Effects of ischaemia and reperfusion on vasoactive neuropeptide levels in the canine infrarenal aortic revascularization model (original) (raw)
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Annals of vascular surgery, 1994
Neuropeptide Y (NPY) is a potent vasoconstrictive polypeptide colocalized with norepinephrine in sympathetic neurons. The effects of ischemia and reperfusion on plasma NPY levels were studied and compared in the mongrel dog after infrarenal aortic cross-clamping. We found a two- to threefold increase in NPY levels during ischemia (initial 10.0 +/- 1.8 pmol/L vs. maximum 24.7 +/- 2.31 pmole/L, p < 0.001). The increase in NPY remained following reperfusion (initial 10.0 +/- 0.8 pmole/L vs. maximum 23.9 +/- 2.31 pmole/L, p < 0.001). These data reveal that NPY is released during ischemia and reperfusion and may be involved in mediating remote vascular events associated with infrarenal aortic cross-clamping.
European journal of vascular surgery, 1994
Endothelin-1 (ET-1) is a potent vasoconstrictive polypeptide produced from vascular endothelial cells. The effects of ischaemia, reperfusion, and exsanguination on plasma ET-1 levels were studied and compared in the mongrel dog after infrarenal aortic cross clamping. Ischaemia produced a trend toward increased ET-1 serum levels (p < 0.07 with Bonferroni correction) that did not reach significance. Plasma ET-1 levels were significantly increased during reperfusion and even further elevations were found following exsanguination. We found a 2-3 fold increase in ET-1 levels following reperfusion (Initial 3.19 +/- 0.27 pg/ml vs. Reperfusion maximum 6.32 +/- 0.72 pg/ml, Bonferroni p < 0.01). Haemorrhagic shock was associated with a 3-4 fold increase in ET-1 levels (Initial 3.19 +/- 0.27 pg/ml vs. Exsanguination maximum 8.37 +/- 0.97 pg/ml Bonferroni p < 0.001). These data reveal that ET-1 is released during reperfusion and exsanguination and may mediate remote vascular events ass...
Attenuation of receptor-dependent and -independent vasoconstriction in the human radial artery☆
European Journal of Cardio-Thoracic Surgery, 2008
Background: Vasodilator strategies used to treat bypass grafts in the operating theatre, such as nitrates, phosphodiesterase inhibitors and calcium channel antagonists have a broad but short-lived effect against a variety of vasoconstrictor stimuli. Treatments that react irreversibly with proteins modulating vasoconstriction have the advantage that their effects can last well into the postoperative period. In addition systemic effects are avoided as the treatment is localised to the treated graft. This study investigated the use of two clinically applied drugs; fluphenazine (SKF7171A, HCl), an irreversible calmodulin antagonist and minoxidil sulphate, an irreversible potassium channel opener. Treatments were tested against receptor and non-receptor-mediated contraction in the human radial artery. Method: Isometric tension was measured in response to angiotensin II, KCl and vasopressin in 108 radial artery rings (taken from 31 patients undergoing coronary artery bypass grafting). Control responses were compared with rings pretreated with fluphenazine or minoxidil sulphate. Vasopressin responses were also compared in the presence of glyceryl trinitrate or the reversible Rho kinase inhibitor Y27632. Results: Fluphenazine pretreatment significantly suppressed vasoconstriction to all agonists tested. Maximal responses to angiotensin II, vasopressin and KCl were reduced by 42 AE 19%, 35 AE 8% and 48 AE 15% respectively, without any measurable effect on the EC 50 . Minoxidil sulphate showed no discernable effect. Vasopressin-induced contraction was also reduced by high levels of glyceryl trinitrate (220 mM; 50 mg/ml) or 10 mM Y27632. Conclusions: The irreversible calmodulin antagonist fluphenazine has potential to be developed as an inhibitor of contraction in arterial graft vessels. The involvement of Rho kinase indicates that other vasoconstrictors and surgical stress can sensitize radial artery to vasopressin-induced contraction. Strategies targeting this pathway also have future potential. #
femoral arterial responses to vasoconstrictor and vasodilator agents in endotoxin shock
Life Sciences, 1994
