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Abstract 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 (KCI), phenylephrine (PE), and prostaglandin F2α (PGF2α). Pulmonary vessels from animals in the Sepsis and Sham groups exhibited significant attenuation of the contractile responses to KCI, PE, and PGF2α compared with the Control group. In contrast, contractility of the aortic rings to KCI, PE, and PGF2α 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 µM) caused an increase in the response to KCI, PE, and PGF2α in pulmonary vessels in Sepsis and Sham rats but not in Control rats. We concluded that (1) sepsis affects vascular contractility differently in vessels from different vascular beds; (2) incision of the abdomen has a direct effect on vascular reactivity and may therefore not be an appropriate control for studies of abdominal sepsis; and (3) the effect of L-NAME on contractile responses of pulmonary artery rings supports the hypothesis that NO synthesis is induced in the pulmonary circulation in sepsis.
Yaghi et al. (Wed,) studied this question.