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

Cardiac prostaglandin release was studied in closed-chest dogs during acute coronary occlusion. Aortic and coronary sinus blood was obtained before, and at intervals after, balloon occlusion of the left anterior descending artery in seven dogs. Samples were assayed for prostaglandins F, E, and A by randioimmunoassay. All dogs demonstrated prostaglandin F release, Mean +/- SE postocclusion aortic levels were 0.26 +/- 0.01 ng/ml; coronary sinus levels were 0.67 +/- 0.01 ng/ml (P less than 0.001). In six dogs, prostaglandin E also was released. Mean postocclusion aortic levels were 0.24 +/- 0.01 ng/ml; coronary sinus, 0.44 +/- 0.01 ng/ml (P less than 0.001). There was no release of prostaglandin A. To examine the site of prostaglandin release, simultaneous samples from the aorta, the coronary sinus, and the great cardiac vein were obtained before and after left circumflex artery occlusion in six additional studies. The great cardiac vein drained effluent from nonischemic myocardium, whereas the coronary sinus drainage included blood from both ischemic and nonischemic zones. All six dogs demonstrated prostaglandin F release from the ischemic region. Mean postocclusion aortic prostaglandin F was 0.32 +/- 0.01 ng/ml. Coronary sinus prostaglandin F was 1.69 +/- 0.03 ng/ml (P less than 0.001), whereas the great cardiac vein level remained at 0.34 +/- 0.01 ng/ml (P greater than 0.05). Prostaglandin E was released from both ischemic and nonischemic regions. Mean aortic prostaglandin E was 0.21 +/- 0.01 ng/ml; great cardiac vein, 0.55 +/- 0.02 ng/ml (P less than 0.001); and coronary sinus, 1.07 +/- 0.04 ng/ml (P less than 0.001). These results have led us to conclude that the different local availability of prostaglandins E and F may influence the cardiac response to ischemia.
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PMID:Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs. 126 7

The effects of nicorandil, a nicotinamide nitrate with K(+)-channel-opening activity, was investigated in several models of ischemia-reperfusion injury in conscious and anesthetized dogs or isolated buffer-perfused rat hearts. In several models of reversible ischemic injury (stunned myocardium) in dogs, nicorandil resulted in an enhanced recovery of regional systolic shortening during reperfusion after a single episode of coronary artery occlusion (10-15 min). These beneficial actions of nicorandil were not shared by the nitrovasodilator sodium nitroprusside but were mimicked by the selective K(+)-channel opener EMD 52692. In a model of irreversible ischemia-reperfusion injury (i.e., 2 h of coronary occlusion followed by reperfusion) in anesthetized dogs, nicorandil produced a marked reduction of myocardial infarct size. An equihypotensive dose of the calcium antagonist nifedipine had no significant effect; however, EMD 52692 produced the same reduction in infarct size as had nicorandil. In isolated, perfused rat hearts subjected to 20 min of low-flow (1.0 ml/min) global ischemia followed by 30 min of reperfusion, nicorandil (7 microM) resulted in a significant improvement in the recovery of isovolumic left ventricular minute work during reperfusion compared with untreated hearts. Finally, the results of in vitro experiments indicated that nicorandil (10(-6) to 10(-3) M) produced a concentration-dependent inhibition of superoxide anion free radical production by human and canine neutrophils. The K(+)-channel opener EMD 52692 also inhibited superoxide production in canine neutrophils. These results indicate that nicorandil is a highly efficacious myocardial protective agent in several animal models of reversible or irreversible ischemia-reperfusion injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotective effects of nicorandil. 128 72

