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  • 1
    ISSN: 0942-0940
    Keywords: Endothelium-dependent relaxation ; hypoxia ; subarachnoid haemorrhage ; vasospasm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Substance P ; vasospasm ; subarachnoid haemorrhage ; isometric tension recording ; cyclic GMP ; rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The vasoactive effects of substance P (SP), as well as the content of cyclic guanine monophosphate (cGMP), were determined in the rabbit basilar artery after subarachnoid haemorrhage (SAH). Out of 47 rabbits, 24 were subjected to a SAH, induced by injecting 5ml of autologous arterial blood into the cisterna magna; 23 were used as controls. In 20 animals (10 SAH and 10 controls), isometric tension recording of isolated rings of the basilar artery — dissected 2 days after SAH — was employed to assess the dosedependent vasodilatation to SP (10−10 to 10−6M) after precontraction with serotonin (10−8 to 10−5M). In 15 animals (8 SAH and 7 controls), the basal cGMP content was measured in the basilar artery 2 days after SAH. In the other 12 animals (6 SAH and 6 controls), the increase in cGMP content was measured in the basilar artery after a 10-minute incubation with SP (10−6M). SP caused significantly less dilatation in animals subjected to SAH than in controls, especially for concentrations between 10−9 and 10−6M (p 〈 0.001). The cGMP content in the arteries 2 days after SAH was significantly lower than in control arteries (31.5 ± 7.3 against 57.3 ± 4.3 pmoles/g tissue). In the preparations incubated with SP, the increase of cGMP was 440 ± 115% in the control arteries, and only 97 ± 30% in the arteries after SAH. It is concluded that the vasodilator activity of SP is significantly impaired after SAH. Moreover, the changes in cGMP content after SAH suggest a link between impaired vasoactive response to SP and decreased production of cGMP after SAH.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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