Effects of Ischemic Preconditioning and Postconditioning in a Renal Ischemia-Reperfusion Injury Model: A Comparative Experimental Study in Rats.

BACKGROUND: Ischemia-reperfusion injury is an unavoidable aspect of transplantation, as well as an important cause of acute kidney injury in clinical practice. Pre- and post-ischemic conditioning are strategies that may provide organs with resistance to major ischemic events. This study evaluates the effects of ischemic preconditioning and ischemic postconditioning, either separately or in combination, after an acute ischemia-reperfusion kidney injury. METHODS: Forty Wistar rats received isoflurane anesthesia and were randomized into 5 groups: 1. the sham group underwent laparotomy; 2. the control group underwent laparotomy and 30 minutes of renal ischemia followed by reperfusion; 3. the preconditioning group underwent laparotomy, ischemic preconditioning, and 30 minutes of renal ischemia followed by reperfusion; 4. the preconditioning and postconditioning group underwent laparotomy, ischemic preconditioning, 30 minutes of renal ischemia, and ischemic postconditioning followed by reperfusion; and 5. the postconditioning group underwent laparotomy, 30 minutes of renal ischemia, and ischemic postconditioning followed by reperfusion. Serum analyses of creatinine and neutrophil gelatinase-associated lipocalin (NGAL) were performed, and renal histology was examined 24 hours later. RESULTS: Severe tubular injury and increases in creatinine were observed in all groups except the sham group. The control group and all ischemic conditioning groups were no different in the degree of renal injury and values of NGAL and creatinine after the injury. CONCLUSIONS: Ischemic preconditioning and ischemic postconditioning, together or separately, are unable to preserve kidney function or exert a protective effect against tubular cell injury after an acute ischemia-reperfusion kidney injury.

Bezold-Jarisch reflex in myocardial infarcted rats.

The Bezold-Jarisch reflex (BJR), produced by the administration of 5-hydroxytryptamine (5-HT, 4-16 micrograms/kg, iv), was evaluated in awake rats bearing short- (1 day) or long-term (30 days) myocardial infarction. Heart chronotropic response produced by acetylcholine was further assessed by Langendorff's isolated heart perfusion technique. Compared to the sham-operated group, infarcted rats showed either hypotension and tachycardia or bradycardia following short- or long-term myocardial infarction, respectively. Whereas the long-term myocardial infarction attenuated 5-HT-induced hypotension and bradycardia by about -25 and -80%, respectively, no significant response changes were observed in short-term infarcted rats. Impairment of BJR correlated significantly (P < 0.01) with the extent of myocardial necrosis in the 30-days infarcted group. Chronotropic responsiveness of the heart to acetylcholine in infarcted rats did not differ from the sham-operated group. Transmural antero-medio-lateral infarcted areas spanned over nearly 37% (1-day group) and 35% (30-days group) of the left ventricular circumference. These results indicate that cardioinhibitory and vasodepressor reflex responses to 5-HT are significantly impaired in chronic myocardial infarction associated with (1) marked hypertrophy of left atrium and/or of non-infarcted left ventricle, which are the main origin of vagal chemosensitive C-fibers, (2) morphological damage of this innervation due to the necrotic injury of the left ventricle, (3), possible attenuation in the vagal afferents located in the lungs and/or (4) enhancement of the chemical sensitivity of cardiac sympathetic afferents.