Biomechanical and phenotypic changes in the vasospastic canine basilar artery after subarachnoid hemorrhage

• Published in: Journal of applied physiology (1985) Vol. 99; no. 5; pp. 2045 - 2052
• Main Authors: Yamaguchi-Okada, Mitsuo, Nishizawa, Shigeru, Koide, Masayo, Nonaka, Yuichiro
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Physiological Soc 01-11-2005; American Physiological Society
• Subjects: Animals; Basilar Artery - metabolism; Basilar Artery - pathology; Basilar Artery - physiopathology; Biological and medical sciences; Biomechanical Phenomena; Brain research; Circulatory system; Collagen - metabolism; Dogs; Female; Fundamental and applied biological sciences. Psychology; Genotype & phenotype; Hemorrhage; Isometric Contraction; Male; Muscle, Smooth, Vascular - pathology; Muscle, Smooth, Vascular - physiopathology; Myosin Heavy Chains - metabolism; Phenotype; Subarachnoid Hemorrhage - pathology; Subarachnoid Hemorrhage - physiopathology; Vasospasm, Intracranial - pathology; Vasospasm, Intracranial - physiopathology; Fissipedia; Carnivora; vascular smooth muscle; Subarachnoid hemorrhage; Central nervous system; Cardiovascular disease; Smooth muscle; Basilar artery; cerebral vasospasm; Encephalon; Biomechanics; Vertebrata; Mammalia; Circulatory system; Dog
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.01138.2004

Department of Neurosurgery, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan
Submitted 14 October 2004
; accepted in final form 22 July 2005
Because it has been argued that active myogenic tone prolongs cerebral vasospasm for >2 wk after subarachnoid hemorrhage (SAH), we attempted to identify the mechanism that plays the main role in sustaining the prolonged cerebral vasospasm. We especially focused on the roles of biomechanical and phenotypic changes in the cerebral arteries in the mechanisms of prolonged vasospasm after SAH. We used the basilar arteries from a "two-hemorrhage" canine model to make serial measurements of maximal contraction capacity and arterial stiffness (papaverine-insensitive tone) until day 28 . We also examined hematoxylin-eosin-stained vasospastic canine basilar arteries for histological changes and immunohistochemically examined them for expression of myosin heavy chain isoforms (SMemb, SM1, and SM2), which are markers of smooth muscle phenotypic changes. Changes in collagen concentration in canine basilar arteries were also measured. Angiographic cerebral vasospasm persisted until day 14 and then gradually diminished; artery diameter returned to the control diameters on day 28 . Maximal contraction capacity decreased until day 21 and showed some recovery by day 28 . Arterial stiffness, on the other hand, progressed until day 28 . Histological examination revealed medial thickening and increased connective tissue until day 21 and a return to control findings by day 28 . The increased connective tissue was not accompanied by changes in collagen concentration, suggesting a role of some other protein in the increase in connective tissue. Immunohistochemical studies with anti-SMemb, anti-SM1, and anti-SM2 antibodies showed enhanced expression of SMemb from day 7 to day 21 and disappearance of SM1 and SM2 on days 14 and 21 . The changes in myosin heavy chain isoform expression returned to normal on day 28 . The above results indicate that biomechanical and phenotypic changes may play a pivotal role in sustaining cerebral vasospasm for >2 wk after SAH, with minimal changes in active myogenic arterial tone.
biomechanics; cerebral vasospasm; vascular smooth muscle
Address for reprint requests and other correspondence: S. Nishizawa, Dept. of Neurosurgery, Hamamatsu Univ. School of Medicine, 1-20-1 Handayama, Hamamatsu, Shizuoka, 431-3192 Japan (e-mail: nisizawa{at}hama-med.ac.jp )