Degree and time sequence of hypothermic protection against experimental ischemic acute renal failure.

Abstract

The purpose of this study was to assess the degree, time sequence, and biochemical correlates of hypothermic protection against ischemic acute renal failure. Rats subjected to 40 minutes of bilateral renal artery occlusion (RAO) were made mildly hypothermic (32 degrees-33 degrees C, by cold saline peritoneal lavage) during the following time periods: 1) RAO only, 2) reperfusion only (beginning at 0, 15, 30, or 60 minutes after RAO and maintained for 45 minutes), or 3) during and after (0-45 minutes) RAO. Continuously normothermic (37 degrees C) RAO rats served as controls. The control rats developed severe acute renal failure (blood urea nitrogen [BUN], 95 +/- 4 mg/dl; creatinine, 2.2 +/- 0.1 mg/dl; and extensive tubular necrosis at 24 hours). Hypothermia confined to RAO was highly protective (BUN, 33 +/- 5 mg/dl; creatinine, 0.62 +/- 0.07 mg/dl; and minimal necrosis). Hypothermia partially preserved ischemic renal adenylate high-energy phosphate (ATP and ADP), increased AMP and inosine monophosphate concentrations, and lessened hypoxanthine/xanthine buildup (assessed at end of RAO). Hypothermia confined to the reflow period (beginning at 0, 15, and 30 minutes) was only mildly protective (e.g., BUN, 58-63 mg/dl); the degree of protection did not differ according to the time of hypothermic onset. Lowering reflow temperature to 26 degrees C had no added benefit. Hypothermia that started at 60 minutes after RAO conferred no protection. Combining ischemic and postischemic hypothermia abolished all renal failure (assessed at 24 hours). This study offers the following conclusions: Mild hypothermia can totally prevent experimental ischemic acute renal failure. Hypothermia is highly effective during ischemia, and it is mildly protective during early reflow; these benefits are additive. During early reflow, hypothermic protection is not critically time dependent. By 60 minutes of reflow, no effect is elicited; this absence of effect possibly signals completion of the reperfusion injury process. Hypothermia's protective effects may be mediated, in part, by improvements in renal adenine nucleotide content and, possibly, by decreasing postischemic oxidant stress.

Ischaemia‐reperfusion injury in the rat kidney: the effect of preconditioning

“…Recent studies have shown the critical eÂect that not significantly diÂerent (P=0.20) from that observed in the IP-only animals (group B). There was no significhanges in core temperature can have on renal preservation [19]. Thus, a decrease of just 2°C can result cant diÂerence between grades of ischaemic damage in group C (RI only) compared with group D (IP+RI) for in significant reductions in ischaemic damage [20].…”

Lowering Perfusate Temperature From 37°C to 32°C Diminishes Function in a Porcine Model of Ex Vivo Kidney Perfusion

“…There further have been historical reports of hypothermia conditioning against ischemia, and to a lesser extent reperfusion, in a murine model. 5 …”

Hypothermic renal perfusion during aortic surgery reduces the presence of lipocalin-2 and preserves renal extraction of dimethylarginines in rats

“…Renal oxygen consumption is reduced to 40% when the renal parenchyma is cooled to 30°C, to 15% at 20°C, and to Ͻ5% at 10°C (6,11,20,39,49). Also, milder disruption in proximal tubules has been seen after 48 h of cold ischemia compared with warm ischemia (48), but glomerular podocytes and peritubular endothelial cells were damaged after cold ischemia.…”