Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether propranolol, which has been shown to reduce the extent of myocardial infarction, reduces microvascular injury which may play a role in exacerbating ischemia. Saline (10 dogs) or propranolol (2 mg/kg i.v., 7 dogs) was injected prior to a one hour occlusion of the left anterior descending coronary artery. Carbon black (1 ml/kg), which labels damaged and leaky vessels, was injected 5 min after release of the occlusion and allowed to circulate for two hours. By morphometric analysis of 1 micron thick sections, 75 +/- 12% of vessels and 84 +/- 7% of myocardial cells showed damage in untreated dogs; only 2 +/- 1% of vessels and 9 +/- 8% of myocardial cells showed damage in the propranolol-treated dogs (P less than 0.001). The number of carbon black-labeled vessels/10 fields/biopsy from comparable areas of ischemic tissue was 55 +/- 7 in untreated dogs and 27 +/- 3 in propranolol-treated dogs (P less than 0.001). The results suggest that propranolol not only protects the ischemic myocardial cell, but also significantly decreases the ischemic microvascular changes.
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PMID:The effect of propranolol on microvascular injury in acute myocardial ischemia. 87 Feb 45

Studies were performed to determine whether an alteration in coronary vascular resistance and a reduction in the reflow phenomenon occurred in the blood-perfused, heparinized canine heart after various periods of myocaridal ischemia. Regional myocardial blood flow was measured with radioactive microspheres. Proximal left anterior descending coronary artery blood flow was measured with a periarterial flow transducer. Reduced reflow to the ischemic portion of the left ventricle and increased resistance in the left anterior descending coronary artery were present after 120 minutes of myocardial ischemia. The reduction in reflow was specific to the subendocardium of the ischemic area. Saline and isosorbide dinitrate (Isordi) did not prevent the increase in coronary vascular resistance or the significant reduction in reflow to the subendocardial portion of the ischemic area. Hypertonic mannitol given so as to increase serum osmolality 40 mosmoles/kg prevented the increase in coronary vascular resistance and modified the reduction in the reflow phenomenon to the subendocardial portion of the ischemic area. Thus, both an increase in coronary vascular resistance and a significant reduction in reflow to the subendocardial portion of the ischemic area occur in the canine heart after 120 minutes of myocardial ischemia. Moreover, the increase in coronary vascular resistance can be prevented and the reduction in reflow to the subendocardial portion of the ischemic area can be modified by the administration of hypertonic mannitol.
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PMID:Reduced myocardial reflow and increased coronary vascular resistance following prolonged myocardial ischemia in the dog. 113 70

The objective of this study was to determine whether ATP-dependent potassium channel activation is involved in the mechanism by which nicorandil reduces postischemic contractile dysfunction produced by a brief period of ischemia (myocardial stunning). Barbital-anesthetized dogs were subjected to 15-min left anterior descending (LAD) coronary artery occlusion followed by 3-h reperfusion. Saline or nicorandil (100 micrograms/kg + 25 micrograms/kg/min) were infused 15 min before and throughout occlusion with or without addition of the KATP channel antagonist, glibenclamide 0.3 mg/kg as an intravenous (i.v.) bolus. Regional myocardial blood flow was measured by radioactive microspheres, and left ventricular (LV) segment function was measured by sonomicrometry. There were no significant differences between the groups in area-at-risk size or collateral blood flow. In contrast, nicorandil significantly reduced mean aortic blood pressure (BP) and the rate-pressure product (RPP) which persisted throughout the occlusion period. In addition, nicorandil markedly accelerated recovery of segment shortening in the ischemic/reperfused region as compared with control dogs. Pretreatment of dogs with glibenclamide blocked none of the hemodynamic effects of nicorandil, but it did prevent improvement in reperfusion segment function. The small dose of glibenclamide used had no effect on hemodynamics or the degree of stunning. Thus, these results suggest that nicorandil attenuates stunning in anesthetized dogs by a direct cardioprotective effect as a result of KATP channel activation in ischemic myocardium.
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PMID:Nicorandil attenuates myocardial dysfunction associated with transient ischemia by opening ATP-dependent potassium channels. 128 Jul 39

The effects of continuous naloxone infusion on the response to intestinal ischemia-reperfusion were studied in a rat model. Naloxone was given as a bolus injection (2 mg/kg bw) followed by a continuous infusion (4 mg/kg bw/h) starting before (-10 min) intestinal ischemia was applied (0-60 min) and continuing 2 h after reperfusion of the intestine. Blood pressure, acidosis and survival were determined. Saline-infused shocked rats and untreated shocked rats served as comparisons and non-shocked animals as controls. Blood pressure was slightly higher before and during the continuous naloxone infusion but did not differ after reperfusion in the three shock groups. Acidosis was less pronounced in naloxone compared to untreated shocked rats. Survival rates were significantly higher in naloxone-treated shocked rats compared to untreated shock and significantly lower in saline treated shocked rats compared to non-shocked controls. In conclusion a naloxone effect on acidosis and survival in shock after intestinal ischemia and reperfusion is possible.
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PMID:Effects of continuous naloxone infusion in intestinal ischemia shock in the rat. 129 83

