Segmental pulmonary vascular resistance following wood smoke inhalation

Abstract

To locate the specific site (i.e., pulmonary arteries, veins, or capillaries) of increased pulmonary vascular resistance after wood smoke inhalation and to demonstrate whether the prostanoids, thromboxane B2 or 6-keto-prostaglandin F1 alpha, play a role in these vascular resistance changes. Prospective, randomized, controlled trial. Laboratory at a university medical center. Five mongrel dogs. The isolated canine left lower lobe preparation was used to measure changes in the pressure drop across the pulmonary arteries, veins, and capillaries. The left lower lobe was surgically isolated and perfused by a pump primed with autologous blood. The arterial and venous occlusion technique and the vascular pressure-flow relationship were used to assess changes in pulmonary vascular resistance. After baseline measurements, the left lower lobe was exposed to wood smoke for 2.5 mins and measurements were repeated. Smoke exposure caused an immediate (5 mins post-inhalation) increase in the total pressure gradient across the lobe (baseline = 9.8 +/- 0.5 torr [1.3 +/- 0.06 kPa]); smoke inhalation = 24.3 +/- 3.9 torr [3.24 +/- 0.5 kPa]; p < .05). Total pressure drop was partitioned longitudinally into pressure drops across arteries, veins, and the middle vessels. The increase in total pressure drop was associated with a moderate increase in the pressure drop across the middle vessels (baseline = 1.1 +/- 0.2 torr [0.14 +/- 0.02 kPa]; smoke inhalation = 5.2 +/- 1.1 torr [0.69 +/- 0.14 kPa]; p < .05); a large increase in the pressure drop across the veins (baseline = 4.8 +/- 1.3 torr [0.64 +/- 0.17 kPa]; smoke inhalation = 20.7 +/- 3.4 torr [2.7 +/- 0.45 kPa]; p < .05), and no significant change in the pressure drop across the arteries (baseline = 3.7 +/- 0.4 torr [0.49 +/- 0.05 kPa]; smoke inhalation = 4.8 +/- 0.5 torr [0.64 +/- 0.06 kPa]; p = NS). Increases in the pressure drop across the middle and venous vessels were transient and no longer significantly different from baseline 15 mins after smoke inhalation. Similarly, analysis of the pulmonary artery/blood flow data demonstrated that the mean slope and pressure intercept were greater than baseline only at 5 mins postsmoke inhalation (p < .05). Thromboxane B2 did not significantly change from baseline values after smoke exposure and prostaglandin F1 alpha demonstrated a slight but significant decrease 30 mins postsmoke. Pulmonary edema was measured gravimetrically (wet/dry weight ratio) and smoke significantly increased lung water in the left lower lobe (wet/dry weight ratio = 6.55 +/- 0.4) as compared with the normal left upper lobe (wet/dry weight ratio = 4.97 +/- 0.2). We conclude that smoke causes an intense but transient increase in the pressure drop across the venous segment that may accelerate the formation of pulmonary edema, which is not mediated by changes in thromboxane B2 or prostaglandin F1 alpha.