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Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,632
Online ISSN 1827-191X
Goetzenich A. 1,2, Schroth S. C. 1, Emmig U. 3, Autschbach R. 2, Pieske B. 4, Rossaint R. 1, Christiansen S. 2,5
1 Department of Anesthesiology University Hospital RWTH Aachen Aachen, Germany
2 Department of Thoracic and Cardiovascular Surgery University Hospital RWTH Aachen, Aachen, Germany
3 Department of Anethesiology and Intensive Care Ospedale Castelli Regione Piemonte - ASL 14, Verbania, Italy
4 Department of Cardiology, Georg-August-University, Göttingen, Germany
5 Department of Cardiac Surgery, University Hospital Schleswig-Holstein Campus Lübeck, Lübeck, Germany
Aim. We investigated the effect of mild hypothermia on the contractility and calcium response of atrial and ventricular myocardium.
Methods. Human atrial tissue was excised during cannulation process from patients undergoing elective open heart surgery following informed consent. Trabeculae were carefully dissected and compared to rabbit atrial and ventricular trabeculae. All probes were electrically stimulated while clamped to a force transducer and suspended in buffer media. Developed force, time to peak tension and time to 50% of relaxation were measured during mild hypothermia (37-31 °C). SR Ca++-content was studied by rapid cooling contractures, Ca++-responsiveness by a stepwise increase of extracellular calcium concentration to 10 mM.
Results. Hypothermia decreased twitch tension and SR Ca++-content in human atrial myocardium but increased contractility and SR Ca++-content in rabbit atrial and rabbit ventricular myocardium. Cooling induced a lengthening of contraction and relaxation times in all preparations. In all preparations the positive inotropic response to calcium was diminished at 34 °C and almost abolished at 31 °C.
Conclusion. In contrast to rabbit ventricular and atrial myocardium, human atrial myocardium showed a negative inotropic effect when exposed to hypothermia. This alteration could be secondary to a declined SR-Ca++ storage and decreased atrial calcium sensitivity. Calcium dependent inotropy is suppressed at temperatures below 34 °C.