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Eur J Cardiothorac Surg 2004;26:564-570
© 2004 Elsevier Science NL
a Department of Thoracic and Cardiovascular Surgery, West German Heart Center Essen, University Hospital of Essen 45147 Essen, Germany
b Department of Experimental Surgery, University Hospital of Essen, 45147 Essen, Germany
Received 19 December 2003; received in revised form 25 May 2004; accepted 28 May 2004.
* Corresponding author. Tel.: +49-201-723-4901; fax: +49-201-723-5471
e-mail: markus.kamler{at}uni-essen.de
Objective: Clinical complications arising from extracorporeal circulation (ECC) have been linked to disturbances in the microcirculation. Hyperoxia, a mainstay of supportive treatment, is clinically used for a variety of pathological states. In previous in vivo animal experiments we found increased leukocyte/endothelial (L/E) cell interaction following ECC due to oxygen derived free radicals. This study was carried out to investigate the link between arterial pO2 during ECC and the potential damage to the microcirculation, supposedly caused by oxygen derived radicals. Methods: Intravital fluorescence microscopy was used on the dorsal skinfold chamber preparation in syrian golden hamsters. ECC was introduced via a micro-rollerpump (0.7 ml/min) and a 60 cm silicon tube (1 mm inner diameter) shunted between the carotid artery and the jugular vein after application of 300 IE Heparin/kg/bw. Experiments were performed in chronically instrumented, awake animals (age: 1014 weeks, weight: 6575 g). Control inspired room air, experimental group 1 inspired 100% oxygen, group 2 received 100% oxygen and 2000 IE of Heparin i.v. (n=7/group), that releases endothelial bound superoxide dismutase, a natural scavenger of oxygen derived free radicals in the hamster. Results: Normobaric inhalation of 100% oxygen increased arterial pO2 from 64±8.1 mmHg to 512±124 mmHg (P<0.05 vs. baseline). ECC under 100% oxygen reduced functional capillary density (FCD) to 70% of baseline values 8 h after ECC (P<0.05). Adherent leukocytes in postcapillary venules and arterioles increased significantly (P<0.05). 2000 IE Heparin prevented the reduction in FCD and decreased the number of adherent leukocytes. Conclusions: Reduction in FCD, increased leukocyte adherence to the microvascular endothelium of postcapillary venules and arterioles under hyperoxia compared to ECC under room air conditions, demonstrates harmful effects of oxygen during ECC in vivo. A high dose of Heparin enhances functional capillary density, thus attenuating the microvascular dysfunction/damage in the period after ECC.
Key Words: Microcirculation Extracorporeal circulation Leukocyte/Endothelial cell interaction Hamster Hyperoxia
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