Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver. Massive myocardial infarction was then induced in intact and CCL4-treated animals. During acute necrosis (Days 1 thru 3), animals were killed at 4, 8, 12 and 24 h on Days 1 and 2, and during myocardial repair on Days 4, 5 and 8. During the induction of cirrhosis, animals developed polydypsia, polyuria, and hyperglycemia; during myocardial infarction, the arteriosclerotic + cirrhotic animals developed severe and persistent congestive heart failure, i.e., hydrothorax. Adrenal and thymus gland weights and corticosterone levels indicated that cirrhosis per se increased pituitary--adrenal activity, particularly in arteriosclerotic animals. Enzyme levels of SGOT and SGPT demonstrated severe hepatic damage due to cirrhosis and acute myocardial infarction. Blood triglycerides and cholesterol responded abnormally in cirrhotic animals during acute myocardial ischemia due to their entrapment within hepatic cells. The cirrhotic animals manifested poor myocardial repair with persistent foci of necrosis, calcification, and a high incidence of large, occlusive, atrial thrombi. It is suggested that cirrhosis interferes with lipid metabolism and adrenal steroid conjugation leading to abnormal levels of mineralocorticoids which favor congestive heart failure, poor myocardial repair, and atrial thrombosis.
 ...
PMID:Effect of CCL4-induced cirrhosis on the pathophysiologic course of acute myocardial infarction in nonarteriosclerotic vs arteriosclerotic male rats. 46 16

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
 ...
PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

Cardiac imaging with dipyridamole infusion has been proposed as an exercise-independent tool for the diagnosis of coronary artery disease. Dipyridamole acts through the accumulation of adenosine, which reduces sympathetic tone in vasomotor nuclei of the brainstem and inhibits norepinephrine release in noradrenergic neurons but also activates arterial chemoreceptors. The aim of this study was to assess whether dipyridamole administration (up to 0.84 mg/kg over 10 minutes, a dosage commonly employed for diagnostic testing) may modulate sympathetic activity either directly or indirectly through blood pressure reduction or myocardial ischemia, which may be evoked by dipyridamole infusion and represent two recognized sympathetic stimuli. Twenty patients were studied with infusion combined with two-dimensional echocardiography and 12-lead ECG monitoring. Blood pressure was recorded each minute by a cuff sphygmomanometer. In all patients, we obtained venous blood samples for epinephrine (an index of adrenomedullary catecholamine release) and norepinephrine (an index of neuronal activity) both in resting conditions and at peak dipyridamole, ie, at the first minute after termination of dipyridamole infusion in negative cases or in the presence of obvious ischemia in positive cases (ie, as soon as a regional ventricular dyssynergy or an ST segment depression greater than 0.1 mV appeared). Epinephrine and norepinephrine determinations were made by a high performance liquid chromatography (HPLC) method. After dipyridamole, there was a significant rise in norepinephrine, while epinephrine did not change significantly. Dipyridamole-induced percentage variations of norepinephrine from baseline were not significantly correlated with mean blood pressure changes (r = .1, p = ns) and were of a similar extent in patients with (n = 10) and without (n = 10) dipyridamole-induced ischemia (+68 vs +73 percent, p = ns). Dipyridamole administration provokes an activation of sympathetic tone which can be detected even in the absence of myocardial ischemia and is not related to blood pressure changes. The increased catecholamine release appears to be of neuronal rather than adrenomedullary origin.
 ...
PMID:Activation of sympathetic tone during dipyridamole test. 164 30

The purpose of the present study was to determine how propranolol modifies the circulatory effects of epinephrine infused to produce plasma concentrations achieved during dental local anesthesia and to evaluate the effects of propranolol on the plasma clearance of epinephrine. The study was performed on six healthy male volunteers ranging in age from 25 to 34 yr. Five measurement series were performed on each of these subjects at the following times: pretreatment control, 15 min after the beginning of the first epinephrine infusion (10 ng/kg/min), 15 min after the cessation of the first epinephrine infusion, 3 min after the intravenous injection of propranolol 40 micrograms/kg, and 15 min after the beginning of the second epinephrine infusion. Plasma epinephrine clearance decreased to 54.7 +/- 9.3% of the control value after propranolol was given. Epinephrine showed initially a predominantly beta-adrenergic action, but this action was inhibited by propranolol. A relative alpha-dominant state may then occur, even when a routine volume of dental local anesthetic is administered to a chronic user of a nonselective beta blocker, and it is postulated that myocardial ischemia may develop in such patients.
 ...
PMID:The influence of propranolol on the cardiovascular effects and plasma clearance of epinephrine. 184 59

