The effects of local sensory blockade (topical anaesthesia) on eccrine sweat glands and cutaneous circulation are not well understood. This study aimed to determine whether topical lidocaine/prilocaine alters eccrine sweat gland and cutaneous blood vessel responses.
Sweating (capacitance hygrometry) was induced via forearm intradermal microdialysis of five acetylcholine (ACh) doses (1 × 10−4 to 1 × 100m, 10-fold increments) in control and treated forearm sites in six healthy subjects. Nitric oxide-mediated vasodilatory (sodium nitroprusside) and adrenergic vasoconstrictor (noradrenaline) agonists were iontophoresed in lidocaine/prilocaine-treated and control forearm skin in nine healthy subjects during blood flow assessment (laser Doppler flowmetry, expressed as% from baseline cutaneous vascular conductance; CVC; flux/mean arterial pressure).
Non-linear regression curve fitting identified no change in the ED50 of ACh-induced sweating after sensory blockade (−1.42 ± 0.23 logM) compared to control (−1.27 ± 0.23 logM; P > .05) or in Emax (0.43 ± 0.08 with, 0.53 ± 0.16 mg cm−2 min−1 without lidocaine/prilocaine; P > .05). Sensory blockade did not alter the vasodilator response to sodium nitroprusside (1280 ± 548% change from baseline CVC with, 1204 ± 247% without lidocaine/prilocaine) or vasoconstrictor response to noradrenaline (−14 ± 4% change from baseline CVC with, −22 ± 14% without lidocaine/prilocaine; P > 0.05).
Cutaneous sensory blockade does not appear to alter nitric oxide-mediated vasodilation, adrenergic vasoconstriction, or cholinergic eccrine sweating dose-response sensitivity or responsiveness to maximal dose. Thus, lidocaine/prilocaine treatment should not affect sweat gland function or have blood flow implications for subsequent research protocols or clinical procedures.
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The effects of local sensory blockade (topical anaesthesia) on eccrine sweat glands and cutaneous circulation are not well understood. This study aimed to determine whether topical lidocaine/prilocaine alters eccrine sweat gland and cutaneous blood vessel responses.
Sweating (capacitance hygrometry) was induced via forearm intradermal microdialysis of five acetylcholine (ACh) doses (1 × 10−4 to 1 × 100 m, 10-fold increments) in control and treated forearm sites in six healthy subjects. Nitric oxide-mediated vasodilatory (sodium nitroprusside) and adrenergic vasoconstrictor (noradrenaline) agonists were iontophoresed in lidocaine/prilocaine-treated and control forearm skin in nine healthy subjects during blood flow assessment (laser Doppler flowmetry, expressed as% from baseline cutaneous vascular conductance; CVC; flux/mean arterial pressure).
Non-linear regression curve fitting identified no change in the ED50 of ACh-induced sweating after sensory blockade (−1.42 ± 0.23 logM) compared to control (−1.27 ± 0.23 logM; P > .05) or in Emax (0.43 ± 0.08 with, 0.53 ± 0.16 mg cm−2 min−1 without lidocaine/prilocaine; P > .05). Sensory blockade did not alter the vasodilator response to sodium nitroprusside (1280 ± 548% change from baseline CVC with, 1204 ± 247% without lidocaine/prilocaine) or vasoconstrictor response to noradrenaline (−14 ± 4% change from baseline CVC with, −22 ± 14% without lidocaine/prilocaine; P > 0.05).
Cutaneous sensory blockade does not appear to alter nitric oxide-mediated vasodilation, adrenergic vasoconstriction, or cholinergic eccrine sweating dose-response sensitivity or responsiveness to maximal dose. Thus, lidocaine/prilocaine treatment should not affect sweat gland function or have blood flow implications for subsequent research protocols or clinical procedures.
Issue Informationhttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12006Issue Information2013-03-26T04:25:30.630744-05:00doi:10.1111/aap.12006John Wiley & Sons, Inc.10.1111/aap.12006http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12006Issue InformationiiTramadol inhibits the contractility of isolated human myometriumhttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12003Tramadol inhibits the contractility of isolated human myometriumN. H. Shah, E. Thomas, R. Jose, J. Peedicayil2013-02-22T02:55:20.140281-05:00doi:10.1111/aap.12003John Wiley & Sons, Inc.10.1111/aap.12003http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12003Original Article15Summary
This study was conducted to determine whether the atypical opioid analgesic tramadol inhibits the contractility of isolated non-pregnant human myometrium. Ten strips of non-pregnant human myometrium stimulated with 55 mm potassium chloride (KCl) were treated with three concentrations (30, 100 and 300 μm) of tramadol to test for any inhibitory effect of tramadol. The effects of concurrent administration of the ß adrenoceptor antagonist propranolol (1 μm), the guanylyl cyclase and nitric oxide synthase inhibitor methylene blue (20 μm) and the opioid receptor antagonist naloxone (100 μm) with tramadol were also studied.
