iNOS is a mediator of the heat stress-induced preconditioning against myocardial infarction in vivo in the rat.

Objective: The inducible isoform of nitric oxide synthase (iNOS) is known to be a trigger of the heat stress (HS)-induced cardioprotection. Since iNOS also appears to mediate various forms of myocardial preconditioning, the goal of this study was to investigate its role as a mediator of the HS response.

Methods And Results: Male Wistar rats were divided in six groups, subjected or not to HS (42 degrees C internal temperature, for 15 min).

Endocannabinoids are implicated in the infarct size-reducing effect conferred by heat stress preconditioning in isolated rat hearts.

Objective: We have investigated the involvement of the endocannabinoid system in the delayed cardioprotection conferred by heat stress preconditioning in the isolated rat heart.

Methods: Rats were divided into eight groups (n=7 in each group), subjected to either heat stress (42 degrees C for 15 min, HS groups) or sham anaesthesia (Sham groups). Twenty-four hours later, their hearts were isolated, retrogradely perfused, and subjected to a 30-min occlusion of the left coronary artery followed by 120 min of reperfusion.

Detrimental implication of B1 receptors in myocardial ischemia: evidence from pharmacological blockade and gene knockout mice.

Objective: The aim of this study was to evaluate the contribution of kinin B1 receptors in myocardial ischemia using both pharmacological blockade and gene knockout mice.

Material And Methods: Hearts (n = 6-8 per group) from wild type or homozygous B1 receptor gene knockout mice were isolated and perfused using the Langendorff technique. After a 30-min stabilisation period, the left coronary artery was occluded for 30 min followed by 60 min of reperfusion.

Free-radical production triggered by hyperthermia contributes to heat stress-induced cardioprotection in isolated rat hearts.

1. Heat stress (HS) is known to protect the myocardium against ischaemic damage. It has been reported that reactive oxygen species (ROS) are abundantly produced during this stress.

Heat stress protects against electrophysiological damages induced by acute doxorubicin exposure in isolated rat hearts.

The use of anthracycline antibiotics as anticancer agents is limited by their cardiac toxicity. Heat stress (HS) is known to confer protection against various myocardial injuries such as ischemia-reperfusion induced damage. This cardioprotective mechanism is associated with an increase in endogenous antioxidative defenses and heat stress proteins (HSPs) synthesis.