To determine whether systemic cardiovascular responses to gram-negative end
otoxemia are mediated by nitric oxide, we evaluated time-dependent changes
in contractility and hemodynamics in a neonatal sheep model subjected to ni
tric oxide synthesis inhibition with L-Name (NW-nitro-L-arginine methyl est
er). Four groups were studied: control (C), endotoxin (E), endotoxin L-Name
where the nitric oxide synthase inhibitor was given prior to endotoxin (EL
N), and a control L-Name group pretreated with L-Name (CLN). The contractil
ity, measured as end-systolic elastance (Ees), increased transiently in the
E group and then returned to baseline. In contrast, Ees declined over time
in the ELN group. In terms of peripheral hemodynamics, both the E and ELN
groups demonstrated significant progressive decreases in blood pressure and
vascular resistance. The results of this study suggest that nitric oxide c
ontributes to the newborn contractile response of the heart to endotoxin, b
ut does not appear to mediate the systemic vascular relaxation response.