| 1. |
- Schoenberg, M H, et al.
(författare)
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Hemorrhagic shock in the dog. I. Correlation between survival and severity of shock.
- 1985
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Ingår i: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:1, s. 21-33
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Tidskriftsartikel (refereegranskat)abstract
- A prerequisite elucidating the pathomechanism of hemorrhagic shock are reproducible experimental models, leading to a predictable outcome. Two concepts have been reported to be a good predictor for the outcome both employing a fixed hypotension level: total oxygen deficit and shed blood volume uptake. To correlate these two models we subjected 31 dogs to a standardized hemorrhagic shock procedure. Besides determination of acid-base status, hematocrit, mean arterial pressure, and cardiac output, these two parameters were measured continuously. Seventeen dogs survived the shock procedure, 14 died within 24 h. During shock, neither oxygen deficit nor any other parameter mentioned above correlated with the final outcome of the shock state. The only significant difference between surviving and non-surviving animals during this period was the amount of uptake. The non-surviving dogs exhibited a higher uptake volume, indicating an incipient collapse of the microcirculation. Terminating the duration of hypotension at an uptake volume of 5% of the maximum shed blood, all animals survived, while after an uptake volume of 15% about 50% of the dogs died. Using uptake volumes of various degrees in a hemorrhagic shock model as the endpoint of the hypotensive stress, it seems possible to produce reliable survival rates.
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| 2. |
- Schoenberg, M H, et al.
(författare)
-
Hemorrhagic shock in the dog. II. Studies on central hemodynamics and regional blood flow.
- 1985
-
Ingår i: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:6, s. 469-82
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Tidskriftsartikel (refereegranskat)abstract
- Oxygen consumption, hemodynamics, and regional blood flow (with the radioactive microspheres technique) were determined in 12 anesthetized dogs subjected to hemorrhagic shock. The animals were kept in hypotension at 40 mmHg, until 15% of the maximum shed blood had been infused to keep arterial pressure stable, whereafter all the shed blood was retransfused. Cardiac output (CO) decreased to 33% and 25% of preshock values in survivors (S) and nonsurvivors (NS), respectively, and after retransfusion it was significantly higher in S. After retransfusion, NS showed a higher arterial pCO2 than S adding a respiratory component to the metabolic acidosis that occurred during and after hemorrhage. Blood flow to the brain was not impeded during shock, but as CO decreased the fraction delivered to the brain was increased 2.6-3.3-fold. Myocardial blood flow decreased to about 28% of preshock values immediately after hemorrhage, and increased to about 54% at the end of hemorrhage. After retransfusion S had a higher myocardial flow than NS. The flow to the gut paralleled the decrease in CO during hemorrhage and immediately after retransfusion NS exhibited an overperfusion in ileum and colon compared to the preshock values. Kidney blood flow fell progressively during the course of hypotension, similarly in S and NS. After retransfusion it was normalized in S but not in NS. The preshock flow to pancreas was significantly higher in S than in NS, but during and after shock the blood flow did not differ between S and NS.
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