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Am J Physiol Heart Circ Physiol (January 15, 2004). doi:10.1152/ajpheart.00837.2003
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Submitted on September 2, 2003
Accepted on January 8, 2004

Systemic Responses to Prolonged Hemorrhagic Hypotension

Luciana N. Torres1*, Ivo P. Torres Filho2, R. Wayne Barbee3, M. Hakam Tiba4, Kevin R. Ward3, and Roland N. Pittman1

1 Department of Physiology, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA; Department of Emergency Medicine, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA
2 Department of Anesthesiology, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA; Department of Physiology, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA; Department of Emergency Medicine, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA
3 Department of Emergency Medicine, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA; Department of Physiology, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA
4 Department of Emergency Medicine, Virginia Commonwealth University Reanimation Engineering Shock Center (VCURES), Richmond, VA, USA

* To whom correspondence should be addressed. E-mail: lntorres{at}vcu.edu.

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 (S) from nonsurvivors (NS) 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's lactate. Arterial and venous blood pressures, gases, acid-base status, glucose, lactate, electrolytes, hemoglobin, O2 saturation (O2Sat), heart and respiratory (RR) rates, total peripheral resistance, O2 delivery and consumption were measured before hemorrhage, soon after reaching 40 mm Hg, and one-half, 1, 2, 3 and 4 hours later. Fifty-three percent of rats survived >=3 h (S); others were considered NS. Nonsurvivors showed a significantly greater degree of metabolic acidosis than survivors. Arterial PO2, RR, O2Sat, O2 content, glucose and pH were significantly higher in S. Rate of RL infusion, arterial K+ and PCO2 were lower in S. Arterial K+ and RR were the only parameters significantly different between S and NS at all time points during HH. Arterial levels of K+ showed the clearest distinction between S and NS 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.




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