Insufflated halothane increases venous admixture less than nitroprusside in canine atelectasis.

Abstract

Although it generally is agreed that halothane is a pulmonary vasodilator, its effect on venous admixture and hypoxic pulmonary vasoconstriction are more controversial. The effects of 2.4% halothane on pulmonary vascular resistance and venous admixture were investigated in an isolated canine lobe made atelectatic. Halothane was administered by three different methods: insufflation, addition to the pulmonary artery blood through a bubble deoxygenator, or a combination of both techniques. Pulmonary vascular resistance was divided into arterial, venous, and middle segmental resistance by a vascular occlusion technique. Middle resistance increased with 3% O2 ventilation (0.0238 +/- 0.0092 cmH2O.ml-1.min-1) or after production of atelectasis (0.0225 +/- 0.0074 cmH2O.ml-1.min-1), compared to control ventilation in the nonatelectatic lung 0.01 +/- 0.0067 cmH2O.ml-1.min-1). Halothane by any delivery method variably decreased middle resistance, with increasing potency from addition of halothane through the bubble deoxygenator (0.0118 +/- 0.0047 cmH2O.ml-1.min-1) to halothane insufflation (0.0072 +/- 0.0058 cmH2O.ml-1.min-1), and finally to a combination of both techniques (0.0026 +/- 0.0041 cmH2O.ml-1.min-1). In contrast to vascular resistance, venous admixture in the atelectatic (8 +/- 5%) and nonatelectatic lobes (7 +/- 4%) was increased with halothane insufflation (11 +/- 4%), addition of halothane through the bubble deoxygenator (26 +/- 16%), and a combination of both techniques (22 +/- 13%). Compared to intravenous nitroprusside (26 +/- 12%), halothane insufflation was less potent in increasing venous admixture when total pulmonary vascular resistances were of similar magnitude (0.0526 +/- 0.0112 and 0.0484 +/- 0.0088 cmH2O.ml-1.min-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)