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This Article Full Text Full Text (PDF) All Versions of this Article: 586/9/2345    most recent jphysiol.2007.150086v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Simpson, J. A. Articles by Iscoe, S. PubMed PubMed Citation Articles by Simpson, J. A. Articles by Iscoe, S. Related Collections Respiratory

¹ Department of Physiology, Queen's University, Kingston, Ontario, Canada K7L 3N6

Repeated episodes of hypoxia and sympathetic activation during obstructive sleep apnoea are implicated in the initiation and progression of cardiovascular diseases, but the acute effects are unknown. We hypothesized that repeated inspiratory occlusions cause acute myocardial dysfunction and injury. In 22 spontaneously breathing pentobarbital-anaesthetized rats, inspiration was occluded for 30 s every 2 min for 3 h. After 1.5 h, mean arterial pressure started to fall; heart rate between occlusions was stable throughout, consistent with only transient increases in sympathetic activity during each occlusion. Three hours of occlusions resulted in ventricular diastolic dysfunction (reduced peak rate of change of ventricular pressure and slower relaxation). Post-occlusions, the left ventricular contractile response to dobutamine was blunted. After 1 h of recovery, left ventricular pressure generation had returned to values no different from those in sham animals in 5 of 9 of the animals. Cardiac myofibrils from rats subjected to occlusions had depressed calcium-activated myosin ATPase activity, indicating myofilament contractile dysfunction that was not due to breakdown of contractile proteins. Haematoxylin and eosin-stained cross-sections revealed multifocal areas of necrosis within the septum and both ventricles. Repeated inspiratory occlusions, analogous to moderately severe obstructive sleep apnoea, acutely cause global cardiac dysfunction with multifocal myocardial infarcts.

(Received 17 December 2007; accepted after revision 3 March 2008; first published online 6 March 2008)
Corresponding author S. Iscoe: Department of Physiology, Queen's University, Kingston, Ontario, Canada K7L 3N6. Email: iscoes{at}queensu.ca