Cerebral vasospasm: contractile activity of hemoglobin in isolated canine basilar arteries

Tanishima, T

doi:10.3171/jns.1980.53.6.0787

Cited by 136 publications

(28 citation statements)

References 31 publications

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“…Perhaps the effects owing to raised ICP in this experimental model might be minimized by removing an equal amount of cerebrospinal fluid prior to blood injection. No particular problems were encountered when performing angi- 13,14,16,19,20,24,26]. Moreover, the reduction in the diameter of "spastic" basilar artery was statistically significant.…”

Section: Discussionmentioning

confidence: 81%

Cerebral vasospasm in a double-injection model in rabbit

Spallone

Pastore

1989

Surgical Neurology

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Spallone A, Pastore FS. Cerebral vasospasm in a double-injection model in rabbit. Surg Neurol 1989;32:408-17.The present study was designed to assess the occurrence of cerebral vasospasm following an experimental subarachnoid hemorrhage model in rabbits. Sixty-nine New Zealand albino rabbits were used in this study. One milliliter of fresh arterial blood was injected through the surgically exposed atlanto-occipital membrane over a period of 20 seconds. The procedure was then repeated 24 hours later. Fifty animals underwent digital subtraction angiography at one of the following prefixed intervals: 1, 3, or 8 days after the second injection hemorrhage. Nineteen animals underwent one angiographic examination prior to the instillation of the intracisternal blood. This procedure was followed by a repeated angiography 3 days after the second experimental subarachnoid hemorrhage. For the purpose of evaluation, the films were magnified 10-fold and the diameter of the basilar artery as well as that of the extracranial vertebral artery at three different levels were measured. We assessed the diameter of the basilar artery as well as the mean ratio extracranial vertebral artery/basilar artery diameters. This ratio was considered to minimize anatomical and technical variabilities. The results in the first 50 animals showed a trend suggesting that spasmogenic activity reaches a peak at about the third day after subarachnoid hemorrhage. These results were confirmed in the latter 19 animals. However, mortality in this group was high: 50%. This double-injection model of subarachnoid hemorrhage in rabbits consistently reproduced cerebral vascular spasm 3 days after repeated subarachnoid hemorrhage. However, its usefulness as an experimental model for subarachnoid hemorrhage is limited practically by the high animal mortality in the protocols where repeated angiographic studies are necessary.

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Section: Discussionmentioning

confidence: 81%

Cerebral vasospasm in a double-injection model in rabbit

Spallone

Pastore

1989

Surgical Neurology

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“…Although the action of EDRF on various vascular smooth muscle cells was inhibited by Hb through inhibition of guanylate cyclase, Hb itself or haemolysate produces contraction of basilar arteries in many species (Tanishima, 1980;Toda et al, 1980;Wellum et al, 1982;Fujiwara & Kuriyama, 1984;Fujiwara et al, 1986;Connor & Feniuk, 1987). Thus, the vasoconstriction that occurs after subarachnoid haemorrhage following rupture of cerebral aneurysms may be related to the actions of Hb (Saito et al, 1977;Fisher et al, 1980;Wellum et al, 1982;Kassel et al, 1985;Boullin, 1985).…”

