title: Blood glucose and lactate levels during hemorrhagic shock reversion by hypertonic NaCl solution.
abstract: 1. Several studies have shown that in irreversible hemorrhagic shock the liver is one of the first vital organs to present metabolic alterations accompanied by an increase in lacticemia. Intravenous infusion of hypertonic solutions increases mesenteric flow as well as liver perfusion, an effect which can be blocked by vagotomy. 2. In the present study we investigate the possible role of the increase in mesenteric flow in the prevention of hepatic failure evaluated by the arterial-venous difference in the generation of glucose from lactate during the reversal of hemorrhagic shock with hypertonic NaCl solution and the possible blockage of this response by bilateral vagotomy. 3. Twenty-eight male dogs, weighing 14-20 kg, were submitted to severe hemorrhagic shock. The animals were then divided into four groups: a) HYPER, 2400 mosm/l NaCl; b) SALINE, 300 mosm/l NaCl; c) HYPERVg, 2400 mosm/l NaCl immediately after bilateral vagotomy; d) SALINEVg, 300 mosm/l NaCl immediately after bilateral vagotomy. Each group received an intravenous infusion of 10% of the shed blood volume of NaCl infusion. 4. Arterial and venous samples were collected to monitor the levels of lactate, glucose and insulin. During hemorrhage, arterial and venous lactate concentrations increased. After infusion, arterial lactate levels decreased from 332 +/- 23% to 115 +/- 12% in the HYPER group in contrast to the SALINE group where it increased from 327 +/- 20% to 422 +/- 19%. 5. The decrease in arterial lactate observed after hypertonic solution infusion (2400 mosm/l), in dogs with intact vagus, suggests an increase of lactate uptake by heart and liver. Thus the beneficial effect of hypertonic solution in the reversal of hemorrhagic shock may be to enhance blood flow and oxygen delivery to the liver which would maintain glucose production and prevent hepatic failure. All the metabolic effects of hypertonic solution were abolished by vagotomy.
authors.affiliation: Departamento de Fisiologia e Biofisica, Universidade de São Paulo, Brasil.
authors.forename: L R
authors.initials: LR
authors.lastname: Lopes
authors.forename: R
authors.initials: R
authors.lastname: Curi
authors.forename: O U
authors.initials: OU
authors.lastname: Lopes
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000096:biosynthesis / Q000378:metabolism*; D004285:Dogs; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007773:Lactates / Q000097:blood* / Q000378:metabolism; D008297:Male; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage*; D012771:Shock, Hemorrhagic / Q000097:blood* / Q000378:metabolism; D013997:Time Factors; D014628:Vagotomy
chemical_list: D001786:Blood Glucose; D007328:Insulin; D007773:Lactates; D012462:Saline Solution, Hypertonic