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Ann Thorac Surg 2003;76:1340-1341
© 2003 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, University Hospital of Ioannina, School of Medicine, DouroutiIoannina 45110 Greece
b Department of Cardiac Surgery, St. Luke’s/Roosevelt Hospital Center at Columbia University, 45 East 89th St, New York, NY 10128, USA
e-mail: cea8{at}columbia.edu
To the Editor:
We read with great interest the article by Caparrelli and associates [1]. We congratulate them on their study of diazoxide administration to reduce neurological injury in a model of spinal cord ischemia.
Theirs was a well-designed study. It consisted of six experimental groups of rabbits and compared the effect of pharmacological versus ischemic preconditioning (IPC) on spinal cord ischemic injury and the effect of systemic hypotension (isoflurane group). The histopathological analysis is of interest because the scoring system used to assess histological damage (0, frank necrosis, to 4, normal histological appearance) allowed a quantitative histological study.
Ischemic preconditioning has been found to protect various organs from ischemic injury, and there is experimental evidence that it also protects the spinal cord after aortic occlusion. Ischemic preconditioning is a biphasic phenomenon, with an early and a late phase of protection, and these two phases have been documented in the spinal cord [2–4]. In this study, Caparrelli and co-workers evaluated the effect of early IPC on spinal cord protection in a group of rabbits that underwent 5 minutes of ischemia, followed by 30 minutes of reperfusion before the 20-minute duration of infrarenal aortic cross-clamping. However, the improvement in the IPC group was not significant compared with that in the control group. Also, in the discussion following the article, Dr Caparrelli said that of the 6 animals that underwent the IPC protocol, 3 demonstrated normal neurological function, and 3 were completely paralyzed. Is this difference in neurological outcome shown in the histological study as well? What was the mean histopathological score of these two subgroups (IPC normal versus IPC paraplegic)?
In a recent study, our group [2] demonstrated that early IPC without hypotension prevents spinal cord injury in pigs, and Griepp and co-workers [5] mentioned indirect clinical evidence of this kind of protection. We used 20 minutes of brief ischemia, 80 minutes of reperfusion, and occlusion of the descending thoracic aorta for 35 minutes. In our study, it was very important to maintain the arterial systolic pressure higher than 100 mm Hg during the 80-minute reperfusion interval. Two animals had an arterial systolic pressure of 80 to 90 mm Hg during the reperfusion period. Although they had a Tarlov score of 4 (our Tarlov scale was 0 to 4) at 24 hours postoperatively, these 2 pigs became paraplegic at 48 hours, and the histological evaluation showed loss of neurons and a moderate grade of inflammation.
Table 1 in the report by Caparrelli and colleagues shows that there was a level of hypotension during the reperfusion interval (Post Intervention column) in the IPC group, although the mean arterial pressure recovered to nearly baseline before cross-clamping was applied. We wonder what the neurological outcome in the IPC group would have been had the mean arterial pressure been maintained at baseline. In other words, was there any difference in mean arterial pressure between the IPC normal and the IPC paraplegic animals during the postintervention period?
References
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