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

Ischemic brain damage can be partially ameliorated by barbiturate therapy applied postinsult. Catabolism-induced brain hyperosmolality during ischemia may contribute to the development of brain edema after restoration of circulation. To determine changes in brain osmolality during ischemia and the effect of barbiturate anesthetics in altering its course, we measured whole and regional (cerebral cortex, diencephalon-midbrain, and cerebellum) brain osmolality for up to 2 hours after decapitation ischemia in unanesthetized and pentobarbital anesthetized rats. Normal (nonischemic) brain osmolality in pentobarbital anesthetized rats was 319 +/- 2 mOsm/1 (mean +/- SEM) and higher than in unanesthetized rats (307 +/- 6 mOsm/1). The rate of increase in whole brain osmolality was 60% slower in pentobarbital anesthetized rats in the first 60 minutes of ischemia and regional brain osmolality increased by a maximum of 32 mOsm/1 compared to 45 mOsm/1 in unanesthetized rats. The potential for edema based on percent change in brain osmolality as well as the rapidity of the change was greater in unanesthetized rats. The significance of the increase in brain osmolality with barbiturate anesthesia and its attenuation of the rate and magnitude of increase during ischemia is discussed.
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PMID:Rat brain osmolality during barbiturate anesthesia and global brain ischemia. 64 23

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

The clinical and pathologic data are presented on three patients who had clinical anoxia-ischemia in combination with serum hyperosmolality. The pathologic lesions consisted of perivascular necrosis, predominantly involving small vessels in the cerebral cortex. No intraluminal thromboembolic material was found in any of the vessels. The lesions are reminiscent of "no-reflow" lesions seen in experimental animals rendered ischemic.
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PMID:Perivascular anoxia-ischemia lesions in the human brain. 116 6

Elevation of extracellular osmolality reduces the extent of myocardial and endothelial cell swelling that accompanies acute ischemia, and the reduction of cell swelling is associated with an increase in collateral blood flow to the ischemic area. However, little is known about the effects of hyperosmolality on the vascular resistance of the collateral coronary vasculature. We compared the effects of hyperosmolar mannitol with those of nitroglycerin and dipyridamole on the vascular resistance of large collateral coronary vessels and of the small arterial vasculature in an isolated heart model of regional ischemia. Elevation of osmolality by mannitol increased collateral blood flow to the ischemic region through at least two mechanisms. First, increasing osmolality resulted in dilation of large arterial conductance vessels, similar to that produced by nitroglycerin. In addition, mannitol produced an effect on the coronary circulation at a microvascular level which, per se or in combination with its effect on larger collateral conductance vessels, increased collateral blood flow to ischemic regions.
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PMID:Hyperosmotic mannitol and collateral blood flow to ischemic myocardium. 250 18

In this study the attention was focused on the possible application of the new low-osmolar water-soluble contrast media in already existing routines for radiologic diagnostic work-up and management of the abdominal emergencies of simple intestinal obstruction and ischemia: Iohexol was a good, or better, alternative to sodium diatrizoate regarding taste acceptance and patient reactions: Seventy-five per cent of patients characterized the taste of iohexol as good or neutral, while 52% gave sodium diatrizoate similar scores. The scores were also consistently in favor of iohexol as compared with sodium diatrizoate for the other chosen criteria; nausea, vomiting and diarrhea, but a larger number of patients may be needed for conclusive evaluation. Water-soluble media may have therapeutic effects on intestinal obstruction when preceded by conventional gastric suction using a short gastric tube: Twenty-three of 25 patients with subtotal small bowel obstruction due to peritoneal adhesions improved following the ingestion of either iohexol or sodium diatrizoate. Hyperosmolar contrast media might stimulate peristalsis and dilute the bowel contents, hence, easing the passage through a subtotally obstructed bowel. In rats, a direct relationship was found between contrast medium osmolality and the degree of intestinal distension, fluid influx to the bowel lumen and the speed of contrast medium progression. The water-soluble, low-osmolar contrast media seem promising as diagnostic aids in examination of the gastrointestinal tract: The low-osmolar contrast media gave better intestinal details on films than both barium sulphate and sodium diatrizoate in rats with intestinal obstruction or ischemia when high volumes of radiopaques were employed. Also in patients iohexol retained its radiographic density in the small bowel better than sodium diatrizoate. The diagnostic efficacy of the water-soluble radiographic media varied directly with their osmolality and the resulting fluid influx to bowel lumen. Hyperosmolality stimulated contrast medium progression and bowel distension, and reduced the radiographic density of the contrast media and the alignment to the bowel wall. Water-soluble contrast media may aid the diagnosis of bowel ischemia and the evaluation of the degree of ischemic injury: No bladder opacification, following absorption of water-soluble contrast media from the simply obstructed bowel, was observed in the majority of the animals and was only faintly present in 8%. Distinct radiographic opacification of the urinary bladder in rats with intestinal ischemia was demonstrated as early as 1-2 hours after the administration of contrast medium.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Water-soluble contrast media in obstructed in ischemic small intestine. A clinical and experimental study. 264 49

