Subject(s)
Analgesics, Opioid/pharmacology , Muscle, Smooth, Vascular/drug effects , Piperidines/pharmacology , Vasodilation/drug effects , Animals , Aorta, Thoracic/drug effects , Endothelium, Vascular/drug effects , Humans , In Vitro Techniques , Rabbits , Rats , Remifentanil , Species SpecificityABSTRACT
BACKGROUND: Remifentanil can cause transient instability in hemodynamic variables. However this change may not be solely the result of autonomic or central nervous system inhibition or of centrally mediated vagal stimulation. In this study, the aim was to examine the direct effects of remifentanil on isolated thoracic aorta strips in vitro. METHODS: Forty-five Wistar rat thoracic aorta rings were isolated, and contraction-relaxation responses were recorded. RESULTS: In aortic rings precontracted with phenylephrine or potassium chloride, remifentanil produced concentration-dependent relaxation in both endothelium-intact and denuded rings (P<0.001). Remifentanil induced significantly greater relaxation in intact rings than in those denuded of endothelium, regardless of whether they were precontracted with phenylephrine hydrochloride or KCl (P<0.001). When the endothelium was present, remifentanil produced greater relaxation in KCl-contracted rings than in PE-contracted rings at lower concentrations (10-9 and 10-8), and similar relaxation at higher concentrations (10-7 and 10-6). However, when the endothelium was removed, relaxation was similar in both solutions, at all concentrations (10-9 to 10-6). In intact rings, pretreatment with L-NO-ARG or indomethacin reduced the degree of remifentanil-induced relaxation. In Ca+ +/- free media, calcium-dependent KCl contractions were inhibited in a dose-dependent manner by remifentanil (P<0.001). CONCLUSION: Remifentanil vasodilates by an endothelium-dependent mechanism, involving prostacyclin and nitric oxide released from the endothelium. Its endothelium-independent vasodilation probably occurs via the suppression of voltage-sensitive Ca++ channels.
Subject(s)
Analgesics, Opioid/pharmacology , Aorta, Thoracic/drug effects , Muscle, Smooth, Vascular/drug effects , Piperidines/pharmacology , Vasodilation/drug effects , Acetylcholine/pharmacology , Animals , Calcium Channel Blockers/pharmacology , Dose-Response Relationship, Drug , Endothelium, Vascular/drug effects , Epoprostenol/physiology , In Vitro Techniques , Nitric Oxide/physiology , Phenylephrine/antagonists & inhibitors , Phenylephrine/pharmacology , Potassium Chloride/antagonists & inhibitors , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Remifentanil , Vasoconstrictor Agents/antagonists & inhibitors , Vasoconstrictor Agents/pharmacologyABSTRACT
In this study, we aimed to clarify the effects of chronically applied static magnetic field (200 Gauss) on specific ATPase activities and bioelectrical and biomechanical responses in isolated rat diaphragm muscle. The mean activities of Na(+)-K+ ATPase and Ca2+ ATPase determined from the diaphragm homogenates were significantly higher in the magnetic field exposed group (n = 20), but that of Mg2+ ATPase was nonsignificantly lower compared to the control group (n = 13). Resting membrane potential, amplitude of muscle action potential, and overshoot values (mean +/- SE) in the control group were found to be -76.5 +/- 0.6, 100 +/- 0.8, and 23.5 +/- 0.6 mV, respectively; these values were determined to be -72.8 +/- 0.4, 90.3 +/- 0.5, and 17.2 +/- 0.4 mV in the magnetic field-exposed group, respectively. The latency was determined to increase in the experimental group, and all the above-mentioned bioelectrical differences between the groups were significant statistically. Force of muscle twitch was found to decrease significantly in the magnetic field-exposed group, and this finding was attributed to the augmenting effect of magnetic field on Ca2+ ATPase activity. These results suggest that magnetic field exposure changes specific ATPase activities and, thence, bioelectrical and biomechanical properties in the rat diaphragm muscle.