Tramadol caused a concentration-dependent inhibition of KCl-induced myometrial contractility, which was statistically significant at all three concentrations of tramadol used. Propranolol significantly reversed the inhibitory effect of 100 μm tramadol on KCl-induced myometrial contractility but not that of 300 μm tramadol. Neither methylene blue nor naloxone reversed the inhibitory effect of tramadol on KCl-induced myometrial contractility.
These results suggest that tramadol inhibits KCl-induced contractility of isolated human myometrium. They also suggest that tramadol relaxes the myometrium due to stimulation of ß1 adrenoceptors. However, the concentrations of tramadol required to relax the myometrium were high and likely to be attained at toxic doses, rather than therapeutic doses, of tramadol.
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This study was conducted to determine whether the atypical opioid analgesic tramadol inhibits the contractility of isolated non-pregnant human myometrium. Ten strips of non-pregnant human myometrium stimulated with 55 mm potassium chloride (KCl) were treated with three concentrations (30, 100 and 300 μm) of tramadol to test for any inhibitory effect of tramadol. The effects of concurrent administration of the ß adrenoceptor antagonist propranolol (1 μm), the guanylyl cyclase and nitric oxide synthase inhibitor methylene blue (20 μm) and the opioid receptor antagonist naloxone (100 μm) with tramadol were also studied.
Tramadol caused a concentration-dependent inhibition of KCl-induced myometrial contractility, which was statistically significant at all three concentrations of tramadol used. Propranolol significantly reversed the inhibitory effect of 100 μm tramadol on KCl-induced myometrial contractility but not that of 300 μm tramadol. Neither methylene blue nor naloxone reversed the inhibitory effect of tramadol on KCl-induced myometrial contractility.
These results suggest that tramadol inhibits KCl-induced contractility of isolated human myometrium. They also suggest that tramadol relaxes the myometrium due to stimulation of ß1 adrenoceptors. However, the concentrations of tramadol required to relax the myometrium were high and likely to be attained at toxic doses, rather than therapeutic doses, of tramadol.
The role of NO in the posterior hypothalamus in amygdala-generated pressor responses in conscious ratshttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12004The role of NO in the posterior hypothalamus in amygdala-generated pressor responses in conscious ratsH. Özyurt Bayraktar, H. Yananlı, B. Terzioğlu, Ş. Oktay, M. Kaleli, M. Z. Gören2013-03-06T04:06:07.236072-05:00doi:10.1111/aap.12004John Wiley & Sons, Inc.10.1111/aap.12004http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12004Original Article716Summary
The nitrergic system modulates cardiovascular functions of the central nucleus of amygdala (CeA) and the posterior hypothalamus (PH) which are involved in the central regulation of the cardiovascular system. The aim of this study was to investigate the contribution of nitric oxide (NO) in the PH in eliciting cardiovascular responses produced through electrical stimulation (ES) of the CeA. Rats were implanted with a stimulation electrode and a parenchymal cannula system into the CeA and a parenchymal cannula or a microdialysis probe into the PH. The next day, the femoral artery was cannulated for haemodynamic measurement. The CeA was electrically stimulated to produce cardiovascular response. The nitric oxide synthetase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 400 nmol/100 nl) or artificial cerebrospinal fluid were injected into the PH or the CeA before the ES of the CeA. The dialysates were collected from the PH to determine the L-citrulline and the L-glutamic acid levels.
L-NAME injection into the CeA but not to the PH suppressed the increases in the mean arterial pressure produced by the ES of the CeA significantly; however, heart rate was not affected by L-NAME injection into either the PH or the CeA. L-citrulline and L-glutamic acid levels in the PH were shown to be increased by the ES of the CeA.
NO is involved between the PH and the CeA which has a considerable role in the central regulation of the cardiovascular system.