Using cardiac microdialysis, we studied release of the adenine nucleotide breakdown products (ANBP) adenosine (ADS), inosine (INS), and hypoxanthine (HYP) into the interstitium of canine myocardium during 20- and 40-min occlusion of the anterior descending coronary artery and reperfusion. Dialysate ANBP concentrations reached maximum values not at the end of ischemia but in the first 10 min of reperfusion. The effect was more pronounced after 20-min ischemia. Further reperfusion led to an ANBP decrease that was more prolonged after 40-min ischemia. Pretreatment with DL-propranolol (0.5 mg/kg, intravenously, i.v.) given 40 min before coronary occlusion had no effect on adenine nucleotide catabolism rate during 20- and 40-min ischemia, but it facilitated washout of ANBP from ischemic zone immediately after the start of reperfusion. A similar effect was elicited by a D-stereoisomer of propranolol with no beta-adrenoceptor blocking activity. Results suggest that the reperfusion injury and probably the no-reflow phenomenon were the cause of enhanced adenine nucleotide catabolism at the beginning of reperfusion and prolonged ANBP washout from the ischemic zone. Reduction of reperfusion injury by propranolol could be related to the membrane stabilizing and antioxidant activity of this agent. Examination of DL-propranolol kinetics in arterial and coronary venous blood plasma showed that drug accumulation in the myocardium was almost maximum at the start of ischemia; therefore, the efficiency of cardio-protection with DL-propranolol was not limited by pharmacokinetic causes. Insertion of an additional microdialysis probe in the myocardium allowed monitoring of extracellular propranolol concentrations.
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PMID:Cardiac microdialysis measurement of extracellular adenine nucleotide breakdown products during regional ischemia and reperfusion in canine heart: protective effect of propranolol against reperfusion injury. 128

The effects of early reperfusion were studied in closed-chest pigs subjected to either 45 min or 3 hr of regional ischemia. Myocardial enzyme release during early reperfusion and electrophysiological stability after two weeks were assessed. Coronary artery occlusion durations of 3 hr and early reperfusion after 45 min were compared. The creatine phosphokinase levels in the coronary effluent were lower after early reperfusion (p less than 0.001). Moreover, in the early reperfusion group, the coronary sinus catecholamine and purine levels rose to higher values than in the 3 hr group. The plasma levels of catecholamines and the plasma renin activity increased rapidly but transiently at reperfusion in the 45 min group. Both the rate-pressure product and the heart rate were elevated at the end of the reperfusion period (p less than 0.001) in the 45 min group. Survival for two weeks was 3 out of 6 animals in the 3 hr group and 5 out of 8 in the 45 min group. In all but one surviving animal, sustained ventricular tachycardias were inducible by programmed stimulation. Abnormally low QRS amplitudes and delayed potentials were found in the signal-averaged electrocardiogram in the early reperfusion group only. In conclusion, early reperfusion causes a reduction of myocardial tissue damage, but simultaneously, neurohumoral parameters showed a greater activation of the sympathetic nervous system and the renin-angiotensin system apparently causing a deleterious increase in oxygen consumption. Therefore, this injurious component of early reperfusion might prevent the potentially beneficial effects of a reduced tissue damage on survival or late arrhythmias.
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PMID:Neurohumoral changes and the inducibility of ventricular tachycardias: effect of early reperfusion on the ischemic porcine myocardium. 135 23

Myocardial ischemia followed by reperfusion was produced in artificially respirated, open-chest rats. Coronary artery ligation for 6 min rarely evoked arrhythmias; however, reperfusion after this period rapidly produced severe dysrhythmias in all control animals. Reperfusion after 12 min of ischemia produced less frequent dysrhythmias than after coronary occlusion for 6 min. Feeding of a linoleic acid-rich diet, applying 12% sunflower seed oil in rat food pellet for 4 weeks, decreased the incidence of reperfusion-induced ventricular fibrillation both after 6 min (2/15 vs. 7/11) and 12 min (0/11 vs. 2/8) of myocardial ischemia and the incidence of other arrhythmias was also decreased. The number of animals developing no arrhythmias during reperfusion was increased (8/15 after 6 min of ischemia, 4/11 after 12 min of ischemia vs. 0/11 and 0/8 in controls, respectively). Our results indicate that increased dietary consumption of linoleic acid decreased the occurrence of life-threatening arrhythmias both during the acute phase of myocardial ischemia and during reperfusion in anesthetized rats.
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PMID:Effect of dietary sunflower seed oil on the severity of reperfusion-induced arrhythmias in anesthetized rats. 137 86

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

The effects of decreasing blood viscosity by normovolemic hemodilution with dextran-40 or normal saline (NS) on myocardial lipid peroxides, superoxide dismutase, infarct size and left ventricular function during acute myocardial ischemia/reperfusion were studied in rabbits. It was found that normovolemic hemodilution with dextran-40 could decrease the content of ischemic myocardial malondialdehyde and preserve ischemic myocardial superoxide dismutase activity after 1 h of coronary occlusion followed by 1 h of reperfusion. However, after administration of NS only a tendency in this aspect exhibited without statistical significance. Besides, hemodilution with dextran-40 reduced infarct size and improved left ventricular systolic function after 1 h of ischemia followed by 23 h of reperfusion. These results suggest that normovolemic hemodilution with dextran-40 may have anti-injury effect on acute myocardial ischemia/reperfusion to a certain degree.
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PMID:The effects of normovolemic hemodilution with dextran-40 on acute myocardial ischemia/reperfusion injury in rabbits. 137 54

