title: Cerebral and intestinal perfusion and metabolism in normocythemic hyperviscous hypoxic newborn pigs.
abstract: We studied the effects of hypoxia on cerebral cortical and intestinal perfusion and metabolism in normocythemic hyperviscous newborn pigs. Seven pigs were made hyperviscous by an injection of cryoprecipitate, increasing viscosity from 5.8 +/- 0.9 to 9.0 +/- 1. 2 (SD) cycles/s. Six normoviscous pigs received 0.9% NaCl. Reducing the inspired O(2) decreased the arterial O(2) content (Ca(O(2))) from 9.5 +/- 1.6 to 3.6 +/- 1.3 ml O(2)/100 ml. Increases in brain and decreases in gastrointestinal blood flow at the lower Ca(O(2)) values were similar between the groups. During hypoxia, blood flow to stomach, distal intestinal mucosa, and large intestines was lower (-50, -23, and -28%, respectively) in the hyperviscous than normoviscous group. At the lower Ca(O(2)) values, cerebral cortical vascular resistance decreased in both groups and intestinal vascular resistance increased (+257%) in the hyperviscous but not in the normoviscous group. During hypoxia, systemic oxygen delivery decreased, extraction increased, and uptake did not change; cerebral cortical O(2) delivery, extraction, and uptake did not change; and intestinal O(2) delivery decreased, extraction increased, and uptake did not change in both groups. Our study demonstrated that 1) during hypoxia, increases in systemic O(2) extraction compensated for decreases in delivery and systemic uptake did not change; vasodilation sustained cerebral cortical O(2) delivery and preserved metabolism; increases in intestinal oxygen extraction offset decreases in delivery and uptake was preserved; and 2) nonpolycythemic hyperviscosity did not have a major influence on cardiovascular or metabolic responses to hypoxia, except for modest effects on intestinal resistance and perfusion to certain gastrointestinal regions. We conclude that, under normocythemic conditions, a moderate increase in viscosity does not have a major impact on hemodynamic or metabolic adjustments to hypoxia in newborn pigs.
authors.affiliation: Department of Pediatrics, Women and Infants' Hospital of Rhode Island, Brown University School of Medicine, Providence 02905, USA.
authors.forename: M
authors.initials: M
authors.lastname: Goldstein
authors.forename: V K
authors.initials: VK
authors.lastname: Rehan
authors.forename: W
authors.initials: W
authors.lastname: Oh
authors.forename: B S
authors.initials: BS
authors.lastname: Stonestreet
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism / Q000502:physiology*; D001682:Biological Availability; D001809:Blood Viscosity; D001921:Brain / Q000378:metabolism; D002560:Cerebrovascular Circulation; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D007413:Intestinal Mucosa / Q000098:blood supply / Q000378:metabolism; D007422:Intestines / Q000098:blood supply*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D013270:Stomach / Q000098:blood supply; D013552:Swine; D014664:Vasodilation
chemical_list: D010100:Oxygen