The hypothesis for this study is that the decreased arterial response to catecholamines may be due to the effect of endotoxemia on vessel tone. One control ring was taken from one femoral artery of a Wistar rat and after endotoxin (ENDT) infusion (iv. 6mg/kg-1 hr.), one ring was removed from the contralateral artery. The post-ENDT rings were tested in four groups which were determined by the mean arterial pressure (MAP) levels at the time of dissection: 100mmHg (120 min), 80mmHg (270 min), 60mmHg (300 min) or 40mmHg (330 min). KC1, phenylephrine (PHE) and arginine-vasopressin (AVP) dose-response curves (DR) were obtained at a preload of 500 mg which allowed the maximum response in control rings. When compared at 500mg preload the maximal active response to all agonists post-ENDT was decreased by about 50%. By increasing the preload on the ENDT rings to 800mg, the active tension became 2.49 times the active tension of the control rings. Length-tension experiments also showed a greater response for post-ENDT rings and a greater preload at maximum response but the ring circumference was the same. In contrast the in vivo femoral artery diameters at 90 min post-ENDT (100 mmHg) were 82.6% of control. Endothelium-dependent relaxation by acetylcholine (ACh) was abolished by ENDT but endotheliumindependent relaxation to nitroprusside (NP) was not affected. It is concluded that the resting tone and active tension of femoral artery smooth muscle is increased by ENDT and the decreased in vivo responsiveness to vasoconstrictor agonists may be the result of vessel constriction due to loss of endothelium. The results also suggest that in vitro comparison of vessels in studies of endotoxin shock be done at the same muscle length rather than at the same preload.
Effects of preanesthetic and anesthetic drugs on endothelium-dependent responses in the rat aorta
General Pharmacology: The Vascular System, 1995
Acetylcholine often fails to induce endothelium-dependent relaxation in human vessels in vifro. Due to the fact that most of these vessels come from surgery, we examined the influence of drugs used in anesthesia on endothelium-dependent responses in rat aorta. 2. Groups of male Wistar rats of the following treatments were utilized: P group, diazepam + promethazine + atropine; I group, pentothal + succinylcholine; IG group, halothane + nitrous oxide; M group, morphine + pancuronium; C group, untreated rats. Dose-response curves to noradrenaline and acetylcholine were determined in rat aorta in vitro, in the presence and absence of endothelium. 3. Acetylcholine induced more relaxation (P < 0.05) in the rat aorta of IG group compared with that of the C group. 4. In the rat aorta from P and IG groups, the contractions produced by several concentrations of noradrenaline were significantly smaller (P < 0.05) when the endothelium was removed. Similar effects occurred in aorta strips of animals previously treated with either atropine, promethazine, cimetidine or halothane. 5. Our results suggest that drugs currently used in anesthesia interfere with some endothelium-dependent effects on isolated rat aorta but according to these results they do not seem to be responsible for the lack of acetylcholine relaxation sometimes described in human vessels in vitro.
Crit Care, 2008
Introduction Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.
Critical Care, 2008
Introduction Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.
European Journal of Pharmacology, 2003
To examine the coronary effects of arginine -vasopressin and its interaction with nitric oxide and prostanoids during partial ischemia and reperfusion, left circumflex coronary artery flow was electromagnetically measured and partial occlusion of this artery was induced for 60 min, followed by reperfusion in anesthetized goats (seven non-treated, six treated with N W -nitro-L-arginine methyl esther (L-NAME) and five with meclofenamate). During partial coronary occlusion, coronary vascular conductance decreased by 20 -31% ( P < 0.01), and the coronary vasodilatation in response to acetylcholine (3 -100 ng) and sodium nitroprusside (1 -10 Ag) was much reduced in every case; the vasoconstriction in response to arginine -vasopressin (0.03 -0.3 Ag) was attenuated in non-treated animals; this attenuation was reversed by L-NAME and was accentuated by meclofenamate. At 30 min of reperfusion, coronary vascular conductance remained decreased by 11 -25% ( P < 0.05 or P < 0.01), and the vasodilatation in response to acetylcholine and sodium nitroprusside as well as the vasoconstriction with arginine -vasopressin was as in the control and comparable in the three groups of animals. These results suggest: (1) that, during ischemia, the coronary vasodilator reserve is greatly reduced and the vasoconstriction with arginine -vasopressin is attenuated, with preservation of the modulatory role of nitric oxide and probable involvement of vasoconstrictor prostanoids in this vasoconstriction; and (2) that, during reperfusion, the coronary vasodilator reserve and the coronary reactivity to acetylcholine and arginine -vasopressin recover, but the modulatory role of nitric oxide in this reactivity may be attenuated. D