Vena cava replacement with a peritoneum-lined vascular graft.

The use of the peritoneum as a venous conduit was analyzed because of the inherent fibrinolytic properties of the mesothelium. A canine model in which the infrarenal inferior vena cava was replaced with interposition grafts (2 cm) of either a peritoneal tube, polytetrafluoroethylene (PTFE), or PTFE lined with peritoneum (lined graft) was studied. Venograms were performed 1 and 6 weeks after graft implantation for the percent area reduction of the lumen. Grafts were explanted at 6 weeks for light and scanning electron microscopy. The percent area reduction at 1 week for all grafts was found to be predictive of graft clotting by 6 weeks. At 6 weeks, one of three peritoneal tube grafts (33%), six of seven PTFE grafts (86%), and four of seven lined grafts (57%) were patent. Histologic studies demonstrated that stenosis of PTFE grafts was due to intraluminal thrombus formation, whereas lined grafts stenosed due to granulation tissue growth between the mesothelium and PTFE. A cellular circumferential intraluminal lining was found in four of four lined grafts, but in none of six PTFE grafts (p < 0.01). Furthermore, none of four lined grafts had intraluminal thrombus, but all of six PTFE grafts did (p < 0.01). Peritoneum-lined PTFE grafts maintain a continuous circumferential cellular lining, but have no improvement in short-term patency compared to PTFE alone.

Alpha-adrenergic receptor antagonism prevents intestinal vasoconstriction but not hypoperfusion following resuscitated hemorrhage.

Resuscitation (RES) after hemorrhage (HEM) results in persistent arteriolar constriction and hypoperfusion of the small intestine (SI) despite restoration of mean arterial pressure (MAP) and cardiac output (CO) to normal values. We postulated that increased adrenergic activity contributes to this vasoconstriction and impairment of flow. A loop of SI from decerebrate rats was exteriorized and suffused with Krebs' solution (37 degrees C, pH 7.4). In initial experiments, the effectiveness of alpha-adrenergic receptor antagonism by phentolamine (PHEN) was assessed. Subsequent groups received either topical PHEN (10(-6) M, n = 6) or saline (n = 6) in the suffusion and were then bled to 50% baseline (BL) MAP for 60 min and resuscitated to BL with shed blood/lactated Ringer's. Intravital microscopy and optical Doppler velocimetry were used to measure large (A1) and small, premucosal (A3) arteriolar diameters and RBC velocity; microvascular blood flow was calculated. MAP and transpulmonary CO were measured. During HEM, control animals developed A1 constriction and hypoperfusion with A3 arteriolar dilation. PHEN treatment prevented A1 constriction and enhanced A3 dilation but did not improve flow. Immediately after RES in controls, microvascular diameters and A1 flow returned to BL; however, over the 2-hr post-RES period there was progressive A1 and A3 vasoconstriction and hypoperfusion despite maintenance of BL MAP and CO. After RES in PHEN-treated animals, A1 flow returned to BL, but progressive hypoperfusion was only partially prevented. alpha-Adrenergic-mediated vasoconstriction contributes to intestinal hypoperfusion after HEM, but other mechanisms are also involved in microvascular responses during RES.(ABSTRACT TRUNCATED AT 250 WORDS)

Microvascular vasoconstriction and mucosal hypoperfusion of the rat small intestine during bacteremia.

Our previous studies have demonstrated that bacteremia induces vasoconstriction and hypoperfusion of the small intestinal microcirculation. The present study used time-transit doppler flowmetry, intravital microscopy, and laser doppler fluximetry to measure superior mesenteric artery (SMA) blood flow, intestinal microvascular blood flow, and mucosal perfusion. The aim of this study was to determine the relative importance of the intestinal macro- and microcirculations in the development of mucosal hypoperfusion. Animals were infused with 5 x 10(8) colony-forming units of Escherichia coli/100 g body weight or saline as control. Bacteremia induced a normotensive, normodynamic state. SMA blood flow was unaffected by bacteremia, but arteriolar vasoconstriction (approximately -30%) and microvascular hypoperfusion (approximately -70%) occurred. Mucosal perfusion decreased by 40% from baseline, and was temporally correlated with microvascular hypoperfusion. From these data, we conclude that the microcirculation has a central role in the development of mucosal hypoperfusion during bacteremia.