Studies on the human umbilical cord Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/sq87bx17h

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  • Studies were initially conducted to determine the action of intravenous serotonin on perfused segments of human umbilical cords in vitro. Intravenous serotonin, via bolus injection or continuous infusion, was found to elevate venous perfusion pressure, while intra-arterial serotonin failed to alter venous pressure. Norepinephrine, administered to the venous perfusate, was shown to elevate venous pressure in approximately one-fifth the cords responding to serotonin. Methysergide (UML-491) failed to alter the response to intravenous serotonin, whether administered to the vein or to the arteries. Longitudinally and spirally cut strips of umbilical artery and vein were prepared and examined in a tissue bath-kymograph apparatus. Both serotonin and norepinephrine caused contractions of these vascular strips. Methysergide was shown to depress the contractions resulting from serotonin but not those from norepinephrine. Increase in venous perfusion pressure in segments of perfused umbilical cord receiving serotonin in the venous perfusate were abolished by removal of the arteries from the cord segment. Insertion of a stainless steel rod into one artery, thus uncoiling the arteries from around the vein, and manual untwisting of the cord segment to accomplish the same end, both abolished the response to intravenous serotonin. Removal of the rod or restoration of the twisted configuration of the cord segment was followed by a return of the response to intravenous serotonin. It is postulated that intravenous serotonin caused the increase in venous pressure by eliciting a contraction of arterial longitudinal muscle fibers, thus tightening the arterial spiral around the vein. The mechanism by which intravenous serotonin caused contraction of arterial muscle fibers remains to be elucidated, however, this study has shown by fluorimetry that approximately one-half of one percent of the serotonin infused into the vein appears in the surrounding bath fluid during the course of a 15 minute perfusion. Perfusion of the arteries in the cord with serotonin failed to produce a detectable level of the drug in the bathing medium. Serotonin administered to the arteries failed to cause contraction of longitudinal fibers in that vessel, although these fibers lie in the internal muscular layer of the artery. This leads to the suggestion that extra-arterial neural elements in the cord may mediate the response to intravenous serotonin. It is suggested that this mechanism could operate in utero to reduce the amount of vasoactive substances reaching the central fetal circulation by reducing blood flow in the cord prior to the drug reaching the fetus itself. If intravenous serotonin can also be shown to increase arterial perfusion pressure in isolated cord segments, this mechanism may further act to maintain constant placental volume by simultaneously regulating arterial and venous flow in the umbilical cord.
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