color fundus photography, fluorescein angiography, and histologic studies in beagles that were fed a 30% galactose diet for up to 66 months. Previously, we have described the appearance of pericyte ghosts, microaneurysms, acellular capillaries, and intraretinal hemorrhages in dogs fed a galactose diet for up to 36 months. These disorders were similar to those observed in humans with background diabetic retinopathy. We report herein that dogs fed galactose for 48 to 60 months experience retinal changes associated with the chronic occlusion of capillary beds and subsequent ischemia of the retina. These changes included the appearance of broad areas of nonperfusion, soft exudates (cytoid bodies), intraretinal microvascular abnormalities, occluded arterioles, preretinal and intravitreal hemorrhages, and apparent new vessel growth around the optic disc. The present study clearly demonstrates that the galactose-fed dog is an animal model in which advanced retinal changes develop, and these changes are similar to those associated with preproliferative human diabetic retinopathy.
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PMID:Diabeteslike preproliferative retinal changes in galactose-fed dogs. 848 28

Peripheral A-delta and C fibers are activated during the production of ischemic or tourniquet pain; however, individual metabolic or molecular factors responsible for neural activation are not known. To elucidate these mechanisms the in vitro corneal nerve preparation was used. Electrophysiologic effects of individual metabolic perturbations associated with ischemia (hypoxia, hypoglycemia, lactic acid, and decreased pH) were investigated on A-delta and C fiber nociceptors. Increased tonic action potential activity occurred in C fibers but not in A-delta fibers after ischemia. The conduction velocity of C fibers was 0.85 +/- 0.2 m/s (mean +/- SD). Under control conditions (n = 43) there was very little fluctuation in the baseline action potential frequency (+/- 3.2%). Hypoxia (n = 12) resulted in a 213 +/- 3.4% (mean +/- SD) increase in C fiber action potential frequency relative to control (P less than 0.001, ANOVA). L-glucose substitution for D-glucose (n = 8) increased C fiber discharge frequency by 653 +/- 28% relative to control (P less than 0.001) as did the combination of hypoxia and L-glucose substitution (n = 6) by 671 +/- 14%. Comparison of hypoxia versus hypoxia and hypoglycemia conditions did not show them to be statistically different (P greater than 0.5). Lactate (10-1000 micrograms/ml) at a pH of 6.9 or 7.4 did not alter the action potential discharge frequency in corneal C fibers (n = 5, P greater than 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of C fibers by metabolic perturbations associated with tourniquet ischemia. 155 Feb 87

Stress gastritis frequently occurs in association with shock or sepsis. Gastric mucosal ischemia appears to be a key feature in these critically ill patients. The University of Wisconsin cold preservation solution (UWS) is an isoosmolar, nonglucose-based perfusate that minimizes hypothermia-induced cell swelling and prevents intracellular acidosis and oxygen-free radical injury, while providing high energy substrates for donor organs. In a prospective, single-blind study, 18 similar Sprague-Dawley rats were randomly divided to receive only 5 per cent dextrose and water (D5W) (Group 1) or a 50 per cent solution of D5W+UWS (Group 2) for 72 hours. At the end of 72 hours the animals were stressed by the cold-restraint model. The mean number of ulcers for Group 2 was nearly half that of Group 1. Also, Group 2 had a significantly lower mean total ulcer length (P less than 0.005) and ulcer index (P less than 0.05). Most of Group 2 had mild gastritis changes (grade 0 to 1), while more than half of Group 1 had severe gastritis (grade 3). Gastric mucosal pH was similar for both groups. Topically applied UWS appears to reduce the severity and incidence of stress gastritis in this experimental model. Because mucosal pH values were similar, it is thought that UWS may alter the effects of gastric mucosal ischemia at a cellular level.
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PMID:Prevention of stress gastritis with tissue preservation solution. 158 84

We measured the parameter lambda, which is the ratio of the distribution spaces of 2-deoxy-D-glucose (DG) and glucose in the brain, in a model of focal cerebral ischemia in the cat. lambda is the parameter in the lumped constant of the [14C]DG technique most susceptible to changes in ischemia. Cats were subjected to occlusion of the middle cerebral artery for a period of 2 h. During the last 60 min of occlusion, [14C]DG was infused in a programmed fashion so as to obtain a stable arterial blood [14C]DG concentration. The brain was funnel-frozen to preserve tissue metabolites and the frozen brain was sampled regionally (4 to 7-mg samples) for local concentrations of glucose, ATP, phosphocreatine (PCr), and lactate. In a separate series of cats, the infusion of [14C]DG was started after 2 h of occlusion and 3 h of recirculation. In both series, lambda declined slightly for increased levels of tissue glucose and increased appreciably as tissue glucose decreased. A similar relationship was observed between lambda and ATP and PCr, although the correlation was not as clear. Since lambda, and hence the lumped constant, increases in ischemia as well as in postischemic tissue, it is important to measure tissue glucose concentration if quantitative values of local cerebral glucose metabolism are desired in this condition.
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PMID:Effect of ischemia and reperfusion on lambda of the lumped constant of the [14C]deoxyglucose technique. 172 44

The advent of treatment modalities with the potential to ameliorate retinal ischemic injury calls for methods allowing their quantitative assessment. We thus established a model of pressure-induced retinal ischemia/reperfusion injury in rats. The intraocular pressure (IOP) was raised to 110 mm Hg by cannulation of the anterior chamber for a duration of 0, 90 or 120 min. The eyes were reperfused for 3 or 7 days. Morphologically, retinal injury occurred in a pattern consistent with retinal and choroidal vascular occlusion. Damage increased in severity with prolonged durations of ischemia. Morphometric determination of the mean thickness of inner retinal layers (MTIRL) revealed significant differences between controls and the 90- or 120-min ischemia groups (p less than 0.05 and p less than 0.01, respectively). The difference in MTIRL between 3 and 7 days of reperfusion was not significant. Replacement of normal saline by a solution of 5% dextrose in the hydrostatic device used to increase the IOP led to a decrease in retinal injury after 120 min of ischemia (p less than 0.01). This model combines a relatively simple methodology, cost-effective execution and a fast, semicomputerized method of quantitation. Depletion of carbohydrates during ischemia may contribute to retinal injury in this model.
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PMID:Pressure-induced retinal ischemia in rats: an experimental model for quantitative study. 177 2


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