The effects of morphine and remifentanil in isolated rat pherenic nerve-hemidiaphragma muscle [·Izole siçan frenik s?n?r-hemidiyafragma kas preparatlarinda re?ifentan?l ve morf?n?n etk?ler?]

In our study, we aimed to investigate the effect of remifentanil and morphine on neuromuscular junction in isolated rat pherenic nerve-hemidiaphragma muscle preparation. Following approvel the protocol by animal ethic commite of Çukurova University, fourty Wistar rats (220-260 gr.) were killed by decapitation and pherenic nerve-hemidiaphragma muscle (70-80 mg weight) were isolated carefully according to the method described by Kelsen ve Nochomovitz. After the thermoregulation and equilibration period for 60 minutes, the voltage of supramaximal stimulation and optimal muscle strenght were determined by both direct and indirect stimulations. Specimens were divided randomly into two groups before the contraction responses were recorded. After control contraction responses were recorded, morphine (0.1, 1, 10 and 100 µM) in group I (n=20) and remifentanil (0.001, 0.01, 0.1 ve 1 µM) in group II (n=20) were added to the bath solution cumulatively and contraction responses (contraction power: KK), contraction time: KS) and 1/2-relaxation time (YGS) were recorded again. In isolated pherenic nerve-hemidiaphragma muscle, control contraction responses contraction power (KK), contraction time (KS) and elaxation time (YGS) determined by direct and indirect supramaximal stimulations were found similar in morphine and remifentanil group. Contraction responses did not change and were found similar with the cumulative addition of opioids (morphine and remifentanil). It is concluded that remifentanil and morphine did not effect neither presinaptic (indirect) nor postsinaptic (direct) depolarization in isolated pherenic nerve-hemidiaphragma muscle produced any relaxation in neuromuscular junction

EFFECTS OF STATIC MAGNETIC-FIELD ON SPECIFIC ADENOSINE-5'-TRIPHOSPHATASE ACTIVITIES AND BIOELECTRICAL AND BIOMECHANICAL PROPERTIES IN THE RAT DIAPHRAGM MUSCLE

WOS: A1995RE76400001PubMed ID: 7677790In 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 the 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. (C) 1995 Wiley-Liss, Inc

The relation between the effects of ketamine on mechanogram and Ca+2 ATPase on nerve-muscle preparation [KETAMIN'IN SINIR-KAS PREPARATLARINDA MEKANOGRAM UZERINE ETKILERININ CA+2 ATP'AZ ILE ILISKISI]

The aim of this study was to determine the effect of ketamine on muscle contraction force and Ca+2 ATPase enzyme activity in the rat phrenic nerve-hemidiaphragm muscle preparation. This study was approved by ethical committee. Wistar strain Albino rats, weighted 200-230 g, were used in this study (n=24). Animals were killed with cervical dislocation and phrenic nerve-hemidiaphragm muscle was prepared. Muscle was placed between two platen electrodes and connected to a isometric force tranceducer which was stimulated hanged in the tissue bath which contains krebs solution at 37°C. Following the 30 minutes of stabilization, muscle was stimulated with direct and indirect electrical pulses supramaximally. The peak tension was recorded with an oscillograph. Initial normal muscle contraction force was recorded before adding 21, 31.6, 42, 52.6, 42, 63, 73.8 µM of ketamine into the solution. After this period, at each concentration enzyme activity was measured in the 10 % hemidiaphragm muscle homogenate, which was prepared in 0.32 % sucrose with 1 mM Mg++ for each ketamine concentration. While, the muscle contraction force was increased at 21, 31.6, 42 µM ketamine concentrations, however concentrations of ketamine (52.6, 63, 73.8 µM) was reduced the peak tension. A proportional dose dependent Ca+2 ATPase enzyme activity reduction with higher ketamine concentrations was determined. According to our results, ketamine decreased the muscle contraction and Ca+2 ATPase enzyme activity

