Hyperoxic preconditioning fails to confer additional protection against ischemia-reperfusion injury in acute diabetic rat heart.

Experimental studies show that detrimental effects of ischemia-reperfusion (I/R) injury can be attenuated by hyperoxic preconditioning in normal hearts, however, there are few studies about hyperoxia effects in diseased myocardium. The present study was designed to assess the cardioprotective effects of hyperoxia pretreatment (≥ 95 % O2) in acute diabetic rat hearts. Normal and one week acute diabetic rats were either exposed to 60 (H60) and 180 (H180) min of hyperoxia or exposed to normal atmospheric air (21 % O2).

Pretreatment with oxygen protects rat kidney from cisplatin nephrotoxicity.

Cisplatin (CP) nephrotoxicity is mainly due to reactive oxygen species. Oxygen pre-exposure as a mild oxidative stress may enhance some endogenous defense mechanisms, so its effect on cisplatin-induced acute renal failure was investigated in present study. Twenty-four rats were divided into four groups.

Delayed cardioprotective effects of hyperoxia preconditioning prolonged by intermittent exposure.

Background: In our previous study, it was indicated that pre-exposing rats to normobaric hyperoxia could induce a late preconditioning against infarction and arrhythmia. In this study, attempts were made to know whether the intermittent pre-exposure to the same environment could prolong the late phase of hyperoxia preconditioning.

Methods: In the first series of experiments, rats were divided into five groups; group 1 was pre-exposed to normal air (NOR) and the other groups to hyperoxic air (O(2)>95%, 120 min once a d) 12, 24, 48, and 72 h (H12, H24, H48, and H72 groups) before 30 min ischemia.

Delayed protective effects of hyperoxia against cardiac arrhythmias and infarction in anesthetized rats.

Background: Previous studies have shown that pretreatment with normobaric hyperoxia has cardioprotective effect in isolated rat heart. The present study was designed to test the hypothesis that pretreatment normobaric hyperoxia could induce delayed cardioprotection effect in an in vivo regional heart ischemia.

Materials And Methods: Experiment 1: Rats were exposed to normobaric normoxia or to normobaric hyperoxia (O(2) > 95%) for 15, 30, 60, 120, and 180 min (H15, H30, H60, H120, and H180 groups, respectively).

Delayed anti-arrhythmic effect of nitroglycerin in anesthetized rats: involvement of CGRP, PKC and mK ATP channels.

Delayed anti-infarct and anti-stunning effects of nitroglycerin (NTG) have well been established in some animal models. The main goals of this study in anesthetized rats were to determine whether NTG has a delayed anti-arrhythmic effect and if so, whether calcitonin gene-related peptide (CGRP), protein kinase C (PKC) and mitochondrial K(ATP) channels (mK(ATP)) are involved in triggering this response. For this purpose, on day 0, male Wistar rats received NTG (120 microg/kg, iv) with or without pre-administration of PKC inhibitor chelerythrine (CHE), capsaicin (CAP) to deplete CGRP from sensory nerves or mK(ATP) channel blocker 5-hydroxydecaonic acid (5HD).