Necdet Dogan

Role of the endothelium on the response to adrenoceptor agonists of rabbit aorta during cooling.

Abstract— The role of the endothelium in the effects of cooling on the response to α1‐ and α2‐adrenoceptor agonists of rabbit aorta was studied. The contractions induced by clonidine (10−9‐ 3 × 10−4M) and xylazine (10−7‐ 10−3M) but not phenylephrine (10−9‐ 3 × 10−4M) and methoxamine (10−9‐ 3 × 10−4M) were enhanced in endothelium‐denuded or NG‐nitro‐L arginine methyl esther (l‐NAME) (10−5M) pretreated rabbit aorta. The senstivily, but not the maximal response, of both α1‐ and α2‐adrenoceptor agonists was significantly lower at 28 °C (cooling) than at 37 °C. Endothelium removal did not affect the action of cooling. These results were taken as evidence for the specificity of α2‐adrenoceptor agonists on the production and release of nitric oxide from vascular endothelium. The results suggest that the endothelium seems to have no role in the cooling‐induced responses of both α1‐ and α2‐adrenoceptors.

Cooling and response to hydrogen peroxide in human saphenous vein: role of the endothelium

In the present work we studied the responses of human saphenous vein to H2O2 and effects of moderate cooling on these responses with analysis of the role of endothelium. H2O2 (10−7–10−2 m) induced concentration‐dependent contraction in the intact human saphenous vein strips at both temperatures. At 28 °C, the maximal contraction induced by H2O2 was significantly lower than that at 37 °C. Compared with intact strips, the sensitivity and the maximal contraction to H2O2 were significantly enhanced in endothelium‐denuded strips at 37 and 28 °C. However, pD2 values and maximal contractions were not significantly different in endothelium‐denuded strips at different temperatures. Pretreatment with NG‐nitro‐l‐arginine methyl ester (l‐NAME) increased significantly the maximal contraction and sensitivity to H2O2 at 37 and 28 °C. The contractions increased by l‐NAME were restored by the pre‐incubation of l‐arginine (10−3 m) at every temperature studied. The contractile responses of intact human saphenous veins to H2O2 were reduced significantly by 10−5 m indomethacin at both temperatures. Our results suggest that H2O2‐induced contraction of human saphenous vein are mediated by its direct effect on the smooth muscle and by the generation of products of the cyclooxygenase pathway from the endothelium. Signalling pathways of these contractile effects are the same at 37 and 28 °C. Under normal temperature conditions, the contraction to H2O2 is possibly modulated by endothelial nitric oxide. Cooling reduces the contraction to H2O2 by increasing release of nitric oxide.

THE EFFECT OF BUPIVACAINE ON COMPOUND ACTION POTENTIAL PARAMETERS OF SCIATIC NERVE FIBERS

The aim of this study was to document the effects of the local anesthetic agent bupivacaine on individual fibers of peripheral nerve. To accomplish this objective, compound action potentials (CAPs) were recorded from isolated frog sciatic nerves treated with bupivacaine for seven individual concentration levels. Numerical and fast Fourier transform (FFT) analysis were performed on these recordings. The areas, latency periods, maximum and minimum derivatives, and power spectrums of the CAPs were computed. The results show that the area and the absolute values of maximum and minimum derivatives decrease linearly as bupivacaine concentration increases. The power spectrum of the CAPs, which resides in the 0-1000 Hz interval, initially shifts to higher frequencies then returns to lower frequency region again with increasing bupivacaine concentration. Due to this result, it is thought that bupivacaine inhibits nerve fibers in a dose-dependent manner. It primarily affects the fibers having the least myelin sheets (motor fibers), then it begins to depress the fast conducting (neurosensorial) fibers as the bupivacaine concentration increases, and finally blocks the unmyelinated C-fibers

Effects of cooling and warming on 5-hydroxytryptamine- and acetylcholine-induced contractions of human umbilical vessels: role of nitric oxide

The effects of cooling (to 28 °C) and warming (to 41 °C) on the vasoconstrictions induced by 5‐hydroxytryptamine (5‐HT) and acetylcholine (ACh) and the role of nitric oxide in these effects were analyzed in human umbilical artery and vein. 5‐HT (10−9–10−4 m) and ACh (10−9–10−4 m) induced concentration‐dependent contractions at 37, 28 and 41 °C. During cooling, the sensitivity, but not the maximal response, of 5‐HT and ACh was significantly higher than at 37 °C; and during warming, again the sensitivity, but not the maximal response, of both contractile agents was significantly lower than at 37 °C. Neither cooling to 28 °C nor warming to 41 °C, after treatment with NG‐nitro‐l‐arginine methyl esther (l‐NAME, 10−4 m), modify the effect of temperature in both vessels. These results suggest that cooling‐ and warming‐induced responses in human umbilical artery and vein are independent of nitric oxide.

