Pulmonary microcirculatory response to localized hypercapnia.

Abstract

Anesthetized bullfrogs were examined to study the effects of localized hypercapnia on the red blood cell (RBC) velocity in pulmonary alveolar microvessels on the exposed lung surface. Before and after the exposure of a small area of the lung surface 6 mm in diameter to a hypercapnic gas mixture, the region was exposed to CO2-free control gas. The RBC velocity was measured by the use of a laser Doppler microscope. Both mean flow velocity (MV) and pulsatile amplitude (PA) were determined from the resulting flow velocity contour. Responses of pulmonary microvessels to hypercapnia were examined by measuring the vessel diameters with an ocular microscale of the microscope while gas mixtures were applied to a 1-mm-diameter region of the surface. During hypercapnia both MV (2.31 +/- 0.27 mm/s) and PA (0.54 +/- 0.15 mm/s) in the alveolar arterioles (luminal diameter = 64 +/- 14 microns) were reduced, each reaching a minimum (2.01 +/- 0.24 and 0.43 +/- 0.19 mm/s, respectively) prior to gradual returns to their initial values. After reintroduction of the control gas, the values of MV and PA approached initial values more rapidly. In capillaries MV (1.44 +/- 0.18 mm/s) and PA (0.28 +/- 0.06 mm/s) decreased to 1.25 +/- 0.10 and 0.15 +/- 0.05 mm/s, respectively. The maximum reduction of PA (-44.6%) therefore clearly exceeded that of MV (-12.4%) in capillary flow. An analog model calculation suggested that the reduction in diameter of the arteriolar system could reduce PA more than MV in the pulmonary capillary network. The time course of the velocity change closely resembled that of the diameter change in relatively large arterioles. Vasoconstriction of the arterioles therefore appeared to be the major cause of these decrements in MV and PA.