Potential beneficial as well as detrimental effects of chronic treatment with lisinopril and (or) spironolactone on isolated hearts following low-flow ischemia in normal and infarcted rats.

This study was designed to demonstrate potential beneficial as well as detrimental effects of lisinopril and spironolactone given in combination. In patients with congestive heart failure or myocardial infarction, the use of angiotensin-converting enzyme (ACE) inhibitors may inhibit aldosterone production. Spironolactone, a specific aldosterone receptor antagonist may exert other independent and additive effects to those of ACE inhibitors.

Dimethyl disulfide exerts insecticidal neurotoxicity through mitochondrial dysfunction and activation of insect K(ATP) channels.

The plant-derived insecticides have introduced a new concept in insecticide research. In response to insect attacks, some plants can release volatile sulfur compounds such as dimethyl disulfide (DMDS) in the atmosphere, which are lethal for the generalist insects. We demonstrate that DMDS induced an uncommon complex neurotoxic activity.

Reactive hyperemia during early reperfusion as a determinant of improved functional recovery in ischemic preconditioned rat hearts.

Objective: Our study was undertaken to clarify the impact of the shear stress-induced reactive hyperemia (associated with reperfusion) in preconditioning-mediated protection.

Methods: In control rat hearts, a 40-minute preischemic perfusion (constant pressure: 70 mm Hg) period was followed by 25-minute global low-flow ischemia (constant flow: 0.3 mL/min) and 30-minute reperfusion (constant pressure).

Mechanisms underlying the coronary vasodilation in the isolated perfused hearts of rats submitted to one week of high carbon monoxide exposure in vivo.

We examined the possible mechanisms for carbon monoxide (CO)-induced effects in hearts isolated from Wistar rats exposed for 1 wk to 530 ppm CO. They were treated by daily intraperitoneal injections of either methylene blue (10 mg/kg), glibenclamide (3 mg/kg), or apamin (125 nmol/kg), known to inhibit vasodilatory mechanisms. Hearts were excised, cannulated, and retrogradely perfused through the coronary artery, using the Langendorff method with a constant perfusion pressure.

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes.

A physiological role of carbon monoxide has been suggested for coronary myocytes; however, direct evidence is lacking. The objective of this study was to test the effect of chronic carbon monoxide exposure on the K(+) currents of the coronary myocytes. The effect of 3-wk chronic exposure to carbon monoxide was assessed on K(+) currents in isolated rat left coronary myocytes by the use of the patch-clamp technique in the whole cell configuration.

Acute ischemic preconditioning and high subchronic CO exposure independently increase myocardial tolerance to ischemia.

This study was designed to investigate whether exposure to carbon monoxide (CO) could alter or raise the ischemic tolerance induced by preconditioning. To this end, isolated rat hearts were aerobically perfused for 20 min. Hearts were then randomized to two groups: (1) a further 20-min aerobic perfusion, and (2) ischemic preconditioning (2 cycles of 5 min of ischemia followed by 5 min of reperfusion).

Beneficial effects of amiodarone and dronedarone (SR 33589b), when applied during low-flow ischemia, on arrhythmia and functional parameters asssessed during reperfusion in isolated rat hearts.

The effects of short-term amiodarone and dronedarone treatments on action potential characteristics and arrhythmia (ventricular tachycardia ) induced by reperfusion after global low-flow ischemia were studied in rat hearts. The actions of amiodarone and SR on recovery of coronary flow and contractile function were also determined. Isolated hearts were stabilized for 40 min and were then submitted to 25-min global low-flow ischemia (constant coronary flow, 0.

Ischemic tolerance of the heart by adaptation to chronic hypoxia is suppressed by high subchronic carbon monoxide exposure.

This study was designed to investigate whether exposure to carbon monoxide (CO) could alter the ischemic tolerance induced by chronic hypoxia. We aimed to determine whether chronic hypoxia-induced cardiovascular adaptation was modified during the return to normoxia or by subchronic CO exposure. The degree of resistance to an in vitro transient ischemia was measured, using the Langendorff method, in hearts from rats previously exposed to chronic hypoxic hypoxia and/or subchronic CO exposure to 600 ppm.

Cardiovascular effects of subchronically low/high carbon monoxide exposure in rats.

This study was designed to determine whether subchronic CO exposure ranging from 15 to 530 ppm induced modifications in the rat cardiovascular system. We investigated the degree of resistance to an in vitro transient ischemia in the hearts exposed in vivo to different CO concentrations for 1-4 weeks. Subchronic CO exposure induced dose and/or time-dependent increases (hematocrit, cardiomegaly and coronary flow).

Electrophysiological approach of the role of Na+/H+ exchange in low-flow global ischemia and in ischemic preconditioning.

We investigated, at first in low-flow global ischemia and then with ischemic preconditioning, the effects of a compound, (4-isopropyl-3-methylsulphonylbenzoyl)guanidine hydrochloride (HOE 642), known to inhibit the Na+/H+ exchange in rat cardiomyocytes. In rat isolated hearts, perfused on a Langendorff apparatus with Krebs-Henseleit carbonate buffer, the action potentials and the contractile function were measured during a 25-min period of global low-flow ischemia (coronary flow, 0.3 mL.