To identify the effect of myocardial ischemia on systemic neurohormones and vascular resistance, 32 untreated, normotensive patients with coronary artery disease underwent incremental atrial pacing until angina. Arterial and coronary venous lactate and arterial values of catecholamines and angiotensin II were determined at control, at maximal pacing rates, and at 1, 2, 5 and 30 minutes after pacing. Based on pacing-induced ST-segment depression (greater than or equal to 0.1 mV) or myocardial lactate production, or both, patients were selected as ischemic (n = 25) or nonischemic (n = 7). Baseline clinical and hemodynamic data were comparable. During pacing, chest pain was similar (20 ischemic vs 7 nonischemic patients). Also, hemodynamic measurements were comparable, except for contractility, which did not improve, and left ventricular end-diastolic pressure, which significantly increased in ischemic patients. Moreover, during ischemia arterial pressures increased significantly (13%) and systemic resistance increased from 1,470 +/- 60 (control) to 1,632 +/- 76 dynes.s.cm-5 5 minutes after pacing (p less than 0.05) in ischemic but not in nonischemic patients. Pacing did not affect neurohormones in nonischemic patients. In contrast, norepinephrine in ischemic patients increased significantly from 1.7 +/- 0.2 (control) to 2.6 +/- 0.3 (maximal pacing) and to 3.0 +/- 0.4 nmol/liter (1 minute after pacing), whereas angiotensin II levels increased from 6.2 +/- 1.4 (control) to 9.3 +/- 2.1 pmol/liter (1 minute after pacing, p less than 0.05). Epinephrine only increased during maximal rates (0.9 +/- 0.1 vs 0.6 +/- 0.1 nmol/liter at control, p less than 0.05). Thus, myocardial ischemia activates circulating catecholamines and angiotensin II, accompanied by systemic vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Systemic neurohumoral activation and vasoconstriction during pacing-induced acute myocardial ischemia in patients with stable angina pectoris. 206 79

Cardiopulmonary bypass (CPB) reperfusion has demonstrated improved resuscitation rates in ventricular fibrillation cardiac arrest models. To investigate the effectiveness of CPB reperfusion in an ischemic cardiac arrest setting, simulating the clinical scenario of myocardial ischemia preceding sudden cardiac death, we developed a canine model of acute myocardial infarction followed by ventricular fibrillation. Sixteen dogs were randomly assigned to two groups. Group 1 (eight) had ventricular fibrillation induced without left anterior descending coronary artery occlusion. Group 2 (eight) had a thrombogenic copper coil placed in the left anterior descending artery and showed ECG evidence of acute myocardial infarction before induction of ventricular fibrillation. CPR commenced after eight minutes of ventricular fibrillation. Epinephrine 0.05 mg/kg and NaHCO3 1.0 mEq/kg were administered at ten minutes. CPB was begun at 12 minutes and continued for one hour. Myocardial ischemic and necrotic areas were determined in four-hour survivors by dual histochemical staining. All animals were resuscitated; all eight group 1 and six of eight group 2 animals survived to four hours. With the onset of CPB, coronary perfusion pressures increased significantly by 68.6 +/- 31.8 (SD) mm Hg in group 1 and 56.2 +/- 34.6 mm Hg in group 2 over those obtained with CPR (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cardiopulmonary bypass in a model of acute myocardial infarction and cardiac arrest. 237 69

Plasma catecholamine levels were obtained during diagnostic heart catheterization from the pulmonary artery and aorta and, similarly, renin levels were determined in the pulmonary artery in 31 patients with coronary heart disease and 18 normal controls. 3 months after aorto-coronary bypass surgery the patients with coronary heart disease underwent repeat heart catheterization and the epinephrine, norepinephrine and renin levels were compared with those obtained before operation. Norepinephrine decreased in the aorta from (means +/- SEM) 475 +/- 57 pg/ml to 360 +/- 38 pg/ml (p less than 0.001) postoperatively (controls 225 +/- 21 pg/ml). Epinephrine decreased from 121 +/- 11 pg/ml to 108 +/- 16 pg/ml (p less than 0.001) postoperatively (controls 84 +/- 9 pg/ml). This shows that postoperative relief from myocardial ischemia is associated with normalization of the preoperatively elevated plasma catecholamine levels).
 ...
PMID:[Changes in the catecholamine plasma level 3 months after aortocoronary bypass operation]. 265 86

