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This Article Full Text Full Text (PDF) All Versions of this Article: 286/5/H1811    most recent 00837.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Torres, L. N. Articles by Pittman, R. N. Search for Related Content PubMed PubMed Citation Articles by Torres, L. N. Articles by Pittman, R. N.

Systemic responses to prolonged hemorrhagic hypotension

Departments of ¹Physiology, ²Emergency Medicine, and ³Anesthesiology, Virginia Commonwealth University Reanimation Engineering Shock Center, Virginia Commonwealth University Health System, Richmond, Virginia 23298-0695

Submitted 2 September 2003 ; accepted in final form 8 January 2004

Studies are needed to provide a rigorous examination of the relevance of monitored variables during prolonged hemorrhagic hypotension (HH). This study was designed to investigate the parameters that describe biochemical and O₂ transport patterns in animals subjected to HH. Systemic parameters that could differentiate survivors from nonsurvivors were identified. An aortic flow probe was implanted in rats (n = 21) for continuous measurement of cardiac output. Experiments were performed 6–9 days after surgery. Rats were bled to a mean arterial pressure of 40 mmHg and kept at that level using Ringer-lactate solution. Arterial and venous blood pressures, gases, acid-base status, glucose, lactate, electrolytes, hemoglobin, O₂ saturation, heart and respiratory rates, total peripheral resistance, and O₂ delivery and consumption were measured before hemorrhage, soon after 40 mmHg was reached, and 0.5, 1, 2, 3, and 4 h later. Fifty-three percent of rats survived 3 h (survivors); others were considered nonsurvivors. Nonsurvivors showed a significantly greater degree of metabolic acidosis than survivors. Arterial PO₂, respiratory rate, O₂ saturation, O₂ content, glucose, and pH were significantly higher in survivors. The rate of Ringer-lactate infusion, arterial K⁺, and PCO₂ were lower in survivors. Arterial K⁺ and respiratory rate were the only parameters significantly different between survivors and nonsurvivors at all time points during HH. Arterial levels of K⁺ showed the clearest distinction between survivors and nonsurvivors and may explain the sudden death experienced by animals during HH. The data suggest that early respiratory and metabolic compensations are essential for survival of prolonged HH.

rat; hemorrhagic shock; potassium; hemorrhage; oxygen delivery and consumption

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