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The effect of intraluminal hyperglycaemia was investigated in the iliac artery of 11 anaesthetised pigs. Following isolation of a test segment, hyperglycaemic blood (40 mmol x [L.sup.-1]) caused a significant dilatation of the artery of 167 ± 208 µm (mean ± SD; n = 6, P = 0.031). Dilatations were reduced by N(G)-nitro-L-arginine methyl esther (250 µg x m[L.sup.-1]) from 145 ± 199 to 38 ± 5 µm), but this was not statistically significant (n = 6, P = 0.18). Intra-arterial infusions of D-glucose (20-40 mmol x [L.sup.-1]x [min.sup.-1]), during graded constrictions, caused statistically significant increases in blood flow (n = 11, P = 0.0013). Vasodilatation was confirmed by measurements of the ratio of immediate pressure steps to flow steps (3P/3F) during the graded obstruction experiments, showing a decrease in instantaneous vascular resistance from a control of 0.62 ± 0.30 to 0.33 ± 0.34 mm Hg x m[L.sup.-1] x [min.sup.-1] (n = 7, P = 0.016). Autoregulation was assessed from the slopes of the plots of steady-state flow versus pressure. There were significant increases in the slope from 2.32 ± 1.03 to 5.88 ± 5.60 mL x [min.sup.-1] x [(mm Hg).sup.-1] (n = 7, P = 0.0078), indicating significant impairment of autoregulation. In conclusion, luminal hyperglycaemia relaxes both arterial and resistance vessel smooth muscle. Key words: vascular smooth muscle, conduit, resistance, hyperglycaemia, autoregulation. L'effet d'une hyperglycemie intra-luminaire a ete examine dans l'artere iliaque de 11 porcs anesthesies. Le sang hyper-glycemique (40 mmol x [L.sup.-1]) provoquait, sur un segment test isole, une dilatation significative de l'artere de 167 ± 208 µm (moyenne ± ET; n = 6, P = 0.031). La dilatation etait reduite par le N(G)-nitro-L- arginine-methyl ester (250 µg x m[L.sup.-1]), de 145 ± 199 a 38 ± 5 µm, mais cet effet n'etait pas statistiquement significatif (n = 6, P = 0.18). Des infusions intra- arterielles de D-glucose (20-40 mmol x [L.sup.-1]x [min.sup.-1]), lors de constrictions graduelles, provoquaient des augmentations significatives du debit sanguin (n = 11, P = 0.0013). La vasodilatation etait confirmee par des mesures du rapport de la pression immediate sur le debit (3P/3F) lors des experiences d'occlusion graduelle, montrant une diminution de la resistance vasculaire instantanee d'un controle de 0.62 [+ or - ] 0.30 a une valeur de 0.33 ± 0.34 mm Hg x m[L.sup.-1]x [min.sup.-1] (n = 7, P = 0.016). L'autoregulation a ete evaluee a partir de la pente des droites du debit a l'equilibre en fonction de la pression. Une augmentation significative de la pente de 2.32 ± 1.03 a 5.88 ± 5.60 mL x [min.sup.-1] x [(mm Hg).sup.-1] (n = 7, P = 0.0078) etait observee, indiquant que l'autoregulation etait significativement perturbee. En conclusion, l'hyperglycemie luminaire relache le muscle lisse tant des arteres que des vaisseaux de resistance. [Traduit par la Redaction] Mots-cles: muscle lisse vasculaire, gros tronc arteriel, resistance, hyperglycemie, autoregulation., Introduction Poor control of blood glucose concentrations in patients with diabetes mellitus is associated with more rapid and severe atherothrombotic disease of arteries than occurs in nondiabetic people and diabetic [...]

Introduction: Elevated luminal homocysteine has been linked with cardiovascular disease; however, whether there is a direct effect of homocysteine on blood vessel endothelium is not clear. In this study, the acute effect of luminal homocysteine on iliac artery endothelial function was assessed in the anaesthetised pig. Methods: Hyperhomocysteinaemic blood was injected into an occluded segment of the iliac in the anaesthetised pig for 20 min, and the effect on atrial diameter during the occlusion and during the reactive hyperaemia assessed. Results: No significant changes in arterial diameter or pressure were observed during the incubation period at homocysteine concentrations of 10, 20, 40 and 100 µM. There was also no difference in the magnitude of the iliac diameter increase in the response to reactive hyperaemia when the incubation period was completed. Conclusion: There is no evidence of endothelial dysfunction in response to an acute 20-min elevation in homocysteine in an intact conduit artery. [ABSTRACT FROM AUTHOR]

Objective: We tested the hypothesis that the rate of adaptation of coronary metabolic vasodilatation and autoregulation is modulated by the cardiac nerves. Methods: Anaesthetised dogs (seven innervated (control) and seven with denervated hearts) were subjected to controlled pressure perfusion of the left main coronary artery. Heart rate was controlled by pacing. Results: The steady state autoregulation curves and metabolic regulation curves were similar in the two groups. A sudden increase or decrease in heart rate was associated with a faster response (22% shorter half-times) in the innervated than the denervated dogs (P<0.001). A sudden increase or decrease in coronary arterial perfusion pressure was associated with a slower response (24% longer half-times) in the innervated than the denervated hearts (P<0.005). Conclusions: We conclude that the speed of response to metabolic and perfusion pressure changes is partly mediated by cardio-cardiac reflexes. Reflex coronary vasodilatation appears to reinforce the metabolic vasodilatation of a heart rate increase and oppose the vasoconstriction in response to increased perfusion pressure. [ABSTRACT FROM PUBLISHER]