Am. J. Respir. Crit. Care Med., Vol 151, No. 3, 03 1995, 706-712.
Vascular reactivity in sepsis: importance of controls and role of nitric oxide
A Yaghi, NA Paterson and DG McCormack
A.C. Burton Vascular Biology Laboratory, Department of Medicine, Victoria Hospital, London, Ontario, Canada.
We have previously reported differential impairment of pulmonary and
systemic vascular contractility in hyperdynamic sepsis. The objectives of
this study were (1) to determine whether the magnitude of this phenomenon
depends on the control group chosen for comparison, and (2) to examine the
role of nitric oxide (NO) in this altered vascular contractility. Rats were
randomized to sepsis induced by cecal ligation and perforation (CLP) or to
one of two control procedures. The Sepsis group had a jugular venous line
for fluid administration, laparotomy, and CLP. Control group 1 (Control)
had only a jugular venous line inserted, while group 2 (Sham) had a jugular
venous line inserted and an abdominal incision. All rats were killed 24 h
after surgery. Vascular contractility of small pulmonary arterial and
thoracic aortic rings was assessed in vitro by obtaining cumulative
dose-response curves to the contractile agonists potassium chloride (KCl),
phenylephrine (PE), and prostaglandin F2 alpha (PGF2 alpha). Pulmonary
vessels from animals in the Sepsis and Sham groups exhibited significant
attenuation of the contractile responses to KCl, PE, and PGF2 alpha
compared with the Control group. In contrast, contractility of the aortic
rings to KCl, PE, and PGF2 alpha was not significantly different in the
three groups studied. Incubation of pulmonary and aortic vessels with
NG-nitro-L-argine methyl ester (L-NAME, 10 microM) caused an increase in
the response to KCl, PE, and PGF2 alpha in pulmonary vessels in Sepsis and
Sham rats but not in Control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
