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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta-Adrenoceptor agonists increase myocardial ischemic injury, mainly by elevating myocardial oxygen consumption. Moreover, it has been shown that isoprenaline may "steal" regional myocardial blood flow (RMBF) from ischemic to non ischemic areas and from epicardium to endocardium. The mechanisms of these two isoprenaline-induced redistributions of RMBF have been investigated by the use of radioactive microspheres in an experimental model of canine myocardial ischemia with simultaneous measurement of ST-segment elevation. Isoprenaline increased RMBF in both epi- and endocardial non ischemic areas and in epicardial ischemic areas, leading to a significant decrease in the endo/epi ratio. After atenolol, isoprenaline still increased RMBF but to a lesser extent and the endo/epi ratio was still decreased. Salbutamol, in doses inducing no significant changes in cardiac parameters or myocardial oxygen consumption, produced effects similar to those of isoprenaline. These results indicate a non-homogeneous beta2-stimulation-induced vasodilation in endo- and epicardium, which might be due either to the higher epicardial coronary vasocilatory reserve or to a heterogeneous distribution of transmural beta2-adrenoceptors. Isoprenaline also decreased the ischemic/non ischemic total blood flow ratio (I/NI) and caused further increases in ST-segment elevation. These effects were abolished by atenolol pretreatment, indicating the deleterious effects of isoprenaline-induced tachycardia in this I/NI decrease and in the ischemic injury.
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PMID:The role of beta-adrenoceptors in coronary blood flow distribution in normal and ischemic canine myocardium. 21 19

16 anesthetized and open chest dogs were studied. Regional myocardial perfusion was assessed using a constant infusion of krypton-81m (half-life 13 sec) into the aortic sinuses and a gamma camera linked to a digital computer. The epicardial electrocardiogram was recorded and the plasma activity of creatine kinase was measured in serial blood samples from the aorta and a local coronary vein draining the area of myocardium supplied by the left anterior descending coronary artery (LAD). These parameters were observed throughout the whole period of a 5-h experiment. Two reversible snares were positioned on the middle portion of this artery. A critical narrowing of this vessel was produced and a peripheral venous infusion of isoproterenol (causing a 5--10% increase in heart rate and a 10--15% fall in blood pressure) was used to increase myocardial oxygen demand. During infusion there was both a relative and absolute fall in regional myocardial perfusion together with evidence of myocardial ischemia in the epicardial electrocardiogram. Provided the infusion was discontinued within 30 min (8 dogs) myocardial perfusion and the epicardial electrocardiogram returned to normal during a 5-h recovery period. In addition there was no efflux of creatine kinase activity from the ischemic area. When infusion was continued for 1 h (4 dogs) permanent alterations in myocardial perfusion and the epicardial electrocardiogram occurred and there was increased creatine kinase activity released from the area of myocardium by the narrowed vessel. Infusion for 40 min in 4 dogs produced permanent alterations in the parameters measured in 2 and complete recovery in the remaining 2. A further 4 dogs were studied in the same way but without a snare on the coronary artery. Isoproterenol given for 1 h produced no effects on any of the parameters either during or after infusion.
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PMID:An experimental model for angina pectoris using krypton-81m. The dynamic balance between myocardial perfusion and metabolism. 47 4

18 patients with non-ischemic heart disease have been studied with reference to the kinetocardiographic changes before and after i.v. administration of dopamine (DOP) (Revivan) or Isoproterenol (ISP) (Aleudrin). For this purpose a simultaneous registration of ECG (lead D2), Kinetocardiogram (KCG) in K25 and K45 was performed. Volume curves were considered as a normal features of KCG, curves showing systolic outward movements during the ejection phase were classified as pathologic. The reduction or disappearance of the systolic movements during the drug administration, were considered as kinetic improvement, the increase of their site was judged as kinetic worsening. During the infusion, 17 KCGs maintained a normal morphological pattern; out of 19 pathological KCGs, 4 did not show any change, and 15, 5 reached a complete normalization. It is pointed out the overlap of the precordial kinetics in the ventricular hypertrophies and in the normal subjects (kinetic improvement), and the possibility to differentiate a systolic outward movement due to synergic contraction of hypertrophied ventricle from a systolic outward movement to be reffered to a diskynetic contraction in the myocardial ischemia (kinetic worsening).
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PMID:[Changes in precordial movements in non-ischaemic heart disease patients after i.v. administration of isoproterenol and dopamine. Comparison between normal and cardiopathic subjects (author's transl)]. 48 99