Remifentanil produces vasorelaxation in isolated rat thoracic aorta strips

PubMedID: 12492799Background: 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. © Acta Anaesthesiologica Scandinavica 47 (2003)

The effects of cocaine on verapamil induced relaxation in the rat thoracic aorta [SICAN TORASIK AORTASINDA VERAPAMILIN OLUSTURDUGU GEVSEMEYE KOKAININ ETKISI]

The effects of cocaine combined with verapamil on the contraction and relaxation responses in the thoracic aorta of rats investigated in this study. The weights of the Wistar rats used ranged between 210 to 300 g. After rats were killed by decapitation, thorax was opened and thoracic aorta was carefully taken out, and as placed in the Krebs solution. The preparations were cut as helical, to make them opened aortic strips (about 2 to 3 mm in width and 10-13 mm in length). Both ends of these strips were bound with a rope, and then placed in the tissue bath which was gassed by a mixture of 5 % CO2 and 95 % O2 and the equilibrated for 120 minutes, under a resting tension of 2 g. The following experiments were performed: First, the muscle was made to contract by adding 10-7 M phenylephrine, the muscle was then made to relax nearly 33 % by adding 10-6 M acetylcholine. Verapamil was then added into the bath solution, by the following cumulative concentrations respectively: 11, 16.5 and 22 µM/L. Following verapamil, cocaine was also added with cumulative concentrations of 19.8, 29.7 and 39.6 µM/L respectively. The responses were recorded with an isometric transducer. It as determined that cocaine antagonized the relaxing effect of verapamil in a dose dependent manner

The effects of ketamine on muscle membrane and intracellular Ca++ stores [KETAMININ KAS HUCRE MEMBRANINA VE INTRASELLULER CA++ DEPOLARINA ETKISI]

The effects of ketamine on the muscle cell membrane and intracellular Ca++ stores were investigated in vitro. Wistar rats (200-230 g) were studied. After decapitation, hemidiaphragma nerve-muscle preparations were placed in an isolated organ bath with Krebs solution (pH=7.4) in which insuflated with oxygen (95 %) and carbon dioxide (5 %) gas mixture. The following experiments were performed: A. 10 nerve-muscle preparations were used for bioelectrical recordings. Preparation was placed in a bath with a capacity of 10 mL and insufflation facilities. Micro electrodes were inserted intramuscularly and membrane potentials and action potentials via the stimulation of nerve recorded with the ketamine concentrations of 30, 50, 70, 90, 100 and 120 µM/L Amplitude, latans and overshoot parameters were calculated from the recorded curves. B. 13 nerve-muscle preparations which were inserted between the platin electrodes were stimulated directly or indirectly with supramaximal electrical stimuli (0.2 ms duration and 0.05 Hz) for biomechanical recordings. After normal strength of muscles were recorded ketamine was added into the bath to obtain the concentration of 21, 31.6, 42, 52.6, 63 and 73.6 µM/L and records were taken. The contraction changes were evaluated. Action potential wets observed to be begun without muscle contraction with the concentration of 73.6 µM/L of ketamine. This result may show that ketamine blocks not only the Na+ channels but also sarcoplasmic Ca++ channels. On, the other hand unchanging contracture stressed that ketamine does not effect on Ca++ reuptake

Remifentanil produces vasorelaxation in isolated rat thoracic aorta strips [7]

PubMedID: 15243971[No abstract available

Effect of propofol on isolated thoracic aorta strips [Izole sican torasik aortasinda propofolun etkileri]