This study examined whether the adenosine potentiator, 5-aminoimidazole-4-carboxamide riboside (AICAr), could limit tissue necrosis during acute myocardial infarction in rabbit hearts with minimal coronary collateral flow. Forty-four rabbits underwent 45 min of ischemia with or without coronary reperfusion for 180 min. Five groups were studied. Saline or AICAr (20 mg/kg, i.v.) was administered as a bolus either 10 min before coronary occlusion or 10 min before the onset of coronary reperfusion. The anatomic risk zone size was assessed by radiolabeled microsphere autoradiography and the area of tissue necrosis was defined using the tetrazolium staining method. Coronary collateral flow in the central ischemic zone was assessed using the radiolabeled microsphere technique. No differences were observed for tissue necrosis (normalized to risk zone size) for saline- and AICAr-treated rabbits (66.2 +/- 10.9% vs. 70.8 +/- 19.9%, p = NS) subjected to 45 min of coronary occlusion without reperfusion. Similarly, tissue necrosis in rabbit hearts with 45 min of coronary occlusion followed by 180 min of reperfusion was not significantly reduced when AICAr was administered either 10 min before ischemia or 10 min before reperfusion (79.8 +/- 17.5 and 76.4 +/- 8.1%, respectively) compared to saline-treated controls (68.1 +/- 22.7%). Coronary collateral flow in these hearts was almost nonexistent. The risk zone size and cardiac hemodynamics were similar between the treatment groups. These results demonstrate that AICAr was unable to limit myocyte necrosis when administered either before ischemia or before coronary reperfusion in this experimental preparation of acute myocardial infarction.
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PMID:Failure of AICA riboside to limit infarct size during acute myocardial infarction in rabbits. 137 90

We have previously shown that gamma-hydroxybutyrate (GHB) protects the small intestine against ischemia/reperfusion injury. This study examined the effects of GHB on cardiovascular function and intestinal microcirculation following hemorrhage. Hypotension was induced in control group of hamsters by controlled hemorrhage to a mean arterial pressure (MAP) of 40 mm Hg. Following 60 minutes of hypovolemia the shed blood was returned. This procedure resulted in complete intestinal mucosal microvascular stasis 2 hours following the return of shed blood. A second group of animals was treated with GHB (600 mg/kg body weight) and, despite the loss of 37% of total blood volume, GHB treatment completely prevented the microcirculatory stasis, following the reinfusion of shed blood. In male Wistar rats treated with GHB (200 mg/kg) after the induction of hemorrhage, blood pressure rapidly increased to pre-hemorrhage levels following treatment, even though the shed blood was not returned. Cardiac output (CO) also increased to pre-hemorrhage levels. Sodium chloride solution, in the same molar concentration as GHB (23% NaCl), produced much smaller, but statistically significant, increases in MAP and CO. In animals given an equal volume of normal saline, a gradual increase in MAP was observed, reaching statistical significance at 75 minutes following treatment. Three hours following hemorrhage, serum levels of creatine kinase were 3-fold higher, whereas aspartate aminotransaminase and alanine aminotransferase levels were 2-fold higher in both normal saline and hypertonic saline-treated animals than in GHB-treated animals. These experiments suggest that GHB can prevent ischemic complications following a hypovolemic episode and may improve survival following severe hemorrhage.
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PMID:The cardiovascular effects of gamma-hydroxybutyrate following hemorrhage. 142 19

The potent and selective AMPA receptor antagonist NBQX was tested for cytoprotective properties in an adult rat model of transient focal neocortical ischemia. Nineteen spontaneously hypertensive rats sustained 2 h of middle cerebral artery occlusion, followed by 22 h of recirculation. Ninety minutes following the onset of ischemia, at the time of, and 30 min following reperfusion, they received i.p. injections of either saline (n = 10) or 30 mg kg-1 of NBQX (n = 9). Saline-treated rats had a mean volume of neocortical infarction ( +/- s.d.) of 181 +/- 31 mm3, while NBQX-treated rats sustained significantly less damage, 125 +/- 19 mm3 (p less than 0.001). Regional cerebral blood flows during ischemia and reperfusion were not affected by the drug. We suggest that the AMPA receptor may play an important role in ischemic cerebral infarction.
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PMID:Delayed AMPA receptor blockade reduces cerebral infarction induced by focal ischemia. 165 10

