Furosemide during sustained left atrial hypertension in functionally anephric dogs: Intravascular and extravascular pulmonary fluid volumes. V

Abstract

The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volume was examined using double-indicator techniques (thermal-green dye) in 11 open-chest anesthetized dogs during the production of sustained left atrial (LA) hypertension by a LA balloon over a period of 195 min. In 6 of these animals data were also acquired after the intravenous administration of furosemide (1 mg/kg). The renal effects of the diuretic were blocked by tying off the ureters and the vascular supply of both kidneys. Left atrial pressure (N = 11) was abruptly increased from 2.2 ± 2.1 mm Hg to 30.2 ± 4.0 mm Hg ( P < 0.01) and maintained at that level for 120 min. Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 60 min for a total of 120 min. At that point EVLW had increased (8.1 ± 0.8 cc/kg at control to 21.7 ± 2.0 cc/kg at 120 min, P < 0.001), as had PBV (6.2 ± 2.1 cc/kg to 9.1 ± 3.1 cc/kg P < 0.01). After furosemide injection ( N = 6), LA pressure declined (mean peak reduction of ∼6 mm Hg at 60–75 min, P < 0.01), aortic and pulmonary arterial pressure both declined ( P < 0.01). However, EVLW remained unchanged, though PBV decreased significantly (peak decrease at 75 min after furosemide administration of 2.0 ± 0.4 cc/kg, P < 0.01). In the untreated dogs, EVLW continued to climb ( P < 0.05 vs treated dogs at 75 min postfurosemide). Thus it is concluded that in a LA balloon model of heart failure where renal diuretic function is eliminated, furosemide acts as a very mild venodilator, redistributing blood from the central to peripheral intravascular circulation, and limiting, but not clearing, the alveolar air spaces. Its major acute effect (<2–4 hr) on gas exchange in vivo must be then its removal of fluid via renal excretion in conjunction with its effect on the venous circulation.