Lack of alteration of endogenous nitric oxide pathway during prolonged nitric oxide inhalation in intensive care unit patients.

OBJECTIVE: To compare hemodynamic and gasometric variables and the plasma concentrations of nitric oxide metabolites (cyclic guanosine monophosphate and nitrate and nitrite), endothelin-1, and renin-angiotensin metabolites before and after the start of nitric oxide inhalation, after prolonged nitric oxide inhalation, and before and after nitric oxide withdrawal. DESIGN: Prospective study. SETTING: Surgical intensive care unit, university hospital. SUBJECTS: Patients with acute lung injury and right ventricular failure. INTERVENTIONS: Nitric oxide inhalation (10-12 ppm) during a median of 2.9 days (12 hrs to 6.5 days). MEASUREMENTS AND MAIN RESULTS: The pulmonary vasodilator effects of inhaled nitric oxide improved arterial oxygenation in patients with acute lung injury (p < .05) and reduced right atrial pressure in patients with right ventricular dysfunction (p < .01). These beneficial effects lasted the whole period of prolonged inhaled nitric oxide therapy up to 6.5 days. However, when inhaled nitric oxide was withdrawn, pulmonary vasodilator effects rapidly disappeared, and Pao2/Fio2 ratio markedly deteriorated in all studied patients to return to pre-inhaled nitric oxide levels. Changes in plasma cyclic guanosine monophosphate and nitrate and nitrite paralleled those of pulmonary vasodilatory effects. An immediate increase in plasma cyclic guanosine monophosphate with a slightly delayed increase in plasma nitrate and nitrite was observed at inhaled nitric oxide start with no attenuation during the prolonged inhaled nitric oxide therapy. A marked decrease toward pre-inhaled nitric oxide levels was seen within hours of inhaled nitric oxide withdrawal. In addition, no alteration of plasma endothelin-1 or renin-angiotensin mediators was observed during or after inhaled nitric oxide therapy. CONCLUSIONS: Our study showed a lack of attenuation in the beneficial effects of inhaled nitric oxide and a lack of alteration of endogenous nitric oxide, endothelin-1, and renin-angiotensin pathways during prolonged nitric oxide inhalation.

The postoperative effects of halothane versus isoflurane on hepatic artery and portal vein blood flow in humans.

UNLABELLED: Animal studies have shown that halothane decreases total hepatic blood flow (THBF) by reducing both arterial (HABF) and portal (PVBF) inflow, whereas isoflurane appears to preserve them. In this study we assessed the effect of halothane and isoflurane on HABF and PVBF in surgical patients by using the pulsed Doppler technique. A validation study was conducted in six cynomolgus monkeys to compare the values of THBF obtained by the pulsed Doppler and indocyanine green clearance methods. Subsequently, six patients (ASA status I and II) undergoing elective open cholecystectomy were studied after surgery by using implanted pulsed Doppler probes. THBF and liver flow partition were compared during 1% halothane and 1.5% isoflurane (end-tidal concentrations). In the animal study, there was good agreement between the techniques (Bland and Altmann representation). In flunitrazepam-anesthetized patients, THBF was 1120 +/- 284 mL/min. Compared with this baseline and for a similar mean arterial blood pressure decrease (10%), THBF was maintained with isoflurane, whereas it decreased by 36% (P < 0.05) under halothane. With isoflurane, PVBF increased (25%; P = 0.067) with a maintained HABF. With halothane, both PVBF (-44%; P < 0.05) and HABF (-20%; P < 0.05) were reduced. Halothane acted mainly as a vasoconstrictor of the hepatic circulation, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on hepatic oxygen supply. IMPLICATIONS: Volatile anesthetics may alter liver circulation with serious adverse effects. Using implanted pulsed Doppler probes in six anesthetized patients, we showed that halothane acted mainly as a vasoconstrictor of the liver vascular bed, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on liver oxygen supply.

Acute respiratory failure secondary to dilatation of herniated stomach.

We report the case of a patient who presented acute respiratory failure (ARF) due to gastric distension secondary to hiatus hernia. This clinical condition may have been induced by an interaction between fluphenazine and ipratropium bromide. This exceptional diagnosis needs to be considered when discussing compressive pneumothorax.