Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Passive intracoronary perfusion of therapeutic agents has been used in the clinical setting to attenuate the effects of brief episodes of myocardial ischemia. The objective of this study was to assess the effects of low-flow coronary infusion with or without Mg2+ on tissue necrosis and cardiac hemodynamics after prolonged regional ischemia. In 33 anesthetized dogs (5 excluded during study), the left anterior descending coronary artery was occluded for 6 h. Dogs were assigned to three groups: the first group (n = 8) was subjected to 6 h coronary occlusion without low-flow perfusion (controls), the second group (n = 10) received a low-flow coronary infusion of Ringer's lactate (Mg(2+)-free), and the third group (n = 10) received a low-flow coronary infusion of Ringer's lactate plus Mg2+ sulfate (15 mM). Tissue necrosis was evaluated using tetrazolium staining and was normalized to the principal baseline predictors of infarct size including anatomic risk zone (microsphere autoradiography) and coronary collateral flow. In control hearts, infarct size comprised 51.1 +/- 4.1% of the risk zone (40.8 +/- 5.1% left ventricular cross-sectional area (LV)). In the Mg(2+)-free and Mg2+ groups, risk zone size was 17.3 +/- 2.2 and 16.8 +/- 1.8% LV (p < 0.05 vs. controls), while infarct size was 23.1 +/- 3.1 and 24.9 +/- 8.1% (p < 0.05 vs. controls), respectively. Coronary collateral flow in the endocardium was similar for all of the experimental groups; however, hearts subjected to ischemia with low-flow perfusion of Ringer's lactate demonstrated significantly higher epicardial coronary collateral flow levels compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium. 145 Oct 22

The limitation of a myocardial necrotic area by some energy-yielding compounds in rat coronary occlusion and their capacity to elevate the ischemia threshold in conscious rabbits were studied. Sodium malate, ascorbic acid and phosphoenolpyruvate were demonstrated to reduce the sizes of necrotic areas and increase the ischemia threshold, whereas cytochrome C and fructose-1,6-diphosphate were effective solely in limiting the infection area. It was concluded that the preventive antianginal effect of energy-yielding and electron-accepting compounds depended on their capacity to accumulate in intact cardiomyocytes.
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PMID:[A comparative evaluation of the cardioprotective and antianginal actions of energy-providing agents]. 145 76

The effect of endothelin-1 (ET-1) and big ET-1 on coronary flow and contractile function was determined in isolated nonischemic and ischemic rat hearts. Both ET-1 (IC50 = 12 pMol) and big ET-1 (IC50 = 2 nMol) reduced coronary flow in a concentration-dependent manner, although ET-1 was > 100-fold more potent. Both compounds decreased contractility, an effect which was lost when coronary flow was held constant, indicating that ET-1 and big ET-1 decrease contractility secondary to reducing coronary flow. Mechanical reduction in coronary flow to levels equivalent to those seen for ET-1 or big ET-1 caused similar reductions in contractility. Both 30 pMol ET-1 and 10 nMol big ET-1 pretreatment significantly reduced the time to contracture in globally ischemic rat hearts, suggesting a proischemic effect. Phosphoramidon (100 microM, endothelin-converting enzyme inhibitor) and BQ-123 (0.3 microM, ETA receptor antagonist) abolished the preischemic increase in coronary perfusion pressure induced by big ET-1 as well as its proischemic effect, whereas only BQ-123 abolished the cardiac effect of ET-1. Neither phosphoramidon nor BQ-123 had an effect on severity of ischemia when given alone. Phosphoramidon was also given i.v. to rats subjected to coronary occlusion and reperfusion and was found to significantly reduce infarct size 24 hr postischemia. Thus, in isolated rat hearts, big ET-1 appears to be converted to ET-1 and is a potent coronary constrictor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of endothelin-1 and big endothelin-1 in modulating coronary vascular tone, contractile function and severity of ischemia in rat hearts. 146 21