Section: Introductionmentioning

confidence: 99%

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

Nishiye¹,

Nakao²,

Itoh³

et al. 1989

British J Pharmacology

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1 Factors inducing dilatation of guinea-pig basilar artery were investigated in intact and endothelium-denuded tissues by measurement of isometric tension and by electrophysiological methods. 2 The amplitudes of contractions induced by 9,1 1,epithio-1 1,12-methanothromboxane A2 (STA2) and by high K+ were enhanced by haemoglobin (oxyhaemoglobin, Hb) in a concentrationdependent fashion (above 1 pM). For the high K'-induced contraction, the initial tonic component was enhanced to a greater extent than the secondary phasic component. Mechanical responses evoked by STA2 and by high K' were greater in endothelium-denuded tissues, but Hb (below 10pM) had no effect on them.3 Hb (10pM) had no effect on the contractile proteins as estimated from the actions of Hb on Ca2+-induced contractions in skinned muscle tissues. Further, Hb had no effect on the release of Ca2+ from intracellular stores but it accelerated the Ca2 + accumulation into the sarcoplasmic reticulum as judged from the caffeine-or STA2-induced contraction generated in intact tissues. 4 Acetylcholine (ACh) relaxed tissues that were precontracted by STA2 but Hb prevented this relaxation, in a concentration-dependent fashion. The ACh-induced relaxation was sustained for over 10min in the absence of Hb, but following application of Hb, ACh caused only a transient relaxation. 5 STA2 (up to 100nM) did not modify the resting membrane potential of smooth muscle cells of the basilar artery. ACh (1O pM) caused transient hyperpolarization which was only slightly inhibited by Hb (10pM) whether or not STA2 was present. The hyperpolarization induced by ACh required the presence of endothelial cells. 6 A23187 (0.01-1 pM) relaxed tissues which were precontracted by STA2, in a concentrationdependent fashion but had no effect on the membrane potential. 7 These results suggest that in guinea-pig basilar artery, ACh induces relaxation of tissues that were precontracted by STA2 by causing release of both endothelium-derived relaxing (EDRF) and endothelial dependent hyperpolarizing factor (EDHF) (sustained and initial transient relaxation, respectively), but via different mechanisms. Hb inhibits the former and to a lesser extent, the latter.Since A23187 produced relaxation of pre-contracted tissue but caused no detectable change in the membrane potential, this agent may release EDRF but not EDHF.

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“…There is currently a great deal of interest in the role of haemoglobin in the modulation of vascular tone, stemming from the observation that it might be responsible for the prolonged constriction of cerebral blood vessels that occurs after cerebral haemorrhage (Echlin, 1971;Osaka, 1977;Bouillin, 1980). Certain blood vessels (cerebral, coronary, mesenteric and femoral) appear to be particularly sensitive to haemoglobin (Tanishima, 1980); it has recently been demonstrated that isolated bovine and canine penile arteries are powerfully constricted by haemoglobin, which also blocks NANC nerve-induced vasodilatation and the dilatation produced by the inhibitory factor extracted from the bovine retractor penis muscle (Bowman & Gillespie, 1983). It seems possible that these effects of haemoglobin are mediated by its ability to inhibit guanylate cyclase, and that cyclic GMP in these vessels may play a role in the determination of vascular tone.…”

Section: Observations)mentioning

confidence: 99%

Cyclic GMP mediates neurogenic relaxation in the bovine retractor penis muscle

Bowman

Drummond

1984

British J Pharmacology

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1 Field stimulation of the non-adrenergic, non-cholinergic inhibitory nerves to the bovine isolated retractor penis muscle evoked a relaxation that was preceded by a rise in the tissue content of cyclic GMP. There was no change in the content of cyclic AMP. 2 The selective cyclic GMP phosphodiesterase inhibitor, 2-o-propoxyphenyl-8-azapurin-6-one (M&B 22948), elevated the tissue's cyclic GMP content, and potentiated both the relaxation and the rise in cyclic GMP produced by inhibitory nerve stimulation. 3 Sodium nitroprusside and an inhibitory factor extracted from the bovine retractor penis muscle mimicked the effects of inhibitory nerve stimulation in that they each produced relaxation associated with a selective rise in cyclic GMP concentration. 4 Haemoglobin (in the form of erythrocyte haemolysate) and N-methylhydroxylamine, which are known to block guanylate cyclase, blocked the relaxation and the rise in cyclic GMP content produced by inhibitory nerve stimulation, inhibitory factor and sodium nitroprusside. Haemoglobin itself caused a rise in muscle tone and at the same time reduced the cyclic GMP content of the tissue. 5 8-Bromocyclic GMP, a permeant derivative of cyclic GMP, produced a relaxation of the muscle that, as expected, was not blocked by haemoglobin. 6 Vasoactive intestinal polypeptide, prostaglandin E1 and forskolin each produced relaxation associated with a selective rise in cyclic AMP content. Their effects were not blocked by haemoglobin or N-methylhydroxylamine. 7 It is concluded that inhibitory nerve stimulation in the bovine retractor penis muscle produces a relaxation that is mediated by cyclic GMP, although some substances relax the muscle without affecting cyclic GMP levels. The results are also compatible with the view that the extracts of muscle contain the inhibitory neurotransmitter.

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Cerebral vasospasm: contractile activity of hemoglobin in isolated canine basilar arteries

Cited by 136 publications

References 31 publications

Cerebral vasospasm in a double-injection model in rabbit

Cerebral vasospasm in a double-injection model in rabbit

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

Cyclic GMP mediates neurogenic relaxation in the bovine retractor penis muscle

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