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

The circulatory effects of norepinephrine (4 micrograms/kg), isoproterenol (10 micrograms/kg) and phenylephrine (20 micrograms/kg) were determined in anesthetized dogs with normal plasma magnesium and with induced hypermagnesemia. Norepinephrine caused a 24% increase in heart rate and a 103% increase in the systemic vascular resistance index in normomagnesemic dogs, while with hypermagnesemia the variations were of 13% and 1%, respectively. Isoproterenol increased heart rate by 48% and 18% in dogs with normo- and hypermagnesemia, respectively. Phenylephrine increased the systemic vascular resistance index (74%) only in the normomagnesemic state. The effects of all the drugs were significantly different (P less than 0.01), without and with the simultaneous administration of magnesium sulfate (plasma magnesium, 1.3 +/- 0.2 mEq/l and 6.8 +/- 1.1 mEq/l, respectively). We conclude that acute induced hypermagnesemia antagonizes the circulatory effects of adrenergic stimulation, a fact that may explain its antiarrhythmic and hemodynamic effects during acute myocardial ischemia.
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PMID:The antiadrenergic effects of hypermagnesemia: an experimental study. 182 14

The aim of this study was to examine the electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on sheep Purkinje fibers in vitro, superfused either with a normal or with a modified physiological salt solution (PSS) designed to mimic some of the conditions occurring during mild myocardial ischemia (hyperkalemia, hypoxia, and acidosis). Intracellular microelectrode recording techniques were used to record resting and action potentials. Noradrenaline (10(-7) to 10(-5) M) and phenylephrine (10(-7) to 10(-5) M) prolonged the action potential of normal fibers in a concentration-dependent manner, the effect of phenylephrine being greater than that of noradrenaline. The only effect of isoprenaline (10(-7) to 10(-5) M) was a slight hyperpolarization. The modified PSS caused marked reductions in resting membrane potential, upstroke, and duration of the action potential. On these depressed fibers isoprenaline, noradrenaline, and phenylephrine all prolonged the action potential, and in the case of noradrenaline the duration of the abbreviated action potential was restored beyond control. This effect of noradrenaline and isoprenaline was more marked under ischemic than normal conditions, whereas the opposite was true of phenylephrine. In the presence of effective alpha- or beta-adrenoceptor blockade, the noradrenaline-induced prolongation of the "ischemia"-abbreviated action potential was attenuated. In some of the preparations exposed to simulated ischemia, noradrenaline caused inexcitability. In conclusion, isoprenaline, phenylephrine, and noradrenaline exhibited different electrophysiological effects on mildly "ischemic" sheep Purkinje fibers compared to their effects on normal fibers.
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PMID:Cardiac electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on normal and mildly "ischaemic" sheep Purkinje fibers. 246 60

Hypertension after carotid endarterectomy has a variable incidence ranging up to 56%. Blood pressure (BP) control is essential due to possible increased risk of morbidity from neurologic deficits or cardiovascular complications. This study evaluated intravenous labetalol for control of hypertension after carotid endarterectomy. Sixty ASA II-IV patients were studied; 20 developed BP high enough for treatment with labetalol. The anesthetic technique was standardized. Labetalol was administered at the conclusion of surgery as a 20-mg bolus over two minutes followed by 40 mg every 10 minutes until the desired BP was achieved (BP less than or equal to 10% above average preoperative BP or less than 150 mmHg, systolic) or 300 mg had been given. The mean total dose of labetalol was 42.0 +/- 33.0 mg (mean +/- SD) and mean time to reach the desired BP was 16.2 +/- 21.4 minutes. Systolic, diastolic, mean arterial pressure and heart rate significantly decreased after labetalol treatment and remained so for the remainder of the 180-minute study period. There was no hypotension, bradycardia, evidence of myocardial ischemia or central nervous system dysfunction present with labetalol treatment. Blood samples were obtained for determination of plasma renin activity, epinephrine, and norepinephrine in 10 patients who developed hypertension and received labetalol, and 10 patients who did not develop hypertension. In the patients developing hypertension, there was a significant elevation in epinephrine just before treatment, that decreased by 30 minutes after treatment. Norepinephrine levels became significantly elevated five minutes after labetalol treatment in the group with hypertension and remained elevated for 120 minutes. Concomitantly, there was a significantly lower plasma renin activity seen in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous labetalol for the treatment of hypertension after carotid endarterectomy. 257 2

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).
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PMID:[Changes in the catecholamine plasma level 3 months after aortocoronary bypass operation]. 265 86