The effects of ischemic preconditioning on epicardial T-Q and S-T segment mapping, local activation, and coronary blood flow were analyzed in nine barbiturate-anesthetized pigs during four coronary occlusion (5 min)-reperfusion (20 min) sequences. In seven sham pigs, one occlusion was performed after a control period of 75 min. The first reperfusion induced a marked coronary hyperemia [11 +/- 4 ml/min (baseline) to 33 +/- 16 ml/min, P < 0.005] and a rapid recovery (30 to 150 s) of epicardial activation delays, T-Q segment depression, and S-T segment elevation in the ischemia area. This recovery was transiently associated with enlargement of intersite T-Q potential variability (alpha: 2.5 +/- 0.6 to 3.4 +/- 0.7 mV, P < 0.05), T-Q segment overshoot to +1.4 +/- 0.9 mV, and S-T segment reelevation. A brief T-Q segment depression (-2.3 +/- 0.9 mV) occurred during early reperfusion in 60 of 91 electrodes overlying the normal myocardium. Compared with the first, the fourth occlusion induced lower S-T segment elevation (3.4 +/- 2.0 to 1.7 +/- 1.9 mV, P < 0.05), and the fourth reperfusion elicited a faster reversal of T-Q segment dispersion (53 +/- 21 to 43 +/- 16 s, P < 0.05), S-T segment elevation (149 +/- 101 to 81 +/- 45 s, P < 0.05), and coronary hyperemia (8 +/- 2 to 5 +/- 1 min, P < 0.05). This trend of changes was not observed during a fourth occlusion in sham pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:T-Q, S-T segment mapping and hyperemia in reperfused pig heart with ischemic preconditioning. 148 98

Ro 40-5967 is a new calcium channel antagonist that binds at the same membrane sites as verapamil, yet has minimal negative inotropic effects. The effects of Ro 40-5967 on the susceptibility to ventricular fibrillation were investigated and compared to diltiazem. Ventricular fibrillation (VF) was induced in 40 mongrel dogs with healed myocardial infarctions by a 2-min coronary occlusion during exercise. Twenty-four animals were found to be susceptible to VF and were given the treatments described below. Pretreatment with Ro 40-5967 (n = 17, 1000 micrograms/kg i.v.) significantly (P < 0.001) reduced the incidence of VF (13 of 17 protected) during the exercise plus ischemia test. Diltiazem (n = 8, 1000 micrograms/kg) completely suppressed VF. Lower doses of diltiazem and Ro 40-5967 did not prevent VF. The hemodynamic effects of Ro 40-5967 were also compared to diltiazem and verapamil. Diltiazem and verapamil, but not Ro 40-5967, increased P-R interval in a dose-dependent manner. Even when reflex tachycardia was controlled by beta-adrenoceptor blockade, Ro 40-5967 still exerted only minimal effects on P-R interval. Verapamil, but neither Ro 40-5967 nor diltiazem, provoked a dose-dependent negative inotropic response. All three drugs elicited large increases in coronary blood flow. These data support the hypothesis that calcium entry may play a critical role in the development of malignant arrhythmias during ischemia. Further, Ro 40-5967 can protect against ventricular fibrillation without significant negative inotropic or dromotropic effects.
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PMID:Ro 40-5967, a novel calcium channel antagonist, protects against ventricular fibrillation. 149 May 22

