Histological changes in neonatal kidneys after cardiopulmonary bypass and deep hypothermic circulatory arrest.

BACKGROUND: Renal failure after open-heart surgery is a serious complication resulting in increased mortality and morbidity. The aim of the study was to find out whether different strategies for open-heart surgery would result in renal histological differences in a neonatal animal model. METHODS: The renal tissue of newborn piglets was examined after mild hypothermic cardiopulmonary bypass (CPB group; n = 10), deep hypothermic circulatory arrest (DHCA group; n = 8), instrumentation without extracorporeal circulation (sham; n = 3), and the data were compared with those of normal porcine neonatal kidneys (control; n = 6). The severity of tissue damage was graded using a 4-point scoring system (0: normal morphology, 3: severe damage). Apoptotic cells and granulocytes were counted. RESULTS: The histological score was higher in all groups compared with controls ( P < 0.05) and higher in the CPB group compared with the DHCA group ( P < 0.05). More apoptotic cells and granulocytes were found in the CPB group compared with controls and the DHCA group ( P < 0.05). CONCLUSIONS: Although changes in the kidney tissue of newborn piglets are detectable after any cardiac procedure, changes are more profound after cardiopulmonary bypass with mild hypothermia.

Ultrastructure of right ventricular myocardium subjected to acute pressure load.

BACKGROUND: Ultrastructural data on acute right ventricular pressure load in pigs are rare. MATERIALS AND METHODS: In control (n = 7) and banding groups (n = 6), right ventricular pressure (micromanometry) and function (sonomicrometry) were measured. Right ventricular pressure was increased 2.5-fold in the banding group by pulmonary artery constriction. Right ventricular biopsies were taken at baseline and after 6 h and processed for electron microscopy. Parameters of cellular injury were determined stereologically. Three perfusion -fixed hearts were investigated qualitatively in each group. RESULTS: Stereology revealed an increase in the sarcoplasmic volume fraction and the cellular edema index in the banding group ( p < 0.05). Mitochondrial surface-to-volume ratio and volume fraction did not show significant alterations. Subendocardial edema and small amounts of severely injured myocytes were observed in the perfusion-fixed hearts after banding. Ultrastructure was normal in controls. After an initial increase, the right ventricular work index declined progressively in the banding group but remained unchanged in controls. CONCLUSIONS: Ultrastructural alterations resulting from acute right ventricular pressure load were characterized by edema of subendocardial myocytes and single cell necrosis. Focal adrenergic overstimulation and mechanical stress are probably more relevant in the pathogenesis of these lesions than ischemia.