This study aims to demonstrate the effect of propofol on isolated rat aorta strips in relation with vascular contraction-relaxation and Na+/K+- Ca++/Mg++ ATP'ase activity. The protocol was approved by ethic committee of Cukurova University. Fifteen wistar rats (200-300 g) were killed by a blow to the head. Thoracic aorta were isolated carefully and were cut with the shape of helical strips and placed in organ baths. Before investigation of the effects of propofol, strips were tested by using acetylcholine followed maximally contraction with phenylephrine (with and without endothelium) propofol was than added to organ baths fluid. Fifteen intact and denuded aorta strips were used to investigate Na+/K+ and Ca++/Mg++ ATP'ase activity. Student's-t test was used for statistical analysis. While approximately 33 % relaxation was occurred on endothelium intact thoracic aorta strips by acetylcholine, acetylcholine-induced relaxation was not observed on endothelium denuded strips. Propofol (3x10-4 M and 3x10-5 M) attenuated the relaxation 16-44 % induced by acetylcholine in endothelium intact thoracic aorta (p<0.001) whereas, caused to relaxation 27-58 % in endothelium-denuded thoracic aorta strips (p<0.001). Na+/K+-Ca++/Mg++ ATP'ase activity in endothelium-intact thoracic aorta strips with 3x10-4 and 3x10-5 M propofol was found significantly lower (p<0.001) than control groups. While Ca++/Mg++ ATP'ase activity in endothelium denuded thoracic aorta strips was found significantly lower (p<0.001), Na+/K+ ATP'ase activity was not found statistically significant compared with control groups. Finally, propofol-induced vasoconstriction is associated with inhibition of NO in endothelium intact thoracic aorta strips, whereas propofol induced vasodilatation is associated with reduced Ca++/Mg++ ATP'ase activity in endothelium intact and denuded thoracic aorta strips

Electromechanical effects of protamine and verapamil in rat papillary muscle

The electromechanical effects of protamine sulfate and the calcium channel blocker verapamil on rat cardiac and skeletal muscles were studied using isolated left ventricular papillary muscle and phrenic nerve- hemidiaphragm preparations. Protamine produced significant decreases in isometric force in the cardiac tissue and contracture developed at concentrations of 40 and 80 mg · L-1. Isometric force also decreased significantly with verapamil at concentrations of 0.757 and 7.57 mg · L-1. Both drugs caused significant decreases in the contractile force of hemidiaphragm muscle when the tissue was stimulated indirectly. Protamine and verapamil caused the resting membrane potential and the amplitude of the action potential to decrease in cardiac tissue and overshoot failed to develop with 80 mg · L-1 of protamine or 7.57 mg · L-1 of verapamil. These bioelectrical changes developed in a dose-dependent manner. It was concluded that protamine had a similar effect to that of calcium channel blockers and it may act through a reduction of cellular calcium. This effect on cardiac tissue may be mediated through the sarcolemmal ion pumps or channels, leading to changes in calcium homeostasis

Is ketorolac tromethamine a local anesthetic?

Ketorolac tromethamine (KT), which is a cyclooxygenase inhibitor, is a non-steroidal antiinflammatory analgesic agent. In this study, it was aimed to investigate the local anaesthetic effect of KT. A total of 24 sciatic nerve bundles (for control and experimental groups, n=12 each) were isolated from winter frogs (Rana cameroni). Desheathed sciatic nerve bundles were then placed in a fluid-electrode chamber. Solutions of frog Ringer procaine (2.1, 4.2, 8.4, 21.0 and 42.0 mM/L), and ketorolac (2.1, 4.2, 8.4, 21.0, 42.0, 84.0 and 115 mM/L) were used in order to bath the nerve bundles. In every solution, the measurements were taken till no further decrement was observed in the amplitude of CNAP, and the tissue samples were then rinsed in frog Ringer solution until the recovery of action potential amplitudes to the normal values, which were accepted to be 100%; amplitudes in the other bath solutions were determined as the percent of these normal values. In a concentration of 42 mM/L, procaine was determined to cause complete, where as KT 20% inhibition in the CNAP amplitudes; complete inhibition by KT was shown to occur in a concentration of 115 mM/L. In other words, KT caused inhibition in a longer period, and to a lesser extent when compared to procaine. The overall evaluation of our results leads to the conclusion that KT causes complete inhibition of CNAP in very high doses and therefore property as a weak local anaesthetic agent limits its effective clinical usefulness