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The nitrergic system modulates cardiovascular functions of the central nucleus of amygdala (CeA) and the posterior hypothalamus (PH) which are involved in the central regulation of the cardiovascular system. The aim of this study was to investigate the contribution of nitric oxide (NO) in the PH in eliciting cardiovascular responses produced through electrical stimulation (ES) of the CeA. Rats were implanted with a stimulation electrode and a parenchymal cannula system into the CeA and a parenchymal cannula or a microdialysis probe into the PH. The next day, the femoral artery was cannulated for haemodynamic measurement. The CeA was electrically stimulated to produce cardiovascular response. The nitric oxide synthetase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 400 nmol/100 nl) or artificial cerebrospinal fluid were injected into the PH or the CeA before the ES of the CeA. The dialysates were collected from the PH to determine the L-citrulline and the L-glutamic acid levels.
L-NAME injection into the CeA but not to the PH suppressed the increases in the mean arterial pressure produced by the ES of the CeA significantly; however, heart rate was not affected by L-NAME injection into either the PH or the CeA. L-citrulline and L-glutamic acid levels in the PH were shown to be increased by the ES of the CeA.
NO is involved between the PH and the CeA which has a considerable role in the central regulation of the cardiovascular system.
Neuromuscular blocking effect of fluoxetine and its interaction with rocuroniumhttp://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12005Neuromuscular blocking effect of fluoxetine and its interaction with rocuroniumJ. C. Patel, M. J. Barvaliya, T. K. Patel, C. B. Tripathi2013-03-06T04:05:46.075768-05:00doi:10.1111/aap.12005John Wiley & Sons, Inc.10.1111/aap.12005http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Faap.12005Original Article1724Summary
As selective serotonin reuptake inhibitors have an inhibitory effect on nicotinic acetylcholine receptors, they may affect the neuromuscular transmission and interact with neuromuscular blockers. This study was designed to observe the effect of fluoxetine on neuromuscular transmission and its interaction with rocuronium using the rat phrenic nerve hemidiaphragm and rabbit head drop methods.
Rat phrenic nerve hemidiaphragms were mounted and stimulated using a train of four pulses (TOF). The effect of fluoxetine was studied on both indirectly and directly stimulated basal twitch responses by plotting cumulative dose response curves (DRCs). DRCs of rocuronium were obtained in the absence, and presence of 5 μm and 20 μm fluoxetine to study its interaction. ED5, ED50 and ED95 values of rocuronium DRCs in absence and presence of fluoxetine were calculated.
Fluoxetine significantly inhibited twitch responses in both indirect and directly stimulated preparations. Fluoxetine (20 μm) caused an increase in the potency of rocuronium such that the ED50 and ED95 values of rocuronium DRCs were significantly decreased. Partially inhibited twitch responses by fluoxetine (100 μm) were not reversed by neostigmine (3.3 μm) or 3,4 diaminopyridine (0.25 μm).
Rabbits were given fluoxetine 0.25 mg kg−1 and 1 mg kg−1 orally for 15 days, and on 15th day, rocuronium infusion was given, and time for head drop was recorded. The time of head drop was significantly reduced in fluoxetine pretreated as compared to control group.
Fluoxetine blocks the neuromuscular transmission and increases the potency of rocuronium-induced neuromuscular block.
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As selective serotonin reuptake inhibitors have an inhibitory effect on nicotinic acetylcholine receptors, they may affect the neuromuscular transmission and interact with neuromuscular blockers. This study was designed to observe the effect of fluoxetine on neuromuscular transmission and its interaction with rocuronium using the rat phrenic nerve hemidiaphragm and rabbit head drop methods.
Rat phrenic nerve hemidiaphragms were mounted and stimulated using a train of four pulses (TOF). The effect of fluoxetine was studied on both indirectly and directly stimulated basal twitch responses by plotting cumulative dose response curves (DRCs). DRCs of rocuronium were obtained in the absence, and presence of 5 μm and 20 μm fluoxetine to study its interaction. ED5, ED50 and ED95 values of rocuronium DRCs in absence and presence of fluoxetine were calculated.
Fluoxetine significantly inhibited twitch responses in both indirect and directly stimulated preparations. Fluoxetine (20 μm) caused an increase in the potency of rocuronium such that the ED50 and ED95 values of rocuronium DRCs were significantly decreased. Partially inhibited twitch responses by fluoxetine (100 μm) were not reversed by neostigmine (3.3 μm) or 3,4 diaminopyridine (0.25 μm).
Rabbits were given fluoxetine 0.25 mg kg−1 and 1 mg kg−1 orally for 15 days, and on 15th day, rocuronium infusion was given, and time for head drop was recorded. The time of head drop was significantly reduced in fluoxetine pretreated as compared to control group.
Fluoxetine blocks the neuromuscular transmission and increases the potency of rocuronium-induced neuromuscular block.