PO2-dependent pulmonary vasoconstriction caused by procaine.

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Abstract
Procaine added to the blood-perfusing excised, ventilated dog lobes in concentrations from 2.5 to 10 mmolesAiter increased pulmonary vascular resistance. This change could be partially reversed by ventilating the lobes with high O2 concentrations. These concentrations of procaine also markedly prolonged the useful lifetimes of the excised lobe preparations. The procaine pressor response may be secondary to histotoxic hypoxia. This is indirectly supported by several observations of other workers. The prolongation of the usable life of the preparations was postulated as due to a decreased permeability of cell membranes which may have led to longer maintenance of nearly normal cellular electrolyte concentrations. These effects of procaine were also produced by tetracaine at about one-tenth the procaine concentration. This study could not resolve the question of whether vascular smooth muscle depolarization is necessary in the process of hypoxic pulmonary vasoconstriction, because the agents used to prevent depolarization seemed themselves to induce cellular hypoxia.

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