The purpose of this study was to evaluate the effect of hyperosmolality on the performance of, and the collateral blood flow to, ischemic myocardium. The myocardial response to mannitol, a hyperosmolar agent which remains extracellular, was evaluated in anesthetized dogs. Mannitol was infused into the aortic roots of 31 isovolumic hearts and of 15 dogs on right heart bypass, before and during ischemia. Myocardial ischemia was produced by temporary ligation of either the proximal or mid-left anterior descending coronary artery. Mannitol significantly improved the depressed ventricular function curves which occurred with left anterior descending coronary artery occlusion. Mannitol also significantly lessened the S-T segment elevation (epicardial electrocardiogram) occurring during myocardial ischemia in the isovolumic hearts and this reduction was associated with significant increases in total coronary blood flow (P < 0.005) and with increased collateral coronary blood flow to the ischemia area (P < 0.005).THUS, INCREASES IN SERUM OSMOLALITY PRODUCED BY MANNITOL RESULT IN THE FOLLOWING BENEFICIAL CHANGES DURING MYOCARDIAL ISCHEMIA: (a) improved myocardial function, (b) reduced S-T segment elevation, (c) increased total coronary blood flow, and (d) increased collateral coronary blood flow.
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PMID:Improvement in myocardial function and coronary blood flow in ischemic myocardium after mannitol. 464 Sep 43

We studied the effects of different metabolic interventions, which stimulate oxidative myocardial carbohydrate metabolism, on ischemic stress during repeated coronary occlusions of three minutes in open-chest dog hearts. Increase of glucose concentration in plasma and decrease of peripheral lipolysis by glucose-insulin-potassium (n = 6) had no substantial beneficial effects on myocardial damage indicated by hemodynamic, electrocardiographic, and metabolic parameters. Infusion of lactate and pyruvate (10 mM, n = 6) was detrimental. Only activation of pyruvate dehydrogenase by dichloroacetate (n = 6) without influence on plasma osmolality reduced epicardial ST-segment elevations (-42%) and myocardial release of potassium (-36%), phosphate (-58%), and lactate (-39%). Elevations of plasma osmolalities by 10 and 20 mOsm with the metabolically inert mannitol increased ECG changes, functional loss and release of potassium, phosphate, and lactate during ischemia in our model. It is suggested, that the oxygen-saving potency of metabolic interventions can exert univocal beneficial effects in experimental and in clinical conditions only when systemic hyperosmolality and hypervolemia are avoided.
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PMID:Different effects of interventions suppressing free fatty acid metabolism on myocardial ischemia. 643 Jun 18

Little is known about blood to brain taurine transport despite substantial evidence suggesting a role of taurine in brain volume regulation during osmotic stress or conditions inducing cell swelling, such as ischemia. We have made measurements of the taurine influx rate constant (K1) with [3H]taurine in three conditions: raised plasma taurine concentrations induced by infusion with 50 mM taurine (10 microliters/100 g/min); osmotic stress induced by i.p. injections of 1.5 M NaCl (2 ml/100 g) or distilled water (10 ml/100 g); and 4 h of middle cerebral artery occlusion (MCAo). In rats with MCAo, additional determinations were made of tissue water and taurine contents, and blood-brain barrier passive permeability with [3H]alpha-aminoisobutyric acid. Taurine infusion increased plasma taurine from 110 +/- 63 microM (SD) to 407 +/- 63 (p < 0.001) and decreased taurine K1 at the blood-brain barrier by 70% (p < 0.001), signifying saturable uptake that maintained unidirectional influx constant. Similarly, although hypo- and hyperosmolality increased and decreased plasma taurine concentration, respectively, a reciprocal relationship between K1 and plasma taurine in these experiments ensured that unidirectional fluxes of taurine into brain were unchanged by osmotic stress. During MCAo, the taurine K1 was reduced 80% in the ipsilateral ischemic tissue compared with the contralateral nonischemic tissue (p < 0.001). This decline may be due to a release of taurine into the brain circulation, because there was a concomitant loss of tissue taurine of 7.4 +/- 2.4 mmol/g dry weight (p < 0.05). Alternately, if taurine uptake is sodium dependent, the decline might reflect a disruption of the endothelial sodium gradient.
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PMID:Blood-brain barrier taurine transport during osmotic stress and in focal cerebral ischemia. 767 78