Role of the nitric oxide on diazoxide-induced relaxation of the calf cardiac vein and coronary artery during cooling.

The effects of cooling (to 28 °C) on the vasodilation induced by diazoxide (10−9–3 × 10−4 m) on carbachol‐pre‐contracted calf cardiac vein and coronary artery and the role of nitric oxide in these effects were analyzed. Diazoxide produced concentration‐dependent relaxation of calf cardiac vein and coronary artery rings pre‐contracted with carbachol (10−6 m). During cooling, the pIC50 values, but not the maximal responses, to diazoxide were significantly lower than at 37 °C in both preparations. Cooling to 28 °C in the presence of NG‐nitro‐L‐arginine methyl ester (10−4 m) did not modify the effect of temperature both in cardiac vein and coronary artery. These results suggest that cooling‐induced changes of diazoxide in calf cardiac vein and coronary artery are independent of nitric oxide.

The relaxant effects of alfentanil and remifentanil on noradrenaline-treated rat aorta

Abstract Background and objective: In this in vitro study on rat thoracic aorta, the effects of indomethacin (a prostaglandin synthesis inhibitor), propranolol (a beta adrenergic receptor blocker), tetraethylammonium (TEA) (a calcium-actived potassium channel blocker), glibenclamide (an ATP-dependent potassium channel blocker) and naloxone (an opioid receptor antagonist) on the responses induced by alfentanil and remifentanil were investigated. Methods: Aortas isolated from rats were cut into spiral strips 12 mm in length, 3 mm wide. Strips were mounted in organ baths at 37°C continuously gassed with 95% and 5% CO2. The responses of the drugs were recorded isometrically on polygraph. Results: In both groups, strips were precontracted with 10-6 Μ noradrenaline (NA). Then alfentanil or remifentanil (10-8 to 10-5 Μ) was administered cumulatively. Both alfentanil and remifentanil significantly produced relaxation (p < 0.05). Indomethacin, propranolol, TEA, glibenclamide and naloxone did not significantly modi...

Warming and response to contractile agents in calf cardiac vein: role of the nitric oxide.

The effects of warming on the response to various contractile agents of calf cardiac vein were studied using 2.5‐mm long cylindrical segments. Concentration–response curves for carbachol (10−9–3 × 10−4 m), 5‐hydroxytryptamine (5‐HT; 10−8–3 × 10−3), potassium chloride (KCl; 10−4–5 × 10−2 m) and calcium chloride (CaCl2; 10−4–10−2) were isometrically recorded at 37 and 41 °C (warming). During warming the sensitivity, but not the maximal response, of carbachol 5‐HT, KCl, and CaCl2 was significantly higher than at 37 °C. Warming to 41 °C after treatment with NG‐nitro‐L arginine methyl esther (10−5 m) did not modify the effect of warming. These results suggest that nitric oxide seems to have no role in the warming‐induced responses in calf cardiac vein.

Effects of fentanyl, remifentanil, and sufentanil in the isolated perfused rat kidney

centration of phenylephrine. Fentanyl induced relaxations were inhibited by glibenclamide (10 −5 M, n = 5) and TEA (10 −3 M, n = 5) ( p 0.05). Both sufentanil- and remifentalin-induced relaxations were not inhibited by indomethacin (10 −5 M, n = 5), L-NAME (10 −4 M, n = 5), propranolol (10 −6 M, n = 5), naloxone (10 −6 M, n = 5) ( p> 0.05) and glibenclamide (10 −5 M, n = 5) but TEA (10 −3 M, n = 5) was effective ( p< 0.05). These results suggest that in isolated perfused rat kidney, K + channels may play a role in fentanyl-, sufentanil- and remifentanil-induced relaxation by opening ATP sensitive-potassium channels and calcium-activated potassium channels. summary