Possible protective role of nitric oxide in myocardial ischemia

Much interest has been focused on the role of endogenous and exogenous NO pathways as regulators of cardiovascular function in health and disease. Despite the great number of studies on the effect of nitric oxide on cardiac functions under basal and ischemic conditions, however their results remains highly controversial.So this study was designed to throw more light on the role of endogenous NO [synthesized of L-argenine] and exogenous NO [from sodium nitroprusside] in modulation of myocardial function in ischemic conditions A total number of 80 isolated hearts from adult male white New-Zeland rabbits weighing 1.5-2 Kg, grouped into 8 groups were used in this study. When administered before 25 min of global ischemia and early in reperfusion it was found the NO donors L. Arginine, SNP induced a significant cardioprotective effect expressed by a reduction in the percentage of post ischaemic cardiac damage. This was manifested by a lesser reduction in heart rate, amplitude of contraction, coronary flow rate and also lesser lactate dehydrogenase [LDH] release when compared with control group. While administration of NOS inhibitor L. NAME or guanylate cyclase inhibitor MB induced cardiac damage manifested by an increase in the percentage of post ischaemic reduction in heart rate, amplitude of contraction, coronary flow rate and an increased LDH release as compared to control group. Co-administration of NO donors with NO inhibitors abolished the cardio protective effect of NO donors. In conclusion it was found that NO has a significant cardio-depressant effect under basal conditions, however it increased coronary flow rate and moreover, NO donors have a significant cardio protective effect, following ischaemia and reperfusion. These findings may have clinical value as it illustrate the role of NO donors as potential therapeutic agents in the treatment and prevention of coronary artery disease

Relative arteriovenous potency of nitric oxide

Much interest has been focused on the role of endogenous and exogenous nitric oxide [NO] pathways as regulators of cardiovascular function in health and disease. Moreover, despite the well documented vasodilator effect of NO, the relative arteriovenous potency of nitric oxide donors and inhibitors and the role of NO in portal circulation remain unclear. So this study was designed to throw more light on the role of NO on different blood vessels in vitro. This work studied the effect of L-NAME, L-arginine,SNP and MB in 3 different doses on the contractile effect of submaximal dose of noradrenaline on isolated dog aortic,femoral artery,femoral vein and portal vein strips. L-NAME and MB induced a significant increase of noradrenaline induced contraction in all vascular strips with all tested doses. However the response of venous strips was significantly higher than arterial strips with the least effect on aortic strips and highest on portal vein strips indicating a higher sensitivity of veins especially portal vein and the importance of NO in maintenance of basal vascular tone in all tested strips. On the other hand L-arginine and SNP induced a significant reduction in the noradrenaline-induced contraction in all vascular strips with all tested doses. This effect was more in veins especially portal vein than arterial strips.This veno-selectivity illustrate a potential role for NO in control of venous tone and in turn preload which is a major risk factor in some cardiovascular diseases as heart failure.Also the high portal sensitivity under basal condition suggest a possible use of NO as therapeutic agents in portal hypertension, however further studies on portal hypertensive subjects are recommended to illustrate its effects under condition of increased portal pressure