[Role of the increased cholinergic activity in prevention of reperfusion-induced arrhythmia in dog experiments].
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Biomedical subjects
Publications and source records attributed to B Tuccillo.
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Histamine is widely present in human tissues and can be released by immunologic and nonimmunologic reactions. Although several direct cardiovascular effects of histamine have been demonstrated in humans, little is known about the direct effects of histamine on the human coronary circulation in vivo. Therefore, we investigated the changes in coronary hemodynamics induced by bolus intracoronary administration of 4 micrograms of histamine to 11 patients with angiographically normal coronary arteries under continuous monitoring of R-R interval from the electrocardiogram, arterial pressure (AP), and coronary sinus blood flow (CBF), measured by thermodilution. Immediately after the end of the intracoronary histamine bolus, with R-R interval and AP unchanged, CBF increased from 144 +/- 20 to 238 +/- 27 ml/min (p less than 0.01) and coronary vascular resistance decreased from 0.7 +/- 0.16 to 0.42 +/- 0.1 mm Hg/ml/min (p less than 0.01). No change in coronary hemodynamics was observed after bolus intracoronary administration of physiologic saline. The effects of histamine on systemic hemodynamics consisted of a transient fall in AP and R-R interval, starting after the onset of changes in coronary hemodynamics. These data show that histamine possesses a direct coronary vasodilator effect in humans, independent of the determinants of myocardial oxygen consumption.
Experimental and clinical studies have shown the action of magnesium salts on myocardial tissue and its antiarrhythmic action on digitalis-induced ventricular arrhythmias. We have evaluated the effects of magnesium sulfate (2.5 mM) on heart rate (HR), coronary flow rate (CFR), left ventricular systolic pressure (LVSP), dP/dt max and voltage epicardial electrogram (VEE) during ischemia and reperfusion in isolated perfused rat heart. Forty-five male rats were randomized into 3 groups. In the control group, after a 15 min period of stabilization, hearts were perfused by ischemic perfusion for 30 min and then reperfused. In group I, magnesium sulfate was given after stabilization and before the ischemic period. In group II, calcium concentration was increased by 0.5 mM and magnesium sulfate was given after stabilization and before the ischemic period. In the control group, we observed during ischemia a reduction in HR, CFR, LVSP, dP/dt max and an increase in VEE. In group I, after the administration of magnesium sulfate, we noted a decrease in HR, LVSP, dP/dt max, VEE and during the ischemic period there was no difference in these parameters with respect to the control group. In group II, the increase of extracellular calcium concentration caused an increase in LVSP, dP/dt max and the administration of magnesium sulfate abolished these effect, bringing the values back to basal values. Reperfusion provoked ventricular arrhythmias in 11/15 and 12/15 hearts in the control group and group II respectively, and only 3/15 in group I (p less than 0.005 group I vs control and group II). Thus, our results demonstrated that magnesium sulfate has varied effects on electrical and mechanical parameters and prevents reperfusion arrhythmias according to the hypothesis of a calcium-antagonist mechanism of magnesium.
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