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Articles in PresS, published online ahead of print September 19, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00629.2002
Submitted on July 19, 2002
Accepted on August 12, 2002
1 Department of Pharmacology, University of Vermont , College of Medicine, Burlington, VT, USA; Department of Surgery, Division of Neurological Surgery, University of Vermont, College of Medicine, Burlington, VT, USA
2 Department of Pharmacology, University of Vermont , College of Medicine, Burlington, VT, USA
3 Department of Surgery, Division of Neurological Surgery, University of Vermont, College of Medicine, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: gwellman{at}zoo.uvm.edu.
Cerebral artery vasospasm is a major cause of death and disability in patients experiencing subarachnoid hemorrhage (SAH). Currently, little is known regarding the impact of SAH on small diameter (100-200 µm) cerebral arteries, which play an important role in the autoregulation of cerebral blood flow. Using a rabbit SAH model and in vitro video microscopy, cerebral artery diameter was measured in response to elevations in intravascular pressure. Cerebral arteries from SAH animals constricted more (~ two-fold) to pressure within the physiological range of 60 to 100 mmHg compared to control or sham-operated animals. Pressure-induced constriction (myogenic tone) was also enhanced in arteries from control animals organ cultured in the presence of oxyhemoglobin, an effect independent of the vascular endothelium or nitric oxide synthesis. Finally, arteries from both control and SAH animals dilated as intravascular pressure was elevated above 140 mmHg. This study provides evidence for a role of oxyhemoglobin in impaired autoregulation (i.e. enhanced myogenic tone) in small diameter cerebral arteries during SAH. Furthermore, therapeutic strategies that improve clinical outcome in SAH patients (e.g. supraphysiological intravascular pressure) are effective in dilating small diameter cerebral arteries isolated from SAH animals.
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