The effects of isoproterenol and dopamine on regional myocardial blood flow were studied in 10 open-chest dogs after acute stenosis of the proximal circumflex coronary artery. Blood flow was determined by the radioactive microsphere technique. Isoproterenol led to a homogenous increase in blood flow in the normal myocardium. In the myocardium with compromised coronary blood flow, isoproterenol led to a relative subendocardial ischemia. This occurred despite increased aortic flow and peak left ventricular dp/dt. Dopamine also increased aortic flow and peak left ventricular dp/dt, but it did not cause regional myocardial ischemia. The findings suggest that dopamine is the preferable inotropic agent in managing low cardiac output in patients with significant coronary artery disease.
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PMID:The effects of isoproterenol and dopamine on regional myocardial blood flow after stenosis of circumflex coronary artery. 83 34

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

Torsades de pointes (TdP) is a life-threatening ventricular tachycardia that occurs in the setting of a prolonged QT interval and is most frequently related to administration of antiarrhythmic drugs. Patients with organic heart disease, with low serum electrolyte levels, with a previous episode of TdP and with bradycardia or baseline QT prolongation may be at increased risk of developing TdP. After initiation of a QT prolonging therapy, the dosage should be modified if the QT interval reaches 560-600 ms. Cessation of medication and immediate hospitalization are indicated in the presence of lightheadedness, syncope, or increased frequency and complexity of ventricular premature beats. The conventional therapy of TdP with isoproterenol or cardiac pacing, although usually effective, has certain disadvantages. Isoproterenol is contraindicated in patients with hypertension or ischemic heart disease, whereas institution of cardiac pacing requires skilled personnel and fluoroscopy. Recently, infusion of magnesium sulfate has been shown to abolish TdP both in the clinical and experimental setting. Compared with conventional therapy, magnesium sulfate has the advantage of safety and simplicity of its administration. In doubtful cases, if does not aggravate a ventricular tachycardia that is not TdP, as may occur with isoproterenol. This advantage and the prompt effectiveness of the drug in four clinical series, including 31 patients, support the use of magnesium sulfate as the first line of therapy for TdP.
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PMID:Torsades de pointes: prevention and therapy. 185 60

The aim of the study was to evaluate the value of analysis of left ventricular systolic intervals during Isuprel test in diagnosis of ischemic heart disease. 30 patients with ischemic heart disease without myocardial infarction in the past (group I) and after myocardial infarction (group II) as well as 15 healthy persons (group III) underwent the study. Electrocardiograms and polycardiograms were analyzed by means of Weissler's method. In patients with CAD during Isuprel test decrease of QS2I, LVETI, LVETI/S1S2 and increase of Q-1, ICT, PEPI, PEP/LVET were stated in comparison with healthy persons. Sensitivity of Isuprel test estimated by ST segment analysis was 80%, specificity 100%, predictive value for CAD confirmation 100% and for its exclusion 71.4%. Diagnostic value of Q-1, QS2I and LVETI intervals and PEP/LVET index did not statistically significantly differ from ST segment diagnostic value. Sensitivity of Isuprel test estimated by means of these intervals analysis was 63.3%, specificity 93.3-100%, predictive value for CAD confirmation 95-100%, and for its exclusion 56-57.7%. Analysis of left ventricular systolic intervals during Isuprel test is a valuable complement of an ECG examination.
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PMID:[Value of the analysis of left-ventricular systolic time intervals in the diagnosis of ischemic heart disease provoked by intravenous infusion of isoproterenol]. 262 7