The most serious effect of high sustained +Gz (head-to-foot inertial load) known to occur in pilots of high performance aircraft is +Gz-induced loss of consciousness (G-LOC), which may result in pilot incapacitation and subsequent loss of life. G-LOC is believed to occur due to a critical reduction in cerebral blood flow (CBF). Recently, using a small animal centrifuge (SAC), we showed that +Gz exposure causes global cerebral ischemia in a rodent animal model. Since ischemia, depending upon the severity and duration, has been associated with increased brain water content or edema, the present study was undertaken. Rats were exposed to six exposures of either +25 Gz (30 s each) or +10 Gz (2 min each) in the SAC at +20 Gz.s-1 G onset rate. The appearance of G-LOC was monitored by the flattening of the electroencephalography (EEG) brain wave recording. G-LOC was observed at 101 +/- 46 and 19.2 +/- 5 s during +10 and +25 Gz exposures, respectively. The brains from these animals were removed 15 min to 24 h after the +Gz exposure and analyzed for edema formation (increase in the percentage of tissue water), metabolites, and cerebral blood volume (CBV). A significant decrease in glucose and an increase in lactate concentration were observed during +Gz exposure. Edema formation was observed 15 min after six exposures of either +10 or +25 Gz. A slight but significant decrease in CBV was also observed in rats exposed to six +10 Gz exposures. Edema formation was transient and resolved within 24 h. We concluded that multiple exposures of either +25 Gz, short duration or +10 Gz, long duration, that resulted in G-LOC, can cause cytotoxic brain edema which probably results from tissue hyperosmolality due to metabolic changes and accumulation of lactate during ischemia.
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PMID:Multiple +Gz exposures cause brain edema in rats. 807 25

Acute mesenteric ischemia is a rare but severe complication after open heart surgery. Its incidence (0.2-0.4%) is quite low, but mortality rates are ranging between 70% and 100%. From October 1992 to December 1996, 4,640 patients underwent open heart surgery with cardiopulmonary bypass: 74.6% coronary artery bypass graft (CABG) operations, 23.2% valve replacement including aortic repairs, and 2.2% corrections of congenital heart diseases or tumors of the heart. The overall mortality rate (30 days) was 3.4%, and after CABG, 2.9%. Twelve patients (0.26%), following CABG (one combined with aortic valve replacement, one with mitral reconstruction, and one with carotid disobliteration) developed signs of acute mesenteric ischemia in the early postoperative period (day 1 to 5). In all patients various abdominal symptoms, leukocytosis, acidosis, hyperlactatemia, hyperosmolality, renal failure, and, finally, hemodynamic instability were observed. Eleven patients underwent emergency laparotomy. Mesenteric angiography was done if possible in still stable patients (n=7); it showed severe stenosis or occlusion prior to the operation in each case. Other diagnostic methods were not reliable. In six patients (55%) during the first look, extensive bowel necrosis was found and in five patients an ischemic intestine but no necrosis was detected. Of these, three patients were affected by extensive bowel gangrene at the second look. In the fourth patient a disseminated peripheral ischemia of the entire small intestine was found intraoperatively. After mechanical release and stimulation normal bowel function could be reestablished. One patient underwent percutaneous transluminal angioplasty prior to the laparotomy. Bowel perfusion was still deteriorated but no necrosis was found intraoperatively. These patients were the only survivors in the investigated group; 10 of 12 patients (83.3%) died in the early postoperative period (day 1 to day 6). Predisposing factors for mesenteric ischemia are: arteriosclerotic patients after CABG (100%), age >70 years (91.7%), hyperosmotic dehydration (100%), and cardiac ischemia in 25%. Mesenteric ischemia is a fatal complication with high mortality rates after open heart surgery, especially in older, dehydrated patients with generalized atherosclerotic vessel disease. As the acute mesenteric ischemia usually starts during anesthesia or in the early postoperative period, setting of immediate diagnosis is very difficult. With the occurrence of typical symptoms diagnostic and therapeutic procedures (angiography and laparotomy) must be done very urgently owing to the life-threatening mesenteric process. When mesenteric gangrene already has taken place, the prognosis is very poor, despite extensive resection. Prevention can be exercised by avoiding perioperative hyperosmotic dehydration of patients at high risk.
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PMID:Acute mesenteric ischemia after open heart surgery. 955 29


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