Role of the carotid sinus in response of integrated venous system to pulsatile and nonpulsatile perfusion.

Effects of pulsatile and nonpulsatile perfusion on capacity system were investigated in 33 open-chest mongrel dogs with extracorporeal circulation. In 28 dogs with intact carotid sinus nerves, after changing from nonpulsatile to pulsatile systemic perfusion the mean arterial pressure decreased by 14 +/- 1.5 mm Hg, peripheral resistance by 423 +/- 15 dyne.cm-5.sec, and venous blood volume by 3.3 +/- 0.4 ml/kg. After changing from pulsatile perfusion to nonpulsatile systemic perfusion the mean arterial pressure increased by 15 +/- 2.2 mm Hg, the peripheral resistance by 431 +/- 15 dyne.cm-5.sec, and venous volume by 3.9 +/- 0.5 ml/kg. The same effects were observed in five dogs with bilateral isolated carotid pulsatile perfusion or nonpulsatile perfusion and systemic nonpulsatile perfusion. These effects were abolished after denervation of pressor receptors and pharmacologic blockade of alpha and beta receptors. It is proposed that with nonpulsatile perfusion carotid sinus-mediated vasoconstriction occurs in the downstream part of the capacitive system, where more pronounced wall musculature with increased number of adrenergic receptors is present. The throttle effect caused by this "resistance" part of venous circulation leads to increase of pressure in the upstream section of the capacitive system, compensates for the constrictive effect of the sympathetic tone, and leads finally to an increased volume of the capacity system. We conclude that venous response to different perfusion modalities is critically dependent on intact carotid sinus nerves and adrenergic receptors in the veins.