Thirty patients with severe pump failure (Killip's degree III or more) complicating acute myocardial infarction (MI) underwent emergency coronary bypass grafting (CABG). Average age was 66 years old and CABG was performed 2.6 days after the onset of MI. The patients were divided into two groups according to the mechanisms that can bring about severe pump failure: 19 patients had large MI alone (G-I). The other 11 patients had severe ischemia occurring either at areas distant from the site of coronary occlusion or in the previous area at risk (G-II). To estimate the ventricular wall motion quantitatively, the left ventricular wall was divided into 17 segments. Each segment was graded on a four-point scale: akinesis, 3; severe hypokinesis, 2; hypokinesis, 1; normal 0. Wall motion score was estimated by summing the number of asynergic segments score. In G-I, Cardiac index (CI (l/min/m2)) increased from 2.03 +/- 0.91 to 2.68 +/- 0.73 and pulmonary wedge pressure (PCWP (mmHg)) decreased from 28 +/- 5 to 15 +/- 5, 72 hours after the surgery (p < 0.01). In G-II, CI increased from 2.17 +/- 0.78 to 3.17 +/- 1.01 and PCWP decreased from 29 +/- 6 to 13 +/- 5 after the surgery (p < 0.01). There was no difference in preoperative and postoperative hemodynamics between two groups. The wall motion score at the risk area did not change postoperatively (from 16 +/- 7 to 17 +/- 9 in G-I, from 15 +/- 8 to 11 +/- 5 in G-II).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Emergency coronary artery bypass grafting in patients with severe pump failure complicating acute myocardial infarction]. 149 Nov 91

The purpose of this investigation was to characterize the effects of nitrous oxide or nitrogen (70%) on systemic and regional hemodynamics and myocardial tissue perfusion after a brief coronary artery occlusion (15 min) and reperfusion (3 h). Two groups of experiments (14 experiments total) were completed with 24 open-chest, barbiturate-anesthetized dogs. Coronary collateral blood flow was diverted from the ischemic zone during coronary artery occlusion to eliminate a source of variability in degree of ischemia produced by differences in degrees of collateral blood flow among animals. Seven of 16 dogs treated with nitrous oxide and 7 of 8 dogs treated with nitrogen survived coronary occlusion and reperfusion (P less than 0.05). Coronary artery occlusion produced paradoxical systolic bulging in the ischemic zone in both groups of experiments. After reperfusion, segment shortening gradually returned toward control levels but remained depressed from the preocclusion state after 3 h in the nitrogen-treated control group. Similar results were observed after reperfusion in the nitrous oxide group; however, segment function in the ischemic region was significantly (P less than 0.05) depressed throughout the 3-h reperfusion period compared with the control group. Transmural coronary collateral blood flow during occlusion was not significantly different (P greater than 0.05) between groups, indicating that differences in recovery of contractile function observed between groups could not be attributed to differences in myocardial oxygen supply. In addition, the similarity in systemic hemodynamics between the nitrous oxide and control groups indirectly suggests that differences in recovery of function could not be attributed to differences in myocardial oxygen demand. The results indicate that 70% nitrous oxide produces greater mortality after coronary artery occlusion and reperfusion and reduces functional recovery of post-ischemic, reperfused myocardium compared with 70% nitrogen in open-chest, acutely instrumented dogs.
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PMID:Nitrous oxide impairs functional recovery of stunned myocardium in barbiturate-anesthetized, acutely instrumented dogs. 153 Jan 67

Neomammalian and paleomammalian (limbic) brain structures control different behaviors and the autonomic support specific to each. Both neural systems are involved in cardiovascular disorders. Our previous studies showed that bilateral cryoblockade of a neomammalian structure (the frontal lobes) reduces blood pressure elevations in experimental hypertension and prevents lethal arrhythmogenesis in experimental myocardial infarction. Other studies showed that bilateral lesions in a paleomammalian structure (amygdala) also reduce the blood pressure elevations. Thus, we hypothesized that cryoblockade of the amygdala would prevent lethal arrhythmogenesis. We found that cooling of cryoprobes implanted bilaterally in the amygdala prevented ventricular fibrillation in five of eight pigs during a 20-minute period of reversible myocardial ischemia, whereas cryoblockade in structures surrounding the amygdala (five pigs), unilateral cryoblockade in the amygdala (two pigs), or sham operations (three pigs) did not prevent ventricular fibrillation (p less than 0.003). In two of the five pigs with amygdaloid blockade, the cooling was reversed at 20 minutes while the coronary occlusion continued (24 hours), and still ventricular fibrillation did not occur. In all other cases, ischemia was reversed at 20 minutes so that the heart could recover; this enabled histochemical documentation that the heart was normal at the time(s) ischemia was induced, and it allowed within-subject control experiments. Amygdaloid cryoblockade produced a small but significant increase in heart rate (10 beats per minute) without a change in blood pressure. We conclude that the paleomammalian brain, like its neomammalian counterpart, mediates brain effects on fatal arrhythmogenesis.
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PMID:Cryoblockade in limbic brain (amygdala) prevents or delays ventricular fibrillation after coronary artery occlusion in psychologically stressed pigs. 153 95

