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  • 1
    ISSN: 0942-0940
    Keywords: Experimental subarachnoid haemorrhage ; 6-hydroxydopamine ; denervation ; ultrastructure of cerebral vessels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Transmission electron microscopy of the middle cerebral artery from cats exposed to subarachnoid injection of blood 3 and 7 days before, showed several damage of the vascular ultrastructure. The intima was thickened with swelling and vacuolization of endothelial cells, with a plump appearance and disruption of tight junctions. The cellular surface was corrugated and the subendothelial space contained proliferating and vacuolated smooth muscle cells capped by elastin and collagen fibres. The internal elastic lamina was also corrugated and disrupted. The adventitial changes were axonic cytoplasmic and mitochondrial swelling, virtual absence of synaptic vesicles, and disruption of the outer axonal membrane, suggesting denervation of cerebral vessels. With administration of 6-hydroxydopamine (6-OHDA), similar ultrastructural changes were observed in the adventitia. These observations indicate that denervation induced by subarachnoid bleeding could be involved in the pathophysiology of cerebrovascular spasm. Subarachnoid haemorrhage, but not 6-OHDA, affects also intima and tunica media, suggesting other mechanisms, in addition to denervation, can participate in the vasospasm.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Keywords Glycated haemoglobin, endothelial dysfunction, nitric oxide, superoxide anions, antioxidants, human microvessels.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. It has been recently shown that glycated human haemoglobin induces endothelial dysfunction in rat vessels by generating superoxide anions that interfere with nitric oxide mediated responses. Our study analysed the effect of glycated human haemoglobin on the endothelium-dependent relaxations of human vessels.¶Methods. Omental microvessels were obtained from patients (without diabetes, hypertension or vascular disease) during surgery and mounted in a small vessel myograph to study their vasoactive responses (vessels from 3–7 patients for each set of experiments).¶Results. Cumulative vasodilatory responses to bradykinin (10 nmol/l to 3 μmol/l) were induced in vessels precontracted with 35–50 mmol/l potassium chloride. Addition of 100 μmol/l N G-nitro-l-arginine methyl ester reduced the relaxation evoked by bradykinin, but preincubation with both N G-nitro-l-arginine methyl ester and 10 μmol/l indomethacin was needed to abolish it. Bradykinin-induced responses were inhibited by 1 μmol/l non–glycated oxyhaemoglobin whereas no effect was obtained with 10 nmol/l oxyhaemoglobin. At these low concentrations (10 nmol/l), glycated human oxyhaemoglobin caused an impairment of bradykinin-induced relaxation when the percentage of glycation was 10 % or higher. This effect was prevented by preincubating the vessels with ascorbic acid (10 μmol/l), superoxide dismutase (100 U/ml) and gliclazide (1 and 10 μmol/l), but not with indomethacin (10 μmol/l), catalase (400–600 U/ml), dimethylthiourea (1 mmol/l) or glibenclamide (10 μmol/l). In vessels preincubated with N G-nitro-l-arginine methyl ester (100 μmol/l), glycohaemoglobin did not add any additional effect.¶Conclusion/interpretation. Highly glycated human oxyhaemoglobin, at physiological plasmatic concentrations, impairs nitric oxide-mediated responses by a mechanism involving superoxide anions but not cyclooxygenase derivatives. [Diabetologia (2000) 43: 83–90].
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  • 3
    ISSN: 1432-1912
    Keywords: Key words Diabetes ; Endothelial dysfunction ; Metabolic control ; Nitric oxide ; Arginine ; Superoxide anions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This work was designed to determine in vivo the influence of the metabolic control of streptozotocin-induced diabetic rats, measured by the levels of haemoglobin glycosylation in blood (HbA1c), on developing vascular endothelial dysfunction. For this, the vasoactive responses to basal and stimulated endothelial nitric oxide (NO) were studied using the technique of the anaesthetized autoperfused rat, analyzing the responses to acetylcholine (ACh) and NG-nitro-l-arginine methyl ester (l-NAME) in non-diabetic and diabetic rats with different degrees of metabolic control (four groups with HbA1c levels of 5.5–7.4%, 7.5–9.4%, 9.5–12%, and 〉12%, respectively). When administered over a noradrenaline-induced vasopressor tone, ACh (0.25, 0.75, 2.5, 7.5 and 25 µg kg-1) induced dose-dependent vasodilatatory responses in all rat groups, reducing both mean arterial pressure and perfusion pressure of the left hindlimb. These responses were similar in non-diabetic and in diabetic rats with good metabolic control (HbA1c 5.5–7.4%), while diabetic rats with levels of HbA1c higher than 7.5% showed significantly lower vasodilatatory responses to ACh. In untreated diabetic rats, the relaxant responses evoked by the NO donor sodium nitroprusside were also impaired. On the other hand, increasing doses of l-NAME (0.1 to 10 mg kg-1) enhanced both mean arterial pressure and left hindlimb perfusion pressure in diabetic and non-diabetic rats. As with ACh, the responses to l-NAME were significantly reduced in diabetic rats with HbA1c levels higher than 7.5%. To determine the mechanism underlying the NO-mediated endothelial dysfunction, the responses to ACh in untreated diabetic rats (HbA1c 〉12%) were studied in the presence of the NO substrate l-arginine, in the presence of the oxygen-derived free radical scavenger superoxide dismutase (SOD), or in the presence of both compounds. Both l-arginine and SOD produced a partial improvement of the ACh-induced vasodilatatory responses, but the effects of these agents were not additive. In this group of animals, SOD also induced a partial recovery of the l-NAME-evoked vasoconstrictions. In non-diabetic and untreated diabetic rats, the plasma levels of NO derivatives and arginine were measured. No significant differences were obtained in the amount of nitrites plus nitrates, while plasma levels of arginine were markedly reduced in the untreated diabetic animals. The results indicate that the endothelial dysfunction associated to diabetes is closely related to the level of metabolic control of the disease. Therefore, it is possible to establish a threshold for developing endothelium impairment from percentages of HbA1c higher than 7.5%. As the responses to the NO synthase blocker l-NAME were analogously impaired, it is reasonable to suggest that diabetic endothelial dysfunction is related to the interference with mechanisms linked both to stimulated and basal production of NO. We suggest that this interference is partially due to a deficit in the substrate availability for NO and to an increased generation of superoxide anions.
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