Key result
Protamine-induced pulmonary hypertension is driven by pulmonary venoconstriction independent of nitric oxide inhibition.
Why the study?
The specific site of protamine-induced pulmonary vasoconstriction and the role of nitric oxide after protamine injection were not determined.
Does protamine induce pulmonary venoconstriction in heparinized pigs, and is this response mediated by nitric oxide?
Does protamine induce pulmonary venoconstriction in heparinized pigs, and is this response mediated by nitric oxide?
Protamine-induced pulmonary hypertension in heparinized pigs is primarily driven by marked pulmonary venoconstriction and is not significantly mediated by nitric oxide release.
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Should not change protamine use in humans; leaves open venoconstriction mechanisms and clinical translation.
HAKIM et al. (1995) studied Protamine-induced pulmonary vasoconstriction. nitrow-L-arginine (LNA) vs. Control (no LNA) was evaluated on Pulmonary vascular resistance (PVR) after protamine injection. In anesthetized pigs, protamine-induced pulmonary hypertension is due to marked pulmonary venoconstriction, and inhibition of nitric oxide release with LNA did not alter the hemodynamic response.
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