Complete radical nephrectomy and vena caval thrombectomy during circulatory arrest.

PURPOSE: A modification of radical nephrectomy for renal carcinoma and vena caval tumor thrombectomy for supradiaphragmatic tumor extension under hypothermic circulatory arrest is presented. MATERIALS AND METHODS: Nephrectomy was performed during the circulatory arrest time in 16 consecutive patients during the last 4 years. RESULTS: Average hypothermic circulatory arrest time increased by 6 minutes. By elimination of manipulation of tumor and thrombus before circulatory arrest potential thrombus fragmentation and embolization were minimized. There were no significant differences in blood loss or complications compared to a prior series of 10 patients undergoing the procedure using conventional techniques. CONCLUSIONS: Performance of complete radical nephrectomy along with venal caval embolectomy during circulatory arrest increases the safety of the procedure without significant morbidity.

Expression of adhesion molecules in rat renal cortex during experimental hydronephrosis.

Unilateral ureteral obstruction (UUO) is associated with an early and steadily increasing infiltration of macrophages into the renal cortical interstitium. As adhesion molecules may play an important role in macrophage recruitment following the mechanical disturbance after UUO, we delineated the time course of intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 mRNA and protein expression. A significant 6.6- (P < 0.001), 2.6- (P < 0.025), 2.6- (P < 0.01), and 2.0-fold (P < 0.005) increase in ICAM-1 mRNA expression was observed at 12, 24, 48, and 96 hours after obstruction, respectively, in comparison to the contralateral unobstructed kidney (CUK). Despite an apparent relief of obstruction, four weeks following reversal of obstruction mRNA levels of ICAM-1 remained equivalent to the 96-hour obstructed kidney group. No significant difference in VCAM-1 mRNA expression was observed between the obstructed kidneys and CUK specimens. Immunohistochemistry revealed focal labeling of ICAM-1 on the apical and basolateral surface of the renal tubules, peritubular interstitium, and vessels of the renal cortex by 12 hours after UUO. In contrast, only faint staining for ICAM-1 protein was observed in the cortex from CUK specimens. The obstructed and CUK specimens exhibited diffuse immunolocalization of VCAM-1 in the cortical tubules and Bowman's capsular epithelium. In situ hybridization showed mRNA transcription for ICAM-1 localized in the peritubular interstitium and cortical tubules from obstructed kidneys. To lend mechanistic insight into the response of ICAM-1 to the mechanical disturbance after UUO, the expression of ICAM-1 mRNA was examined when freshly isolated proximal tubules were exposed to angiotensin II (1 to 100 microM) immediately after preparation. Levels of ICAM-1 mRNA were elevated 1.4-, 7.1-, and 3.7-fold when exposed to 10 microM, 100 microM, and 1000 microM of angiotensin II for one hour, respectively, when compared to control cultures. The addition of losartan to proximal tubules for one hour prior to angiotensin II stimulation decreased ICAM-1 levels to control values. In summary, this investigation demonstrates that ICAM-1 is important in the initiation of macrophage recruitment into the renal cortex of the obstructed kidney. These findings provide evidence that angiotensin II, produced after ureteral ligation as a result of tubular injury and dysfunction, may play a central role in the release of ICAM-1 from the proximal tubule epithelial cells.

Computer automated structure evaluation of quinolone antibacterial agents.

The Computer Automated Structure Evaluation (CASE) program was used to study a series of quinolone antibacterial agents for which experimental data pertaining to DNA gyrase inhibition as well as MICs against several strains of gram-positive and gram-negative bacteria are available. The result of the analysis was the automatic generation of molecular fragments relevant to the respective biological endpoints. The potential significance of these major activating-inactivating fragments to the biological activity is discussed.