Differential responses to pial vessels between nitric oxide donor, nitroprusside and trimethaphan in cats

The reactivity of cerebral vessels to different stimuli varies according to artery and vein and also its vessel size. Whether nitric oxide (NO) mediates ischemic and hypoxic vasodilatation is controversial. We therefore attempted to address this question by means of a direct measurement of diameter of pial artery and veins during hypotension induced by a NO donor, nitroprusside (NTP), or a ganglionic blocker, trimethaphan (TMP), referring to (together with) that during hemorrhagic hypotension. In addition, comparisons were made between effects of these two vasodilating drugs on the cerebrovascular reactivity to hypercapnia. Using twenty-one cats anesthetized with halothane (0.9%, end-tidal), the diameter of pial arteries and veins were measured by the image-splitting technique through the cranial window. Each of these vessels were classified into three groups according to their reference diameter: I; 24-50 μm, II 51-100 μm, III; 101-352 μm. The mean arterial pressure was reduced to approximately 50 torr by either HEM or by the administration of the drugs. Diameters of arteries were increased during hypotension induced by NTP, HEM or TMP; smaller arteries dilated more than did the larger ones. Consistent and significant dilatation of all veins was observed only during NTP-induced hypotension. During TMP-induced hypotension, dilatation of arteries was independent of vessel size. C0 2 responsiveness of arteries to hypercapnia was reduced during HEM or TMP-induced hypotension, whereas it was maintained during NTP-induced hypotension. Arteries are dilated by hemorrhagic hypotension smaller arteries less than 50 μm dilated more than did the larger ones, and NTP produces similar responses. NTP-induced hypotension may not modify the C0 2 reactivity, while hemorrhagic and TMP-induced hypotension may impaire the reactivity. NTP produces potent vasodilatation in smaller veins.