The possible antianginal effect of allopurinol in vasopressin-induced ischemic model in rats

Abstract

The anti-anginal effects of allopurinol were assessed in experimental model rats of angina and their effects were evaluated with amlodipine. In the vasopressin-induced angina model, oral administration of allopurinol in dose of 10 mg/kg revealed remarkably analogous effects in comparison with amlodipine such as dose-dependent suppression of vasopressin-triggered time, duration and severity of ST depression. In addition, allopurinol produced dose dependent suppression of plasma Malondialdehyde (MDA) level, systolic blood pressure, cardiac contractility and cardiac oxygen consumption; while in contrast, amlodipine minimally suppressed the elevation of plasma MDA level. Endothelial NO synthase (eNOS) expression, serum nitrate were strikingly increased, however lipid profile was significantly reduced. Seemingly, allopurinol was found to be more potent than amlodipine - a calcium channel antagonist. To conclude, it was explicitly observed and verified that on the ischemic electrocardiography (ECG) changes in angina pectoris model in rats, allopurinol exerts a significant protective effects, reminiscent of enhancement of vascular oxidative stress, function of endothelial cells, improved coronary blood flow in addition to the potential enhancement in myocardial stress. Moreover, our findings were in conformity with several human studies.

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

“…Effects on the levels of endothelial NO synthase (eNOS) expression and serum nitrate were the main underlying mechanism 22 . All of these mechanisms can exert similar effects in kidney IRI.…”

Mentha longifolia alleviates experimentally induced angina via decreasing cardiac load

“…Six‐week‐old male Wistar rats (King Abdulaziz University) were randomly divided into three experimental groups (8 animals each): control (C), angina (A), M. longifolia ‐treated (M) groups. Experimental angina was induced by intravenous injection of vasopressin (2 IU/kg) (Al‐Zahrani et al, ) under general anesthesia. M. longifolia extract was suspended in deionized water and administered daily by oral gavage in a dose of 200 mg/kg for three days before induction of angina.…”

Reactive Oxygen Species Cause Exercise-Induced Angina in a Myocardial Ischaemia-Reperfusion Injury Model

“…Angina refers to cardiac pain or discomfort triggered by strenuous activities. Several experimental angina models, such as vasopressin-, methacholine- and isoproterenol-induced angina models, have been used for studying angina [ 16 , 17 , 18 ]. Further, several indirect indicators such as ST-segment, blood pressure, and biochemical markers of myocardial injury are used to evaluate angina [ 29 , 30 , 31 ].…”

“…Although several mechanisms, such as inflammation, apoptosis, microvascular dysfunction, and oxidative stress, are involved in I/R injury [ 15 ], the relationship of angina and I/R injury is still insufficiently understood. Even though vasopressin, methacholine, and isoproterenol, which evoke vasospasm, have been used as experimental animal models for angina [ 16 , 17 , 18 ], they have less translational potential.…”