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Phyo Kim, Robert R. Lorenz, Thoralf M. Sundt Jr. and Paul M. Vanhoutte

E ndothelium-dependent relaxation is abolished in the canine basilar artery during chronic vasospasm after subarachnoid hemorrhage (SAH). 17, 18 The present study was undertaken to determine the cause of the observed loss of endothelium-dependent relaxation. Bioassay experiments 7, 26 were performed to examine whether the loss is due to reduced release of endothelium-derived relaxing factor (EDRF) or to alterations in sensitivity of vascular smooth muscle to the factor. Materials and Methods Study Groups Fourteen mongrel dogs of either sex, each

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Kazuhiro Hongo, Neal F. Kassell, Tadayoshi Nakagomi, Tomio Sasaki, Tetsuya Tsukahara, Hisayuki Ogawa, Dennis G. Vollmer and R. Michael Lehman

T he obligatory role of endothelium in the arterial relaxation response to acetylcholine (ACh) was first demonstrated by Furchgott and Zawadzki 12 in isolated rabbit aorta. The substance released from the endothelium to elicit this relaxation was later termed “endothelium-derived relaxing factor” (EDRF). 2 Since then, a large number of vasodilators have been shown to induce endothelium-dependent vascular relaxation in a wide variety of mammalian vessels. 2, 6, 9, 10 Recently, it has been suggested that the EDRF is not only released by vasoactive agents, but

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David H. Edwards, James V. Byrne and Tudor M. Griffith

E ndothelial cells play a central role in the regulation of vascular tone by releasing the potent endogenous nitrovasodilator endothelium-derived relaxing factor (EDRF) both basally 14, 15 and when stimulated by agents such as acetylcholine, purine nucleotides, and substance P. 12 Although there is controversy whether EDRF is nitric oxide (NO) 18, 34 or a nitrosothiol, 31 it is nevertheless established that EDRF is avidly bound by hemoglobin. 20 This provides a mechanism whereby hemoglobin could contribute to the cerebral vasospasm that complicates

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Kenji Kanamaru, Shiro Waga, Hiroshi Tochio and Kazuhiko Nagatani

. Rabbits fed a high-cholesterol diet for 50 days showed a decreased cerebral blood flow, which returned to normal with administration of lipid-lowering drugs. 12 Significant cerebrovascular atherosclerosis would be expected only after many months of consuming a high-cholesterol diet. 8 It has recently been reported that vasoactive substances can cause relaxation of blood vessels by releasing endothelium-derived relaxing factor (EDRF) from the endothelial cells. 5 These observations have led to the proposal that dysfunction or denudation of the endothelium in

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Kenji Kanamaru, Bryce K. A. Weir, J. Max Findlay, Christel A. Krueger and David A. Cook

I t has been demonstrated that experimental subarachnoid hemorrhage (SAH) and the administration of hemoglobin can impair endothelium-dependent relaxation. 13, 20, 22, 23, 25, 29, 31 However, it remains controversial if the inhibition of endothelium-derived relaxing factor (EDRF) by hemoglobin is a critical cause of cerebral vasospasm or a result of prolonged vasospasm. 13, 20, 22–25, 29, 31, 38 Despite the fact that most arterial ring segment studies have shown the inhibitory effects on EDRF by hemoglobin 13, 22, 23, 25, 29 and SAH, 20, 31 some

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Tadayoshi Nakagomi, Neal F. Kassell, Tomio Sasaki, R. Michael Lehman, James C. Torner, Kazuhiro Hongo and Joung H. Lee

✓ The effect of endothelium removal on the contractile responses to KCl, hemoglobin, serotonin (5-HT), norepinephrine (NE), prostaglandin (PG)F2α, PGD2, and PGE2 was investigated in canine and rabbit basilar arteries by an isometric tension-recording method. In canine basilar arteries, endothelium removal elevated the dose-response curves to 5-HT, PGF2α, and PGD2, and PGE2, but not to KCl, hemoglobin, or NE. In rabbit basilar arteries, on the other hand, removal of the endothelium elevated the dose-response curves to 5-HT, NE, PGF2α, and PGD2, but not to KCl or hemoglobin. Neither contractile nor inhibitory response was elicited by PGE2 in rabbit basilar arteries. Contraction induced by 5-HT and NE following endothelium removal had a much more pronounced effect in rabbit basilar arteries than in canine basilar arteries.

These results suggest that, following endothelium removal, abolition of the spontaneous release of endothelium-derived relaxing factor is the most probable mechanism of the enhanced vasocontraction. Since endothelial damage results from subarachnoid hemorrhage, the aforementioned mechanism of vasocontractile enhancement may play a role in the pathogenesis of cerebral vasospasm.

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Yasukazu Kajita, Yoshio Suzuki, Hirofumi Oyama, Toshihiko Tanazawa, Masakazu Takayasu, Masato Shibuya and Kenichiro Sugita

N itric oxide or a closely related factor formed from L-arginine is strongly implicated as a major endothelium-derived relaxing factor (EDRF). 7, 13, 28 Endogenous nitric oxide released from the endothelium induces relaxation after stimulation by such agents as acetylcholine, substance P, vasopressin, and others, 7, 37, 38 but synthesis and release of nitric oxide in vascular tissue under basal conditions appear to be essential to the maintenance of basal tone in cerebral blood vessels. 5, 15, 27, 31, 38 It is assumed that basal release of nitric oxide must

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Phyo Kim, Thoralf M. Sundt Jr. and Paul M. Vanhoutte

V arious clinical and experimental studies of cerebral arteries in chronic vasospasm have demonstrated structural damage to each layer of the arterial wall, including the endothelium. 11, 18, 24, 32 The morphological alterations of the endothelium include vacuolization and detachment, and are observed at the early phase after subarachnoid hemorrhage (SAH). 3, 24, 32 Various vasodilator agents require the presence of the endothelium for their action. 4 In response to those agonists, the endothelium releases a factor (endothelium-derived relaxing factor, EDRF

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Shuji Kazuki, Tomio Ohta, Ryusuke Ogawa, Masao Tsuji, Yoji Tamura, Yasushi Yoshizaki and Takashi Takase

vascular wall. 25, 39 However, the mechanism of delayed cerebral vasospasm has not yet been clarified. It has been recognized recently that the endothelium plays an important role in both vasocontraction and vasodilation. 49 In vasodilation, endothelium-derived relaxing factor (EDRF) was identified by Furchgott and Zawadzki. 11 In vasocontraction, Yanagisawa, et al., 54 isolated a potent vasoconstrictive peptide, endothelin (ET), from cultured porcine aortic endothelial cells. Because ET is a very potent and long-lasting vasoconstrictor, it is believed to contribute

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Tadayoshi Nakagomi, Neal F. Kassell, Tomio Sasaki, Shigeru Fujiwara, R. Michael Lehman, Hiroo Johshita, Gregory B. Nazar and James C. Torner

-established that the relaxation induced by ACh 9, 11, 15, 16, 18 and other vasoactive agents, such as adenine nucleotides, 9, 11 substance P, 16 bradykinin, 5, 16 and histamine, 38 is mediated indirectly by the release of a relaxant substance from the endothelial cells, which has been termed the “endothelium-derived relaxing factor” (EDRF). The present experiments reveal that the endothelium-dependent relaxation of the basilar arteries induced by ATP is inhibited following SAH while that induced by ACh is not. Three major causes for this impairment of endothelium