RESUMO
This report is the author's in vivo study of basilar artery reactivity to physiologic and pharmacologic stimuli in a newborn animal model. Isoflurane-anesthetized and ventilated piglets(less than 3 days of age) were placed supinely, the pharyngeal muscles retracted, and a 9 mm diameter hole was drilled in the clivus. The dura was incised in a circular fashion and coagulated, and a stainless steel and glass window with inflow and outflow ports was affixed to the clivus with dental cement. Using a color camera mounted on a triocular stereomicroscope, images of the basilar artery were recorded to Super-VHS tape, and stimulus-induced changes in vessel diameter were determined off-line from the videotape record using an image analysis system. Induction of moderate hypercapnia(PaCO2=69+/-3 mmHg) dilated the basilar artery 21+/-4%(p=0.002;n=5);hypocapnia(PaCO2=21+/-0.5 mgHg) constricted the artery 10+/-3%(p=0.05;n=5). A reduction in cerebral perfusion pressure induced by hemorrhagic hypotension to a mean arterial pressure(M ABP) of 34+/-0.5 mmHg was associated with a 9+/-1.6% reduction(p=0.0005;n=11) in basilar artery diameter. Superfusion of the clival window with the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine(L-NMMA)(100 microM) decreased artery diameter 20+/-5.6%(p=0.01;n=6). Superfusion of 10 microM and 100 microM adenosine caused dose-dependent increases in artery diameter of 9.3+/-4%(p=0.02;n=4) and 13+/-5%(p=0.03;n=5), respectively. These results indicate that, while reactivity to CO2 is intact in the newborn basilar artery, autoregulatory adjustment in brainstem blood flow in newborns may be limited due to basilar artery constriction in response to systemic hypotension. Nitric oxide provides a tonic vasodilative influence on basilar artery tone in the neonate.