Hemorrhagic shock resuscitation with carbon monoxide saturated blood

被引:40
作者
Cabrales, Pedro
Tsai, Amy G.
Intaglietta, Marcos
机构
[1] La Jolla Bioengn Inst, La Jolla, CA 92037 USA
[2] Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA
关键词
apoptosis; microcirculation; capillary perfusion; reoxygenation; tissue injury;
D O I
10.1016/j.resuscitation.2006.06.021
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The response to exchange transfusion with red blood cells (RBCs) saturated with carbon monoxide (CO) in amelioration of microvascular function and providing tissue protection in hemorrhagic shock resuscitation was investigated in the hamster chamber window model. Shock was induced by the withdrawal of 50% of blood volume (BV). Blood volume was restored 1 h after hemorrhage with a single volume infusion (resuscitation) of 25% BV with fresh RBCs (saturated or unsaturated with CO) suspended in human serum albumin (HSA). Hemorrhage, shock and resuscitation were monitored continuously in terms of mean arterial pressure (MAP), microvascular blood flow, capillary perfusion and systemic gas parameters. Eight hours after resuscitation, Annexin V and propidium iodide (PI) were injected into the window chamber to study tissue viability, and labeled cells were observed by using intravital epifluorescence microscopy. TUNEL staining was performed on the tissue to confirm in vivo results. Systemic and microvascular restoration were not different with or without CO up to 90 min after resuscitation. CO concentration decreased over 90 min, increasing oxygen carrying capacity and gradually reoxygenating the tissue. CO saturated blood partially mitigated cell injury at 8 h after resuscitation. The precise cellular mechanisms involved require further elucidation. CO is a novel experimental strategy to improve tissue viability and requires the appropriated preclinical studies to confirm its efficacy. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:306 / 318
页数:13
相关论文
共 32 条
[1]   INSITU END-LABELING DETECTS DNA STRAND BREAKS IN APOPTOSIS AND OTHER PHYSIOLOGICAL AND PATHOLOGICAL STATES [J].
ANSARI, B ;
COATES, PJ ;
GREENSTEIN, BD ;
HALL, PA .
JOURNAL OF PATHOLOGY, 1993, 170 (01) :1-8
[2]  
BITENSKY M, 1995, METHOD USING CO EXTE
[3]   Carbon monoxide generated by heme oxygenase 1 suppresses endothelial cell apoptosis [J].
Brouard, S ;
Otterbein, LE ;
Anrather, J ;
Tobiasch, E ;
Bach, FH ;
Choi, AMK ;
Soares, MP .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (07) :1015-1025
[4]   Early difference in tissue pH and microvascular hemodynamics in hemorrhagic shock resuscitation using polyethylene glycol-albumin-and hydroxyethyl starch-based plasma expanders [J].
Cabrales, P ;
Nacharaju, P ;
Manjula, BN ;
Tsai, AG ;
Acharya, SA ;
Intaglietta, M .
SHOCK, 2005, 24 (01) :66-73
[5]   Increase plasma viscosity sustains microcirculation after resuscitation from hemorrhagic shock and continuous bleeding [J].
Cabrales, P ;
Intaglietta, M ;
Tsai, AG .
SHOCK, 2005, 23 (06) :549-555
[6]   Hyperosmotic-hyperoncotic versus hyperosmotic-hyperviscous: Small volume resuscitation in hemorrhagic shock [J].
Cabrales, P ;
Tsai, AG ;
Intaglietta, M .
SHOCK, 2004, 22 (05) :431-437
[7]  
CABRALES P, 2006, AM J PHYSL HEART CIR
[8]   Remodeling of hepatic microvascular responsiveness after ischemia/reperfusion [J].
Clemens, MG ;
Bauer, M ;
Pannen, BHJ ;
Bauer, I ;
Zhang, JX .
SHOCK, 1997, 8 (02) :80-85
[9]  
Eguchi Y, 1997, CANCER RES, V57, P1835
[10]   TECHNICAL REPORT - A NEW CHAMBER TECHNIQUE FOR MICRO-VASCULAR STUDIES IN UNANESTHETIZED HAMSTERS [J].
ENDRICH, B ;
ASAISHI, K ;
GOTZ, A ;
MESSMER, K .
RESEARCH IN EXPERIMENTAL MEDICINE, 1980, 177 (02) :125-134