Calcium antagonists may have a valuable role in ameliorating the extent and duration of myocardial ischemia following infarction. The precise cellular effects of these agents are being revealed through studies using the model of transient coronary occlusion induced by coronary angioplasty. The class of calcium antagonists is not uniform, and these diverse agents may have a favorable effect on ischemia through one or more of the following mechanisms: direct cardioprotective effects, prevention of calcium accumulation in the mitochondria in ischemic cells, reduction in oxygen consumption or in coronary artery vasoconstriction or coronary spasm, prevention of ischemia-induced arrhythmias, and increased coronary blood flow to ischemic tissue directly or through enhancement of collateral flow. Recent studies of diltiazem, nifedipine, nicardipine, nisoldipine, and amlodipine, as representative agents, are reviewed.
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PMID:Perspective: the cellular influences of calcium antagonists on systemic and coronary hemodynamics. 154 39

The role of anions in the initiation of ischemia- and reperfusion-induced arrhythmias is unknown. We examined the antiarrhythmic effects of isotonic substitution of extracellular Cl- with NO3- by using the rat Langendorff preparation (n = 12 per group). During 30 minutes of regional ischemia, the incidence of ventricular fibrillation (VF) was reduced from 50% in hearts perfused with control solution (containing a Cl-:NO3- ratio of 100:0) to 25%, 0% (p less than 0.05), 0% (p less than 0.05), and 0% (p less than 0.05) by perfusion with solution containing Cl-:NO3- ratios of 75:25, 50:50, 25:75, and 0:100, respectively. The incidence of reperfusion-induced VF was also reduced from 58% to 25%, 8% (p less than 0.05), 8% (p less than 0.05), and 0% (p less than 0.05), respectively. Similar effects were produced in hearts reperfused after briefer durations of ischemia (10 or 15 minutes). Substitution of NO3- for Cl- also facilitated spontaneous termination of VF. Heart rate and occluded zone size were not affected by anion manipulation. Coronary flow was affected by NO3-, but changes did not correlate with arrhythmias. During ischemia, electrocardiographic changes indicative of class III activity (widening of the ventricular complex) were produced by anion substitution. These changes occurred selectively in the ischemic tissue with no significant influence before ischemia onset. However, the relation between this effect and arrhythmia reduction was not linear and a cause-effect relation is therefore unlikely. In separate groups of hearts (n = 12 per group), switching from 100:0 to 0:100 Cl-:NO3- solution or vice versa 10 seconds after coronary occlusion or just before reperfusion demonstrated that 1) protection against ischemia-induced VF resulted partly from an action in the ischemic zone and partly from an action in the nonischemic zone, and 2) protection against reperfusion-induced VF resulted principally from an action occurring during reperfusion and within the reperfused tissue. To assess whether benefit was offset by deleterious effects on contractile function in nonischemic tissue, we constructed Starling curves in isolated rate hearts. The 0:100 Cl-:NO3- solution had no effect on compliance or contractility at physiological end-diastolic pressures but reduced the slope of the peak systolic pressure-volume relation by approximately 20% as end-diastolic pressure was increased above 10 mm Hg. In conclusion, anions appear to play a hitherto unrecognized role in arrhythmogenesis in ischemia and reperfusion. Manipulation of anion homeostasis may represent a novel target for antiarrhythmic drug development.
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PMID:Anion manipulation: a new antiarrhythmic approach. Action of substitution of chloride with nitrate on ischemia- and reperfusion-induced ventricular fibrillation and contractile function. 155 Nov 89


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