Previous results on the effects of angiotensin-converting enzyme (ACE) inhibition in myocardial ischemia are conflicting. To determine whether acute ACE inhibition may influence myocardial perfusion deficit during ischemia and reduce ischemia-reperfusion injury, anesthetized open-chest dogs underwent 2-h left anterior descending coronary artery (LAD) occlusion followed by 6-h reperfusion. After 1-h coronary occlusion, each dog was randomized to receive either captopril [5 mg/kg intravenous (i.v.) bolus and 0.25/kg/h infusion for 7 h] or saline. Whereas arterial pressure was reduced (p = 0.001), captopril did not influence myocardial perfusion deficit: Blood flow in the central ischemic zone represented 17.1 +/- 2.8% of the flow in the nonischemic zone versus 20.5 +/- 3.8% before treatment (NS). The values of the control group were 17.8 +/- 2.5 and 16.7 +/- 2.4%, respectively. In addition, there was no difference in infarct size: 35.9 +/- 3.3% of the area at risk in captopril-treated dogs versus 40.0 +/- 3.6% in controls. Analysis of subgroups based on the level of the collateral flow indicated, however, that ACE inhibition had an adverse effect on infarct size in dogs with high collateral flow: 31.9 +/- 4.6% in captopril dogs versus 17.6 +/- 4.7 (p = 0.048). This effect was related to a decrease in collateral flow because animals exhibiting the highest increase in perfusion deficit presented the greatest increase in infarct size (r = -0.92, p = 0.003). Although in dogs with low collateral flow, ACE inhibition appeared to exert a slight beneficial effect on infarct size, we conclude that at least in this dog model, acute ACE inhibition could exacerbate myocardial injury.
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PMID:Importance of the flow perfusion deficit in the response to captopril in experimental myocardial infarction. 137 9

Acute coronary occlusion during PTCA represents a significant procedural complication occurring in approximately 4-5% of cases, most frequently because of coronary dissection, spasm, or thrombosis. In these cases the first step in the management of acute ischemia is 1) a brief evaluation of its hemodynamic consequences and 2) the assessment and treatment of its cause. Spasm and intracoronary thrombus formation are usually readily identifiable and treatable using intracoronary nitroglycerin and thrombolytic therapy. In our catheterization laboratory the current approach to occlusive coronary dissection is represented by the use of autoperfusion dilatation catheters and by stent application. The atherectomy devices and the laser "welding" of the dissected intimal segment represent other alternatives that are still under clinical evaluation in this particular setting. If coronary occlusion is refractory to these efforts and coronary blood flow is not reestablished rapidly, emergency coronary bypass surgery is required to salvage jeopardized myocardium. In this case myocardial ischemia may be lessened by the insertion of an intra-aortic balloon pump. In our experience, the incidence of death (4%) and myocardial infarction (37%) for emergency CABG after a failed angioplasty, is similar to that reported by other Authors. The duration of myocardial ischemia and the presence of cardiogenic shock before operation are the most important determinants of major complications such as death and acute myocardial infarction.
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PMID:[Surgical indications and results of myocardial revascularization in complications of PTCA]. 142 76

The effect of different doses of perfluorocarbon emulsion (5, 10, and 15 ml/kg) on the hemodynamics and contractility of heart was studied on anesthetized dogs. The emulsion was introduced intravenously by the 60th minute of acute myocardium ischemia caused by partial coronary occlusion. When pO2 = 120 mm Hg, the emulsion was efficient only at doses of 10 and 15 ml/kg (an increase in cardiac ejection, in the rate of contraction and relaxation of the myocardium, reduction of vascular resistance). However, the efficiency of the emulsion at a dose of 15 ml/kg was lower, possibly, due to hypervolemia and cardiodepressive effect of introduction of excess quantity of the surface-active substance proxanol, a component of the emulsion.
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PMID:[Effects of different doses of perfluorocarbon emulsion on hemodynamics and contractility of ischemic heart]. 144 24


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