Previous attempts to define the etiology of coronary arterial spasm have been focused on mechanisms such as autonomic nervous dysfunction and/or enhanced platelet activation. In the present study, humoral regulation was investigated in patients with vasospastic angina and scintigraphically documented transient myocardial perfusion abnormalities after a peripheral cold pressor test. Serial changes in angiotensin II, epi- and norepinephrine as well as thromboxane B2 (the stable derivate of thromboxane A2), and malondialdehyde were determined at baseline (I), immediately after 5 minutes cold water hand immersion (II), and following 10 minutes recovery (III). Angiotensin II and epinephrine remained unchanged during observation (I vs II, II vs III: P = NS). Norepinephrine was elevated after cold (I vs II: P less than 0.001) and normalized after 10 minutes (I vs III: P = ns). Thromboxane B2 and malondialdehyde increased continuously (I vs III: P less than 0.05 and I vs III: P less than 0.002, respectively). Further radiothin-layer chromatography results indicate an activation of platelet function during myocardial ischemia. Our results do not establish a cause-effect relationship but, together with other evidence, they may suggest that thromboxane A2 is unlikely to be the cause of spasm. It might, however, play an important role in the maintenance of vasoconstriction.
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PMID:Humoral regulation during cold-induced coronary arterial spasm. 280 8

Blood catecholamines (dopamine, adrenaline and noradrenaline) were measured in the coronary sinus and artery of 35 patients divided into 2 groups: coronary patients with stable angina of effort, functional class II-III (group 1) and patients with NCD (group 2), before and during a cardioselective load test (atrial stimulation). Developing myocardial ischemia was associated with a significant rise of noradrenaline in arterial and coronary venous blood. The use of isoptin changed noradrenaline balance, resulting in increased noradrenaline level in the coronary sinus, while coronary flow increased, as did the anginal threshold. Noradrenaline rise may well be an additional antianginal factor mediating the action of isoptin.
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PMID:[Effect of isoptin on catecholamine levels in arterial and coronary venous blood during an attack of myocardial ischemia]. 281 Oct 43

Serotonin (5-hydroxytryptamine) has multiple cardiovascular actions. The presence of serotonin in the heart suggests it may be an endogenous source of inotropic support during physiologic or pathologic stress. Serotonin may increase cardiac contractility by augmenting release of norepinephrine at sympathetic nerve endings. Norepinephrine release is markedly elevated in patients with heart failure. To explore the role of serotonin in enhancing norepinephrine release in patients with heart failure, ketanserin, a specific serotonin antagonist, was used as a physiologic tool to examine the effect on transmyocardial norepinephrine flux. Ketanserin (10 mg bolus, 4 mg/hr infusion for +/- 40 min) was administered intravenously to nine patients with congestive heart failure (NYHA III or IV) secondary to congestive cardiomyopathy (N = 7), or ischemic heart disease (N = 2). Plasma catecholamines (norepinephrine, epinephrine, dopamine) were measured in the aorta (Ao) and the coronary sinus (CS) of patients at rest and during supine leg exercise before and after administration of ketanserin. Baseline norepinephrine levels were markedly elevated at rest and during exercise in all patients. Norepinephrine levels were significantly higher in the CS than in the Ao (rest, CS 1185 +/- 235, Ao 878 +/- 381 pg/mL, P less than .05; exercise, CS 2239 +/- 697, Ao 1453 +/- 697 pg/mL, P less than .05). Baseline epinephrine levels were within normal limits. In contrast to norepinephrine levels, epinephrine levels were consistently higher in the Ao than in the CS, indicating unimpaired extraction or uptake across the heart. The relationship between norepinephrine and epinephrine concentration in the Ao and CS suggested a net overflow of norepinephrine in the CS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of 5-hydroxytryptamine blockade with ketanserin on myocardial uptake of epinephrine and norepinephrine in patients with congestive heart failure. 368 May 95

