Abstract
Helically cut strips of 4th- and 5th-order pulmonary arteries were obtained from dogs and rabbits and studied in a muscle bath. Isometric contractions of these strips were recorded. The effects on resting tensions and on the tensions following induction of contractions by several stimuli were observed during periods of O2 deprivation and of variation of bath pH and 6.6 to 8.0. The stimuli for contractions included electrical current, serotonin, norepinephrine, angiotensin, acetylcholine, and potassium chloride. Neither hypoxia nor pH alteration changed resting tension. Hyposda depressed the tensional responses to all stimuli, and acidification depressed responses to all stimuli except addition of norepinephrine to the bath solution. No evidence could be found that hypoxia either increased excitability or contractility or in itself caused arterial contraction. The ability to maintain the tensions of the arterial strips clearly depended on the presence of 02. Hypoxic pulmonary vasoconstriction in vivo is therefore probably not a manifestation solely of changes of vascular muscle. The phenomenon of hypoxic pulmonary vasoconstriction also is probably not a manifestation of arterial contractions caused by hypoxic acidosis, since acidosis typically depressed strip tension. Experiments relating the contractile response of arterial strips to muscle cell membrane potential were presented and discussed. From these experiments it was suggested that tensional responses to all stimuli used were functions of the membrane potential difference.