No abstract

Long‐chain soluble polymers (LSPs) have been shown to have profound hemodynamic effects at very low concentrations. At only 5 ppm in blood, LSPs increase blood flow and reduce vascular resistance. Despite studies showing therapeutic value in cases of hemorrhage, myocardial infarction, and atherosclerosis, the mechanism of action is unknown. The purpose of this study was to determine the dose‐dependency of LSPs on systemic and microcirculatory variables. Sprague‐Dawley rats were anesthetized and their spinotrapezius muscles isolated for transillumination. The experimental group (n=2) was given serial injections of the LSP polyethylene oxide (mol wt 4500 kDa) dissolved in saline to reach blood concentrations of 0.12, 0.4, 1.2 and 4 ppm. The control group (n=8) was given serial injections of the same volumes of saline. At 4 ppm, mean arterial pressure was lower in the LSP group (90 ± 2 mmHg vs 108 ± 17 mmHg). Interstitial PO2, as measured by phosphorescence quenching, was higher in the LSP group at 0.12 ppm (67 ± 3 mmHg vs 60 ± 4 mmHg) and 0.4 ppm (66 ± 2 mmHg vs 60 ± 4 mmHg). These findings are consistent with previous reports of this polymer.Support: NHLBI HL18292 and HL079087

This study compared the effects on O2 transport of two resuscitation fluids: a hemoglobin‐based O2 carrier (HBOC‐201, Biopure Corp., Cambridge, MA), and 5.9% human serum albumin (HSA), a non‐oxygen carrying colloid solution. Intravital microscopic measurements were made on the spinotrapezius muscle of anesthetized, male Sprague‐Dawley rats. Interstitial (ISF) PO2 was measured using phosphorescence quenching microscopy at baseline, post‐hemorrhage and post‐resuscitation time points. Following hemorrhage (40% blood volume) the animal was maintained in this condition for 30 minutes before resuscitation. Local tissue O2 consumption (VO2) was proportional to the rate of decline of PO2 following arrested flow from rapid inflation of a Saran bag placed around the microscope objective. In both groups (HBOC, N=4; HSA, N=4), baseline ISF PO2 (~60 mmHg) decreased significantly during hemorrhage (to ~2 mmHg), and increased after resuscitation (to ~40 mmHg). Significant vasoconstriction and elevation of mean arterial pressure (MAP) was observed with HBOC‐201. Infusion of nitroglycerin (N=2) along with HBOC‐201 diminished arteriolar vasoconstriction, eliminated the rise in MAP, and increased ISF PO2 (to ~55 mmHg). The findings support the hypothesis that vasoconstriction and elevation in MAP by HBOCs is due to nitric oxide scavenging.