In order to investigate whether brief, repeated episodes of acute myocardial ischemia impair the function of the intrinsic sympathetic efferent post ganglionic cardiac nerves, 12 cycles of left anterior descending coronary artery occlusions (5 mins) and reperfusions (10 mins) were successfully performed in 10 dogs. Following each brief occlusion percentage systolic shortening in the ventral myocardium was reduced, consistent with myocardial stunning. Stellate ganglion stimulation increased intramyocardial pressures in the ventral and lateral regions of the left ventricle before and after each of the artery occlusions in which stimulations were performed. Isoproterenol and tyramine also augmented intramyocardial pressures in those regions. When the coronary artery was occluded permanently in seven of the dogs tested, stellate ganglion stimulation continued to augment intramyocardial pressure in the ventral region of the left ventricle for up to 35 mins. These results indicate that following repetitive episodes of brief occlusion of a coronary artery that are reported to 'stun' the involved myocardium in a transmural distribution, sympathetic efferent post ganglionic axons can augment inotropism in the affected zone. Furthermore, when a coronary artery is totally occluded thereafter for up to 35 mins these efferent sympathetic post ganglionic nerves continue to function. It is concluded that sympathetic efferent post ganglionic neurons innervating the ventricle can augment cardiac inotropism in a region of stunned myocardium.
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PMID:Functional integrity of sympathetic efferent postganglionic axons in a region of stunned myocardium. 281 59

Patients with hypertension or ischemic heart disease are often treated with beta-adrenoceptor antagonists, yet the degree of beta-adrenoceptor blockade has rarely been studied in relation to anesthesia. We have constructed isoproterenol dose-response curves in four groups of patients under general anesthesia: group I, 27 elderly normotensive patients not receiving drugs; group II, 14 hypertensive patients treated with cardioselective beta-adrenoceptor antagonists; group III, 15 hypertensive patients receiving nonselective beta-adrenoceptor antagonists; group IV, 13 patients receiving an infusion of labetalol at 0.15 mg X kg-1 X hr-1. Geometric mean CD25, the dose of isoproterenol required to increase the heart rate by 25 beats/min was 4.4 micrograms (3.5-5.6, 95% confidence interval (CI) of the mean) in group I, and 27 micrograms (19-38, 95% CI), 39 micrograms (29-52, 95% CI), and 95 micrograms (62-147, 95% CI) in groups II, III, and IV, respectively. All differences were significant (P less than 0.01), except those between groups II and III (P less than 0.1). No signs of myocardial ischemia and only a few transient arrhythmias were observed. Isoproterenol dose-response curves are a safe means to assess the degree of beta-adrenoceptor blockade during anesthesia and the postoperative period.
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PMID:Assessment of beta-adrenoceptor blockade during anesthesia in humans: use of isoproterenol dose-response curves. 285 67

The isoprenaline test was performed in 89 patients with CHD and cardialgias of various origins. The diagnosis was verified by coronarography and bicycle ergometry in 60 patients. Isoprenaline was administered via intravenous drip, with the initial rate of 2-3 micrograms/min eventually increased until clinical or electrocardiographic signs of myocardial ischemia emerged, or the heart rate reached 130 beats per minute. When compared with coronarographic and bicycle-ergometric results, the isoprenaline test was shown to be highly sensitive and specific (64.3 and 95.2%), as evidenced by the electrocardiographic positive-result criteria, and superior to bicycle ergometry in its diagnostic possibilities. The isoprenaline test is recommended for the diagnosis of coronary heart disease in cardiologic and therapeutic hospital units. The test can be a method of choice in cases where rationed exercise tests are impossible to achieve.
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PMID:[Importance of the intravenous isoprenaline test in diagnosing ischemic heart disease]. 408 72


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