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Isolated Preparations (isolated + preparation)
Selected AbstractsBiphasic effects of NMDA on the motility of the rat portal veinBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2000Z L Rossetti The effect of NMDA on the motility of the rat portal vein was studied in an isolated preparation. NMDA induced a concentration-dependent (10,7,10,4 M) increase of the contraction frequency (maximum increase, 148±6% of control at NMDA 10,4 M). The NMDA-induced excitatory response was prevented by the competitive NMDA receptor antagonists (±)-2-Amino-5-phosphonopentanoic acid (AP-5, 5×10,4 M) or (RS)-3-(2-carboxypiperazine-4-yl) propyl-1-phosphonic acid (CPP, 10,4 M). Tetrodotoxin (TTX, 10,6 M) or atropine (10,4 M) abolished the NMDA-induced increase of the portal vein motility and reversed the excitatory effect to a concentration-dependent inhibition (maximum inhibition, 52±8 and 29±7% of controls, respectively, at NMDA 10,3 M). Removal of the endothelium abolished the NMDA-induced inhibitory response. Sodium nitroprusside concentration-dependently (10,7,10,5 M) inhibited the portal vein motility, while L -NG -nitro-arginine methyl ester (L -NAME, 10,4 M) reversed the inhibitory effect of NMDA (in the presence of TTX), restoring the portal vein spontaneous activity to control values. These results show that NMDA modulates the portal vein motility in a biphasic manner: via indirect activation, through prejunctional NMDA receptors presumably located on intrinsic excitatory neuronal afferences, or via direct inhibition, through endothelial NMDA receptors activating the nitric oxide pathway. Overall these findings support the hypothesis of the existence of a peripheral glutamatergic innervation modulating the contractile activity of the rat portal vein. British Journal of Pharmacology (2000) 129, 156,162; doi:10.1038/sj.bjp.0703002 [source] Effects of Direct Sympathetic and Vagus Nerve Stimulation on the Physiology of the Whole Heart , A Novel Model of Isolated Langendorff Perfused Rabbit Heart with Intact Dual Autonomic InnervationEXPERIMENTAL PHYSIOLOGY, Issue 3 2001G. André Ng A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n= 10) had baseline heart rates of 146 ± 2 beats min,1 which could be increased to 240 ±11 beats min,1 by sympathetic stimulation (15 Hz) and decreased to 74 ± 11 beats min,1 by stimulation of the vagus nerve (right vagus, 7 Hz). This model has the advantage of isolated preparations, with the absence of influence from circulating hormones and haemodynamic reflexes, and also that of in vivo preparations where direct nerve stimulation is possible without the need to use pharmacological agents. Data are presented characterising the preparation with respect to the effects of autonomic nerve stimulation on intrinsic heart rate and atrioventricular conduction at different stimulation frequencies. We show that stimulation of the right and left vagus nerve have differential effects on heart rate and atrioventricular conduction. [source] Effect of exogenous glutamate and N-Methyl-D-aspartic acid on spontaneous activity of isolated human ureterINTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2007Slobodan M Jankovic Objectives: While the neurotransmitter role of glutamate in the gastrointestinal tract has been shown, its effects on smooth muscle of the human ureter have not previously been investigated. In our study we have investigated the effects of exogenous glutamate on the spontaneous activity of isolated human ureter, taken from 14 adult patients after nephrectomy. Methods: The segment of ureter, excised 3 cm distal from the pyeloureteral junction, was isolated in an organ bath. Both longitudinal tension and intraluminal pressure of the segment were recorded simultaneously. Results: Glutamate administered in the lumen of the isolated ureteral segments (7.8 × 10,7 M/L,3.5 × 10,2 M/L) was ineffective. When added to the isolated organ bath from the serous side of the ureteral segment, glutamate (7.9 × 10,6 M/L,10.6 × 10,3 M/L) and N-Methyl-D-aspartic acid (NMDA) (9.1 × 10,8 M/L,3.1 × 10,5 M/L) produced a concentration-dependent increase in spontaneous