Central catecholaminergic nerves have been shown to participate in the integration of cardio-cardiac reflexes induced by coronary artery ligation in the rat. In this study we measured the turnover of dopamine, norepinephrine and epinephrine in microdissected brain regions to identify some of the specific neural loci involved in this integration. Three groups of rats, treated with alpha-methyltyrosine, an inhibitor of catecholamine biosynthesis were examined: left coronary artery ligation, left coronary artery ligation with the left ventricle painted with lidocaine, and sham operation. An untreated group of resting rats was also examined. Dopamine, norepinephrine and epinephrine turnover was increased in ligated rats in nucleus tractus solitarius (right and left), nucleus commissuralis, A1-region, locus coeruleus, nucleus cuneatus, and area postrema in the pons-medulla and nucleus dorsomedialis in the hypothalamus. Norepinephrine and dopamine (but not epinephrine) turnover was increased in nucleus ambiguus in the brain stem and nucleus paraventricularis in the hypothalamus. A ligation-induced increase in norepinephrine turnover, alone, was exhibited by the A2-region and nucleus gigantocellularis in the medulla and nucleus supraopticus and nucleus hypothalamicus posterior in the hypothalamus. Dopaminergic nerves to the nucleus gigantocellularis appeared to be inhibited following coronary ligation. The catecholamine stores of 11 nuclear regions were not influenced by coronary artery occlusion. Topical lidocaine, applied to the ischemic left ventricle, only, of ligated rats, completely restored regional brain catecholamine turnover to that found in sham-operated animals. In conclusion, we have identified discrete loci in the brain in which catecholamine turnover (as measured by alpha-methyltyrosine induced disappearance) is increased by the stimulation of left ventricular receptors during acute myocardial ischemia in the rat.
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PMID:The identification of specific brain nuclei in which catecholamine turnover is increased by left ventricular receptors during acute myocardial infarction in the rat. 718 30

Although it is well known that myocardial ischemia induces the depletion of myocardial ATP and sustained myocardial dysfunction, the mechanisms causing impaired myocardial function have not been elucidated completely. To clarify the relationship between ATP depletion and myocardial contractility, we investigated the influence of myocardial ATP depletion on spontaneous beating in cultured rat ventricular myocytes. Furthermore, because catecholamines have been used to improve myocardial contraction in the ischemic heart, we attempted to determine whether the ATP depletion per se alters the contractile responses to alpha 1- and beta-adrenoceptor stimulation. After 24 hr of culture in the presence of a metabolic inhibitor, 2-deoxyglucose (2DG, 5mM), myocardial contractility decreased to 19% of the vehicle level, and returned to normal after the removal of 2DG. The beating rate did not show any alterations in the vehicle, in the presence of 2DG (2DG [+/+]) or after the removal of 2DG (2DG [+/-]). Norepinephrine (NE) caused significant decreases in beating rate and increases in contractility in all groups. Isoproterenol (ISP) caused significant increases in beating rate and contractility in all groups. In the 2DG (+/+) group, the contractility was significantly lower as compared to other groups during NE or ISP stimulation. However, the percent change of contractility was similar to those of other groups after NE or ISP stimulation in the 2DG (+/+) group. These results suggest that decreased myocardial ATP causes the decreased contractility and does not affect the alpha 1- or beta-adrenoceptor-mediated responses.
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PMID:Effects of 2-deoxyglucose, a metabolic inhibitor, on spontaneous contraction and adrenoceptor responsiveness in cultured rat ventricular myocytes. 758 56

The purpose of this study was to determine the effect of dietary magnesium supplementation on blood pressure and cardiovascular function of Sprague-Dawley normotensive and mineralocorticoid-salt (DOCA-salt) hypertensive rats. The rats were pair-fed for 5 wk a purified diet containing either a normal or magnesium-supplemented diet (1.5 or 10 g/kg diet). Magnesium supplementation significantly lowered blood pressure levels in hypertensive rats, but not in normotensive rats. Heart rate was not affected in either group. The blood pressure-lowering effect of magnesium supplementation in DOCA-salt hypertensive rats was associated with a lower in vivo cardiovascular reactivity to norepinephrine and angiotensin II. Norepinephrine reactivity in isolated aortae from DOCA-salt hypertensive rats was not modified by magnesium supplementation. However, endothelium-dependent relaxation to acetylcholine was improved and could be related to the release of endothelial relaxant factors. Magnesium supplementation did not affect cardiac hemodynamics in isolated heart from either normotensive or DOCA-salt hypertensive rats. Furthermore, no protective effects upon myocardial ischemia and ventricular arrhythmias were demonstrated. These findings suggest that the lowering effect of magnesium supplementation on blood pressure in hypertensive rats may be related to a vascular effect of magnesium that reduces vascular tone. Mechanisms related to the pathophysiological development of mineralocorticoid-salt hypertension may be involved.
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PMID:Dietary magnesium supplementation modifies blood pressure and cardiovascular function in mineralocorticoid-salt hypertensive rats but not in normotensive rats. 772 84


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