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The purpose of this study was to examine and compare the effects of atrial natriuretic peptide and furosemide on pulmonary gas exchange, hemodynamics, extravascular lung water, and renal function in a dog model of oleic acid-induced pulmonary edema.Prospective, comparable, experimental study.Laboratory at a university hospital.Eighteen male beagle dogs were studied under mechanical ventilation with pentobarbital anesthesia.Oleic acid (0.08 mL/kg) was injected and allowed for 1 hr to achieve pulmonary edema with hypoxemia at Fio2 of 0.3. After lung injury, dogs were divided into three groups; control group (n = 6) receiving saline (2.5 mL/hr for 5 hrs), atrial natriuretic peptide group (n = 6) receiving atrial natriuretic peptide (1 microg x kg(-1) x min(-1) for 5 hrs), and furosemide group (n = 6) receiving furosemide (1 mg x kg(-1) x hr(-1) for 5 hrs).Hemodynamics, arterial blood gases, extravascular lung water, and renal function were measured hourly for 7 hrs after injury. Oleic acid increased extravascular lung water and induced hypoxemia. In the atrial natriuretic peptide group, extravascular lung water was significantly (p.05) lower and Pao2 was significantly (p.05) higher than in the control and furosemide groups, respectively. Pulmonary hypertension induced by oleic acid was attenuated by atrial natriuretic peptide infusion but not by saline or furosemide. Increased natriuresis/diuresis did not significantly differ between the atrial natriuretic peptide and the furosemide group, whereas creatinine clearance in the atrial natriuretic peptide group was significantly higher than that in the furosemide group.These findings suggest that atrial natriuretic peptide improves pulmonary gas exchange by reducing extravascular lung water and pulmonary arterial pressure, possibly independently from natriuresis/diuresis in oleic acid-induced pulmonary edema.

The suprarenal abdominal aortic cross-clamping during aortic aneurysm repair causes renal dysfunction after surgery. Atrial natriuretic peptide (ANP), a hormone synthesized by the cardiac atria, induces diuresis-natriuresis and increases glomerular filtration rate. Therefore, we tested the hypothesis that prophylactic ANP infusion could limit the development of acute renal failure after aortic cross-clamping.Prospective, comparative, experimental study.Laboratory at a university hospital.Twelve male beagle dogs (10-13 kg) with mechanical ventilation under pentobarbital anesthesia.A catheter was inserted into the femoral vein, and lactated Ringer solution (10 mL/kg/hr) was administered throughout the study period. Two groups of animals were studied: the control group (n = 6), which received saline vehicle before and after suprarenal abdominal aortic cross-clamping for 1.5 hrs; and the ANP group (n = 6), which received ANP (1 microg/kg/min) for 5 hrs, starting from 10 mins before suprarenal abdominal aortic cross-clamping until the end of procedure.Changes in systemic and renal hemodynamics, blood gases, and renal function were measured at baseline and 1, 2, 3, 4, and 5 hrs after aortic cross-clamping. After aortic cross-clamping, urine volume, renal blood flow, and creatinine clearance significantly (p.01) decreased, and serum creatinine concentrations significantly (p.01) increased, but these effects were limited by continuous ANP infusion.The present study shows that ANP infusion preserved renal function after suprarenal abdominal aortic cross-clamping in dogs. These results justify a trial of ANP infusion in humans during aortic aneurysm repair.

Objective To investigate whether ONO-1714, a putative selective inhibitor for inducible nitric oxide synthase, modulates systemic hemodynamics, arterial blood gases, lactate concentrations, gastric mucosal perfusion, and renal and hepatic functions in endotoxic shock. Design Prospective, randomized, controlled animal study. Setting Laboratory at a university hospital. Subjects Eighteen male beagle dogs (12-19 kg) under pentobarbital anesthesia. Interventions Dogs were mechanically ventilated and monitored with a pulmonary arterial catheter and a gastric tonometer. They were divided in three groups: a) lipopolysaccharide (LPS) plus vehicle group (n = 6), which received LPS (250 ng/kg/min for 2 hrs) and saline 1 hr later; b) LPS plus ONO (0.05) group (n = 6), which received ONO-1714 (0.05 mg/kg) 1 hr after the start of LPS; c) LPS plus ONO (0.1) group (n = 6), which received ONO-1714 (0.1 mg/kg) 1 hr after the start of LPS. Measurements and main results Hemodynamics, blood gas parameters, gastric intramural pH, urine output, and serum levels of lactate, transaminases, bilirubin, and creatinine were measured during a 6-hr observation period. LPS induced hypotension, lactic acidosis, gastric mucosal acidosis, and renal and hepatic dysfunction. ONO-1714 reversed the LPS-induced hypotension and lactic acidosis without deteriorating cardiac output, oxygen delivery, or gastric mucosal acidosis. Conclusions These findings suggest that ONO-1714 is a useful agent to reverse hypotension and lactic acidosis in a canine endotoxic shock model.

Objective: To elucidate the relationship between airway pressure (Paw) and the distribution of gas-liquid interface during partial liquid ventilation (PLV). Design: Prospective, controlled study. Setting: A research laboratory at a university medical center. Subjects: Ten Japanese white rabbits. Interventions: Ten rabbits were tracheostomized and mechanically ventilated (FIO 2 = 1.0, tidal volume = 40 mL, respiratory rate = 25 breaths/min) under general anesthesia. In the oleic acid lung injury group (n = 5), oleic acid (0.10-0.12 mUkg) was intravenously administered to make a lung injury model. When PaO 2 became

The effect of mechanical ventilation with PEEP of 0, 10, and 20 cm H2O (continuous positive-pressure ventilation [CPPV]) on hepatic blood flow (HBF) and intrahepatic oxygen delivery was studied in 26 mongrel dogs anesthetized with fentanyl. Hepatic arterial and portal venous blood flow was measured by an electromagnetic flowmeter. CPPV caused a significant decrease in HBF, which was related to the PEEP level. A linear correlation was seen between HBF and cardiac output. Intrahepatic oxygen delivery decreased more than HBF and cardiac output. The reduced oxygen delivery was due mainly to the decrease in portal venous oxygen content.