activity of the isolated preparations, while kainic acid (6.3 × 10,8 M/L,10.5 × 10,5 M/L) and (+/,)- trans -1-Aminocyclopentane- trans -1,3-dicarboxylic acid (ACPD) (7.7 × 10,8 M/L ,6.5 × 10,5 M/L) were ineffective. Conclusions: The results of our study suggest that an excitatory neurotransmitter glutamate stimulates spontaneous activity of the human ureter through activation of NMDA ionotropic receptors, located on smooth muscle cells or intramural nerve fibers [source] Is the efficiency of mammalian (mouse) skeletal muscle temperature dependent?THE JOURNAL OF PHYSIOLOGY, Issue 19 2010C. J. Barclay Myosin crossbridges in muscle convert chemical energy into mechanical energy. Reported values for crossbridge efficiency in human muscles are high compared to values measured in vitro using muscles of other mammalian species. Most in vitro muscle experiments have been performed at temperatures lower than mammalian physiological temperature, raising the possibility that human efficiency values are higher than those of isolated preparations because efficiency is temperature dependent. The aim of this study was to determine the effect of temperature on the efficiency of isolated mammalian (mouse) muscle. Measurements were made of the power output and heat production of bundles of muscle fibres from the fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus muscles during isovelocity shortening. Mechanical efficiency was defined as the ratio of power output to rate of enthalpy output, where rate of enthalpy output was the sum of the power output and rate of heat output. Experiments were performed at 20, 25 and 30°C. Maximum efficiency of EDL muscles was independent of temperature; the highest value was 0.31 ± 0.01 (n= 5) at 30°C. Maximum efficiency of soleus preparations was slightly but significantly higher at 25 and 30°C than at 20°C; the maximum mean value was 0.48 ± 0.02 (n= 7) at 25°C. It was concluded that maximum mechanical efficiency of isolated mouse muscle was little affected by temperature between 20 and 30°C and that it is unlikely that differences in temperature account for the relatively high efficiency of human muscle in vivo compared to isolated mammalian muscles. [source] Calcitonin gene-related peptide facilitates serotonin release from guinea-pig colonic mucosa via myenteric neurons and tachykinin NK2/NK3 receptorsBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2004Shu-ichi Kojima The ability of calcitonin gene-related peptide (CGRP), to alter the outflow of 5-hydroxytryptamine (5-HT) from the guinea-pig proximal colon, was evaluated using three different isolated preparations: whole colon, mucosa-free muscle layer and submucosa/mucosa preparations. In the presence of the monoamine oxidase A inhibitor, clorgyline, CGRP elicited a concentration-dependent increase in 5-HT outflow from the whole colon, but not from mucosa-free muscle layer preparations. The CGRP-evoked 5-HT outflow was sensitive to tetrodotoxin (TTX) or hexamethonium, but was not detectable in submucosa/mucosa preparations. HCGRP8,37 (3 ,M) inhibited the submaximal effect of CGRP on the 5-HT outflow. [Cys(ACM)2,7]hCGRP had a slight stimulant influence on the 5-HT outflow. The selective NK2 and NK3 receptor antagonists, SR48968 or SR142801, respectively, prevented the enhancing effect of CGRP. By contrast, a selective NK1 receptor antagonist L703606, failed to block the effect of CGRP. The enhancing effect of CGRP was mimicked by the NK2 receptor agonist [, -Ala8]-neurokinin A (NKA)4,10 and the NK3 receptor agonist senktide. The effect of [, -Ala8]-NKA4,10 on the 5-HT outflow was unaffected by TTX, while the effect of senktide was prevented by TTX, hexamethonium or SR48968. The present data also demonstrated a synergistic action of the NK2 and NK3 receptor agonists on the CGRP-evoked 5-HT outflow. We concluded that CGRP facilitates 5-HT release from the guinea-pig colonic mucosa through an action on myenteric neurons and that this effect is mediated by endogenously released tachykinins, acting via tachykinin NK2/NK3 receptors in cascade. British Journal of Pharmacology (2004) 141, 385,390. doi:10.1038/sj.bjp.0705624 [source] | |||||||||||||