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Effects of nitrates on splanchnic and hepatic circulation

It has only recently been discovered that exogenously administered nitrates exhibit their vasodilatory effect by release of an endothelium-derived relaxant factor, which may in turn be identical with nitric oxide. The intravenous or oral administration of nitrates such as nitroglycerin (NTG) will generally result in vascular dilatation, which can, however, be modified by homeostatic vascular reflexes often involving sympathoadrenal activation. The vasodilatory action of nitrates appears to be more pronounced in veins than in arteries (1). During normal resting conditions the total splanchnic blood perfusion will constitute at least 20% of the total left ventricular output, which implies that changes in splanchnic vascular resistance will significantly affect overall systemic vascular resistance. The liver receives two-thirds of its blood supply in desaturated form through the portal vein. One third of its blood flow, but approximately half of its oxygen supply, is received from the hepatic artery which acts as an important oxygen supply regulator for the liver. The main characteristics of the splanchnic circulatory bed are given in Table 1 . Regional haemod ynamic responses to various vasoactive drugs as well as to various forms of general anaesthesia may show substantial variation between different studies. The reason for this is the variety of factors that can influence vascular responses, as shown in Table 2. In anaesthesia and intensive care practice TNG is frequently administered intravenously, both to awake patients and to patients during general or regional anaesthesia. During general anaesthesia the splanchnic vascular bed generally tends to be underperfused in relation to other vascular beds and it is therefore important that the addition of various vasoactive drugs does not increase this imbalance.