| Autor: |
Figueiredo, Luiz Francisco Poli de, Cruz, Ruy Jorge, Silva, Eliezer, Macae, Margareth, Yada-Langui, Silva, Mauricio Rochae e |
| Předmět: |
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| Zdroj: |
Journal of Investigative Surgery; Sep/Oct2005, Vol. 18 Issue 5, p257-264, 8p, 1 Chart, 6 Graphs |
| Abstrakt: |
Splanchnic hypoperfusion has been implicated as the motor of multiple organ dysfunction. Hypertonic saline has shown to benefit microcirculatory blood flow. In hemorrhaged animals, we tested the hypothesis that small-volume 3% NaCl/10% dextran 40 (3%HSD) promotes global and regional improvements, including gastric mucosal acidosis reversal. Seventeen dogs (18.8 ± 1.2 kg) were bled (20 mL/min) to a mean arterial pressure of 40–45 mm Hg, which was maintained at these levels for 15 min. They were randomly assigned to two groups: Blood ( n = 9), total shed blood retransfused at 40 mL/min; or a 4-min bolus injection of 3%HSD ( n = 8), in a volume equivalent to 25% of total shed blood. All animals were followed for 30 min thereafter. Gastric mucosal PCO 2 (gas tonometry), portal vein PCO 2 , superior mesenteric artery blood flow (SMA, ultrasonic flowprobes), and systemic and regional O 2 -derived variables were evaluated throughout the protocol. Hemorrhage induced significant reductions of arterial pressure, cardiac output, and SMA blood flow, while portal–arterial and gastric–arterial PCO 2 gradients increased. Total shed blood transfusion, as well as 3%HSD bolus injection, promptly restored all parameters, except for the increased gastric–arterial PCO 2 gradient. We conclude that persistent gastric mucosal acidosis cannot be adequately predicted by global and splanchnic O 2 derived variables in following hemorrhage and resuscitation with total shed blood transfusion or small-volume hypertonic–hyperoncotic solution. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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