ABSTRACT
Acute renal failure due to bilateral ureteral obstruction is a rare complication after appendectomy in children. We report a case of bilateral ureteric obstruction in a 14-year-old boy nine days after surgery for an acute appendicitis. After saline-filling of the urinary bladder, transabdominal ultrasound demonstrated bilateral hydronephrosis of moderate degree. No abscess was found with CT but presence of millimetric stones on both distal ureters was shown, with bilateral calyceal dilatation. Cystoscopy revealed inflammatory changes in the bladder base. Following introduction of bilateral ureteric stents, there was rapid normalisation of urinary output and serum creatinine.
ABSTRACT
The protective effects of captopril were evaluated in vitro on isolated perfused rat hearts after a global ischemia of 20 min. The hearts were randomly allocated in 2 groups. In the first one (n = 6) captopril was added at a concentration of 270 microM. The second one was utilized as control (n = 6). Aortic flow and minute work respectively decreased on reperfusion by 35% and 49% in captopril group and by 65% and 71% in controls (p < 0.001). No changes occurred in heart rate. Aortic systolic pressure and coronary flow decreased in the 2 groups, but not significantly. Myocardial enzyme release during reperfusion showed significant lower levels of CPK and LDH in the captopril group as compared to controls (p < 0.001 after 41 min). The occurrence of serious ventricular arrhythmias was considerably higher in controls with respect to the captopril group. Irreversible ventricular fibrillation occurred only in control hearts (50%). These data indicate that captopril exerts a protective effect during myocardial ischemia and reperfusion by preventing serious ventricular arrhythmias, reducing enzymatic release and a lower decrease in cardiac performance, without an increase in heart rate.
Subject(s)
Captopril/therapeutic use , Heart/drug effects , Myocardial Reperfusion Injury/prevention & control , Myocardium/enzymology , Peptidyl-Dipeptidase A/metabolism , Animals , Creatine Kinase/drug effects , Creatine Kinase/metabolism , Drug Evaluation, Preclinical , Hemodynamics/drug effects , In Vitro Techniques , L-Lactate Dehydrogenase/drug effects , L-Lactate Dehydrogenase/metabolism , Male , Myocardial Reperfusion Injury/enzymology , Myocardial Reperfusion Injury/physiopathology , Peptidyl-Dipeptidase A/drug effects , Random Allocation , RatsABSTRACT
The protective effects of exogenous phosphocreatine were evaluated in vitro on isolated perfused rat hearts during reperfusion of ischemic myocardium. The hearts were randomly allocated in 2 groups. In the first (n 6) phosphocreatine was added at a concentration of 10 mM. The latter was utilized as control (n 7). In both groups the results showed a slight decrease in the post-ischemic myocardial performance. Aortic systolic pressure and flow respectively decreased on reperfusion by 17% and 12.5% in the phosphocreatine group and by 25.6% and 35% in the control group. Coronary flow was reduced by 10% in the phosphocreatine and by 18% in the control group. No statistically relevant differences were reported within or between the groups. No changes in heart rate occurred in the same period in the phosphocreatine and in the control group. Myocardial enzyme release during reperfusion showed significant lower levels of CK and LDH in the phosphocreatine group compared to controls (p less than 0.001 after 65 min and p less than 0.025 after 75 min between the 2 groups). The occurrence of serious ventricular arrhythmias was considerably higher in controls with respect to the phosphocreatine group. The overall incidence of major rhythm disturbances was 66% in the phosphocreatine group and 100% in the control group. Irreversible ventricular fibrillation (57%) occurred only in control hearts. The present findings indicate that phosphocreatine exerts a protective effect during myocardial ischemia and reperfusion, especially by preventing serious ventricular arrhythmias and by reducing myocardial enzyme release.