The aim of this study was to elucidate the role of platelet aggregation as a risk factor for ischemic heart disease (IHD) and the relationship between fatty acids and platelet function. Platelet aggregation upon adenosine diphosphate (ADP), adrenaline and thrombin were measured in middle aged men in east and west, two regions of Finland with a nearly twofold difference in IHD mortality. Platelet aggregation results were correlated with the fatty acid compositions of plasma lipid fractions, adipose tissue triglycerides and platelet phospholipids. There was no significant east-west difference in platelet reactivity to ADP, adrenaline and thrombin. ADP-induced platelet aggregation showed significant negative correlations with all the platelet C20-C22 n-3 polyunsaturated fatty acids (PUFA), but significant positive correlations with the percentage of 18:2n-6 in adipose tissue and plasma cholesterol esters (CE) and triglycerides (TG). Adrenaline-induced aggregation correlated negatively with the percentage of 20:5n-3 in plasma CE and TG, and positively with the total percentage of saturated fatty acids in platelets. Aggregation upon thrombin had a negative correlation with the 20:3n-6/20: 4n-6 ratio in plasma CE and a positive correlation with 18:2n-6 in adipose tissue. The percentages of the major PUFA in platelets correlated significantly with the same fatty acids in plasma CE and phospholipids PL. Platelet 20: 5n-3 had a highly significant negative correlation with the percentage of 18: 2n-6 in plasma and adipose tissue lipids. Platelet 20: 4n-6 was unrelated to its precursors in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Dietary fats and platelet function among Finnish men. 292 2

To assess the effects of elevated epinephrine levels on cardiovascular performance in patients with coronary artery disease (CAD), epinephrine was infused intravenously into eight patients with normal coronary anatomy and 22 patients with CAD at dose rates of 0.06, 0.12, 0.18, and 0.24 micrograms/kg/min. Hemodynamic responses to epinephrine were not significantly different between the two groups. However, contractility increased significantly more (P less than 0.05) and end-systolic volume decreased significantly more (P less than 0.025) in normal subjects than in those with CAD. Plasma norepinephrine concentrations increased significantly (P less than 0.05) at 0.24 micrograms/kg/min epinephrine, indicating activation of sympathetic nervous system. Epinephrine ischemic thresholds ranged from 652 to 3362 pg/ml. Patients with CAD compared with normal subjects had more frequent ventricular arrhythmias (55% vs. 25%), chest pain (50% vs. 13%), and ischemic ECG changes (73% vs. 13%). These results indicate that although epinephrine induced myocardial ischemia in CAD, hemodynamics and ventricular pump function were maintained.
 ...
PMID:Effects of 1-epinephrine on hemodynamics and cardiac function in coronary disease: dose-response studies. 334 21

Lysophosphoglycerides accumulate in ischemic myocardium and induce electrophysiologic alterations in normoxic tissue in vitro closely resembling those seen with ischemia in vivo. Delayed afterdepolarizations and triggered activity may be particularly important in the pathogenesis of arrhythmias in the ischemic heart. The present study was performed to determine whether lysophosphatidylcholine (LPC), at concentrations comparable to those present in ischemic myocardium, can induce delayed afterdepolarizations and/or triggered activity in normoxic canine Purkinje fibers. In the present study, as little as 75 microM LPC was found to induce delayed afterdepolarizations and as little as 100 microM LPC was found to induce delayed afterdepolarizations and triggered activity even at low cycle lengths. The amplitude of the induced delayed afterdepolarizations was enhanced by augmentation of the extracellular concentration of calcium (7 mM) or by exogenous epinephrine (10(-9) to 10(-6) M). The amplitude was decreased by verapamil (1 mg/l) or Mn++ (2.5 mM). Epinephrine at a concentration of 10(-6) M also initiated triggered activity in Purkinje fibers exposed to LPC (75 microM), a response blocked by l-propranolol (2 X 10(-7) M and 10(-6) M) but not by the alpha 1-adrenergic blocking agent BE-2254 (10(-6) M). Delayed afterdepolarizations induced by LPC (75 microM) and epinephrine (10(-6) M) persisted even in the presence of acidosis (pH 6.7) and hyperkalemia ([K+]o = 7 mM). Thus, delayed afterdepolarizations and triggered activity induced by LPC may contribute to the induction and/or maintenance of arrhythmias early after the onset of myocardial ischemia. However, because of the reversal of these effects after superfusion with media devoid of LPC, they may occur with ischemia in vivo but not be seen in tissue isolated from ischemic regions and evaluated in vitro.
 ...
PMID:Induction of delayed afterdepolarizations and triggered activity in canine Purkinje fibers by lysophosphoglycerides. 379 82


1 2 3 Next >>