We evaluated the biochemical and hemodynamic response to hypertonic saline solution plus dextran in isoflurane-anesthetized pigs infused IV with Escherichia coli endotoxin (5 micrograms/kg of body weight for 0 to 1 hour + 2 micrograms/kg for 1 to 4 hours). After 120 minutes of endotoxemia, pigs were treated with a bolus (4 ml/kg over 3 minutes) of either normal saline solution (NSS; 0.9% NaCl), or hypertonic saline solution plus dextran (HSSD; 7.5% NaCl + 6% dextran-70). Administration of HSSD significantly (P < 0.05) increased serum osmolality and concentrations of sodium and chloride for approximately 2 hours during endotoxemia. Plasma total protein concentration decreased significantly (P < 0.05) for 2 hours after treatment with HSSD, indicating hemodilution and increased plasma volume. Although HSSD transiently increased cardiac index (CI) for approximately 15 minutes, this effect was not sustained; however, the endotoxin-induced decrease in CI was ameliorated from 120 to 180 minutes. In pigs of the endotoxin + NSS group from 180 to 240 minutes, CI decreased significantly (P < 0.05), compared with baseline and control values. The endotoxin-induced increases in mean pulmonary arterial pressure and pulmonary vascular resistance were not attenuated by HSSD. At 135 minutes, total peripheral vascular resistance was transiently lower (for approx 15 minutes) in pigs treated with HSSD, compared with control pigs. The endotoxin-induced increase in plasma lactate concentration was not attenuated by HSSD, indicating continued peripheral O2 debt. We conclude that, despite sustained increases in serum osmolality and concentrations of sodium and chloride, HSSD has only transiently beneficial cardiopulmonary effects during endotoxemia in pigs.

To determine blood supply in the area, dye or radioopaque contrast material was injected into the named arteries supplying the terminal colon and rectum in 10 dogs. The cranial rectal artery appeared to supply most of the blood to the terminal colon and rectum. The middle and caudal rectal arteries supplied variable and relatively insignificant amounts. The intrapelvic rectum had a less adequate blood supply than did the terminal colon or proximal rectum. A ventral midline laparotomy and pubic osteotomy were performed in an additional 11 dogs to provide access to the terminal colon and rectum. When the cranial rectal artery was ligated and the colorectal junction was transected and anastomosed, the intrapelvic rectum developed marked congestion, edema, and discoloration. Rectal fluorescence, after IV administration of fluorescein, was either poor or absent. Histologically, partial- to full-thickness mucosal necrosis was evident in most tissue specimens taken from the rectum, and muscle necrosis was evident in some. These findings suggest that, in dogs, the cranial rectal artery should be preserved if at all possible and, if the cranial rectal artery is ligated, most of the intrapelvic rectum should be resected to ensure adequate blood supply to the anastomosis.