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A case of unilateral suprarenal abscess is reported. This is the third such reported case, and the first reported case successfully treated with preservation of the kidney. Diagnosis and treatment were aided significantly by a thorough preoperative radiological evaluation, including angiography.

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.

Although alpha-adrenergic stimulation can increase coronary vascular resistance, it remains unknown whether the vasoconstriction can override intrinsic coronary regulatory influences to produce ischemia. Methoxamine, 2 to 4 mg, was infused into the circumflex coronary artery of 23 chloralose-anesthetized open chest dogs, and resulted in a 68% increase in coronary vascular resistance. The functional consequence of this increased coronary vascular resistance was assessed by gated radionuclide ventriculography and ST-T wave changes on the electrocardiogram. In six dogs (Group I), aortic pressure changed trivially (less than 5 mm Hg) to allow distinction between direct effects of the flow reduction and indirect effects of increased aortic pressure. In this group, coronary blood flow decreased 33% from a control value of 44 +/- 10 ml/min (p less than 0.001) and left ventricular ejection fraction decreased from 0.54 +/- 0.12 to 0.46 +/- 0.10 (p less than 0.025). In eight dogs (Group II) in which aortic pressure increased by more than 5 mm Hg, left ventricular ejection fraction decreased from 0.46 +/- 0.07 to 0.39 +/- 0.09 (p less than 0.002). Pressure gradients were measured between the aorta and a distal coronary artery branch to calculate small and large vessel resistances separately in four other dogs (Group III). The resistance of small coronary arteries accounted for 92% of the total increase in coronary vascular resistance produced by methoxamine. In five other dogs (Group IV), intracoronary methoxamine, 2 mg, produced ST-T wave changes suggestive of ischemia as it increased coronary vascular resistance by 33%.(ABSTRACT TRUNCATED AT 250 WORDS)