The effect of the sitting position on cerebral blood flow (CBF), spinal cord blood flow (SCBF), and cerebral metabolic rate for oxygen (CMRo2) was studied in anesthetized dogs with and without increased intracranial pressure. Blood flow measurements were made at four time periods: (a) initial supine; (b) after 5 min in the sitting position; (c) after 60 min in the sitting position; and (d) 15 min after resuming the supine position. Six dogs (group 1) served as a control group with a normal intracranial pressure (ICP). In five dogs (group 2) ICP was elevated with a parietal epidural balloon 1 h before the first measurements of blood flows were made. Saline was injected incrementally into the balloon so as to reach a steady-state ICP of 30 mm Hg for 1 h. Elevation of ICP in group 2 resulted in significantly lower CBF, SCBF, and CMRo2 compared with group 1. Postural changes in group 1 did not result in any significant change in blood flow measurements whereas in group 2, after 1 h in the sitting position, there were significant decreases in CBF and SCBF compared with the initial supine measurements. There was, however, no corresponding decrease in CMRo2 in group 2 with change in position. These data suggest that both the brain and spinal cord may be at risk for ischemia during sitting position procedures under general anesthesia in the presence of elevated ICP.
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PMID:Intracranial and spinal cord hemodynamics in the sitting position in dogs in the presence and absence of increased intracranial pressure. 230 45

Reversible, prolonged functional and metabolic abnormalities result from brief coronary occlusions with subsequent reperfusion (stunned myocardium). In the present study the effects of a new antiarrhythmic, vasodilator agent with intracellular calcium antagonist properties in vascular smooth muscle, KT-362 (5-[3-[( 2,3,4-dimethoxyphenyl]-ethyl)amino-1-oxopropyl]- 2,3,4,5-tetrahydro-1,5-benzothiazepine fumarate) on postischemic functional (percentage of segment shortening) recover and regional myocardial blood flow (radioactive microspheres) in the stunned myocardium were investigated in anesthetized dogs subjected to a 15-min coronary artery occlusion followed by 3 hr of reperfusion. Saline or KT-362 (300 micrograms/kg/min i.v.) were infused 15 min before and throughout occlusion of the left anterior descending coronary artery. There were no significant differences between groups in ischemic bed size or collateral blood flow, however, during ischemia and after reperfusion, KT-362 produced a significant decrease in the heart rate-systolic pressure product, an index of myocardial oxygen demand. In addition, there was a significant decrease in the incidence of reperfusion-induced ventricular fibrillation in the drug-treated animals. KT-362-treated dogs showed a marked improvement in myocardial segment function of the ischemic-reperfused region at 1, 2, and 3 hr of reperfusion as compared to the saline-treated animals (3 hr percentage of segment shortening of pretreatment: saline group, 14 +/- 10; KT-362 group, 59 +/- 7). These results demonstrate that KT-362 has a favorable effect on the functional recovery of the ischemic-reperfused myocardium and incidence of ventricular fibrillation, and may be of potential benefit as a new therapeutic agent for the treatment of coronary heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotective effects of a new vascular intracellular calcium antagonist, KT-362, in the stunned myocardium. 253 31

Both Trolox (a water-soluble analogue of alpha-tocopherol) and ascorbic acid were more effective than superoxide dismutase or catalase in protecting myocyte cell cultures from free radical attack (induced by hypoxanthine and xanthine oxidase). In a canine model of two hours of left anterior descending coronary artery occlusion followed by four hours of reperfusion, Trolox and ascorbic acid reduced the area of infarction within the area at risk. The Trolox group received 500 mL of deoxygenated saline solution containing 2.0 g of Trolox, 3.0 g of ascorbic acid, and 18 mg of EDTA (ethylenediaminetetraacetic acid) infused into the ascending aorta 30 seconds before and four minutes after reperfusion. Saline controls received 500 mL of deoxygenated saline solution containing 18 mg of EDTA. The angioplasty group had unmodified reperfusion by simple release of the occlusion. The area at risk and the area infarcted were estimated with Evans blue and triphenyl tetrazolium hydrochloride stains, respectively. The ratio of the area infarcted to the area at risk was significantly lower with Trolox (angioplasty, 30.4% +/- 5.1%; saline, 20.8% +/- 2.9%; and Trolox, 8.7% +/- 4.0%; p less than 0.01). In summary, the antioxidants Trolox and ascorbic acid effectively reduced myocardial necrosis after ischemia.
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PMID:Myocardial salvage with trolox and ascorbic acid for an acute evolving infarction. 271 29


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