IN-VIVO ANGIOPLASTY PREVENTS THE DEVELOPMENT OF VASOSPASM IN CANINE CAROTID ARTERIES - PHARMACOLOGICAL AND MORPHOLOGICAL ANALYSES

Background and Purpose To study the effects of in vivo transluminal ba lloon angioplasty (TBA) on the structure and function of the arterial wall, a canine model of hemorrhagic cerebral vasospasm of the high cer vical internal carotid artery (ICA) was used. This model was also used to determine whether TBA performed before clot placement could preven t the development of vasospasm. Methods Twelve dogs underwent surgical exposure of both distal cervical ICAs, followed by baseline angiograp hy. One randomly selected ICA in each dog was then subjected to in viv o TBA and repeated angiography. Both distal ICAs were then surrounded with blood clots held by silicone elastomer sheaths. Seven days later angiography was repeated, and all animals were killed. The ICAs in fou r animals were perfusion-fixed in situ for morphological analysis by e lectron microscopy, and the arteries in the remaining eight animals we re removed and immediately immersed in oxygenated Krebs' solution. Con tractile responses of isolated arterial rings from each ICA were recor ded after treatment with KCl, noradrenaline, serotonin, and prostaglan din F-2 alpha, while relaxations in response to the calcium ionophore A23187 and papaverine were recorded after tonic contraction to noradre naline had been established. The morphology and pharmacological respon ses of ICAs that had been exposed to blood with or without prior TEA w ere compared with data obtained from control arterial segments of inta ct, more proximal regions of the ICAs from each animal. Results TBA re sulted in immediate angiographic enlargement of the ICA lumen that was still evident 7 days later despite the placement of clotted blood aro und the artery. Scanning and transmission electron microscopy demonstr ated flattening of the intima and internal elastic lamina in these dil ated arteries, associated with patchy losses of endothelial cells. In contrast, ICAs that had been exposed to clotted blood but had not unde rgone prior TBA developed consistent angiographic and morphological va sospasm. In comparison with control vessels and nondilated vasospastic vessels, vessels dilated with TBA and then exposed to clotted blood s howed significantly diminished responses to all compounds tested, with the exception of prostaglandin F-2 alpha. Conclusions These results i ndicate that in vivo TBA results in a degree of functional impairment of vascular smooth muscle that persists for at least 7 days. This resu lt is consistent with previous observations of the acute effects of TB A in isolated arteries. Furthermore, these results support the hypothe sis that normal smooth muscle function is required for the development of vasospasm. Finally, these results indicate that TBA performed befo re the onset of vasospasm prevents its development.