Objectives Nitric oxide released from vascular endothelial cells is a potent vasodilator and inhibits platelet adhesion. It has been suggested that decreased nitric oxide production from dysfunctional endothelial cells is implicated in the pathophysiology of pre-eclampsia. In this study evidence was sought for abnormal production of nitric oxide in pre-eclamptic women.Participants Blood was collected from 20 women presenting with pre-eclampsia, from 20 matched healthy pregnant controls and from 12 nonpregnant women of childbearing age.Methods Serum nitrate, the stable end metabolite of nitric oxide, was measured by vanadium 111 chloride reduction and chemiluminescence.Results Sera fiom women with pre-eclampsia had significantly higher nitrate concentrations (mean 47.4 pmol/L [SD 13-61) compared with healthy pregnant (mean 31.2 pmol/L. [SD 9.141) and nonpregnant (mean 32.1 pmol/L [SD 10.01) controls.Conclusions These results do not support the hypothesis that decreased endothelial cell nitric oxide production may be important in the pathophysiology of pre-eclampsia. On the contrary, serum nitrate levels are increased which may reflect either increased production of nitric oxide from an unidentified source or decreased elimination through the kidneys.

Adverse events during coronary artery bypass graft (CABG) surgery have been described in patients receiving angiotensin converting enzyme (ACE) inhibitors, including hypotension on induction of anaesthesia and an increase in vasoconstrictor requirements after cardiopulmonary bypass (CPB). Omitting regular ACE inhibitor medication before surgery may improve cardiovascular stability during anaesthesia. We evaluated prospectively the effect of omitting regular ACE inhibitor medication before CABG surgery on haemodynamic variables and use of vasoactive drugs. We studied 40 patients with good left ventricular function, allocated randomly to omit or continue ACE inhibitor medication before surgery. Arterial pressure, cardiac output, systemic vascular resistance and use of vasoactive drugs were recorded during anaesthesia and in the early postoperative period. Patients who omitted their ACE inhibitors had greater mean arterial pressure during the study and required less vasopressors during CPB. However, these patients required more vasodilators to control hypertension after CPB and in the early postoperative period. There was no difference in hypotension on induction of anaesthesia or in the use of vasoconstrictors after CPB. We conclude that omitting ACE inhibitors before surgery did not have sufficient advantage to be recommended routinely.

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We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

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