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  • 1
    Electronic Resource
    Electronic Resource
    Dynorphins directly inhibit neuronal nicotinic acetylcholine receptors in PC12 cells (2000)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 12 (2000), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The authors have previously reported that dynorphin A (1–17), an endogenous kappa opioid agonist, inhibits the current mediated through neuronal nicotinic acetylcholine receptors (nAChRs) without the involvement of opioid receptors or G-proteins. We have further characterized this action to elucidate the mechanisms. The nicotine-induced current was studied in PC12 cells using patch-clamp techniques. In the whole-cell configuration, four kinds of dynorphins with different lengths, dynorphin A (1–17) (1–13) (2–13) and (1–8), similarly inhibited the nicotine-induced inward current at 1 μm and accelerated the current decay. The inhibition by dynorphin A (1–17) was not antagonized by the increasing concentrations of nicotine. The current–voltage relationship revealed that dynorphin's inhibition was voltage independent at the membrane potentials from −30 to −70 mV. The inhibition was not affected by pretreatment with pertussis toxin (PTX) or inclusion of staurosporine into the pipette solution. The inhibitory effect of dynorphin A (1–17) was well preserved in the outside-out patch configuration. Analysis of the nicotine-induced noise and single-channel kinetics revealed that dynorphin A(1–17) reduced open time without changing the amplitude of the unitary current. We found that the inhibitory effect on neuronal nAChRs is shared by all four dynorphins studied. The inhibition appears to be non-competitive and voltage independent. The outside-out recording together with other experiments indicated that a major part of this inhibition is not mediated through cytoplasmic messengers, but based on the direct action of dynorphins on neuronal nAChRs leading to the reduction of open time.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2000.00012.x
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  • 2
    Electronic Resource
    Electronic Resource
    Pulmonary hypertensive response to declamping of the aorta during abdominal aortic reconstructive surgery—role of metabolic derangement and anaphylatoxin in the reaction (1990)
    Springer
    Journal of anesthesia 4 (1990), S. 29-34 
    Details
    ISSN: 1438-8359
    Keywords: Aortic aneurysm ; Aortic declamping ; Pulmonary hypertension ; Anaphylatoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Metabolic parameters and anaphylatoxin activities in mixed venous blood were measured in 16 patients undergoing abdominal aortic reconstructive surgery to study the mechanism of pulmonary hypertensive response after aortic declamping. This reaction was confirmed by a rise in ratio between mean pulmonary arterial pressure and mean systemic arterial pressure (Pp/Ps). Aortic declamping was followed by a significant increase in lactate level and lactate-pyruvate ratio (L/P ratio) as compared with pre-declamping level (P ≪ 0.01). Although anaphylatoxin C3a concentration rose significantly after declamping (P ≪ 0.01), C5a showed no change at any stage. When the patients were divided into two groups according to the degree of Pp/Ps change by declamping, significant elevation of L/P ratio and C3a level were observed in the group with higher increase (Post-/Pre-declamp value ≧1.25) of Pp/Ps compared to the lower (≫1.25) group. After declamping, in the higher Pp/Ps group, a positive correlation existed not only between Pp/Ps change and aortic clamp time, but also between L/P ratio and C3a level. The present results suggest that muscular metabolic derangement distal to the aortic clamp may play an important role in the development of post-declamping pulmonary hypertensive response through anaphylatoxin C3a. (Wakamatsu M, Minamoto Y, Okumura F: Pulmonary hypertensive response to declamping of the aorta during abdominal aortic reconstructive surgery. J Anesth 4: 29–34, 1990)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054000040029
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  • 3
    Electronic Resource
    Electronic Resource
    Anesthetic management for implantation of the left ventricular assist device (1987)
    Springer
    Journal of anesthesia 1 (1987), S. 183-186 
    Details
    ISSN: 1438-8359
    Keywords: Cardiac anesthesia ; Ventricular assist device ; Heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054070010183
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  • 4
    Electronic Resource
    Electronic Resource
    Fentanyl antagonizes diazepam on carotid sinus baroreflex control of circulation in rabbits (1993)
    Springer
    Journal of anesthesia 7 (1993), S. 210-217 
    Details
    ISSN: 1438-8359
    Keywords: Carotid occlusion ; Drug interaction ; Arterial baroreflex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the effects of a combination of fentanyl and diazepam on carotid sinus baroreflex in conscious rabbits, we examined the responses of mean systemic arterial pressure (MAP), heart rate (HR) and total peripheral resistance (TPR) to bilateral carotid occlusion (BCO). Seven rabbits were given 0.5 mg·kg−1 of diazepam i.v. followed by 10 mg·kg−1 of fentanyl i.v. at 5 min intervals (group 1), and the drugs were given in the reverse order to 5 other rabbits (group 2). BCO was repeated in conscious state (control) and after each drug injection. MAP responses did not differ from control response in either group when both drugs were given. In group 1, however, diazepam decreased HR response to 71.4% of control, and increased TPR response by 36%. Fentanyl administration reversed diazepam-induced changes in BCO responses to the control level. In group 2, fentanyl decreased TPR response to 61.6% of control and increased HR response by 41.5%. Administration of diazepam following fentanyl restored HR and TPR responses to control levels. Carotid sinus baroreflex gain was 3.1 ± 0.4 (mean ± SEM) in control and 3.1 ± 0.4 after administration of both drugs in 12 rabbits. The results suggest that a sedative dose of either fentanyl or diazepam antagonizes the other drug’s action on the carotid sinus baroreflex. The combination of fentanyl and diazepam has little influence on carotid sinus baroreflex control of the circulation in rabbits. (Sakamoto M, Ohsumi H, Sumida T, et al.: Fentanyl antagonizes diazepam on carotid sinus baroreflex control of circulation in rabbits. J Anesth 7: 210–217, 1993)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054030070210
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of continuous negative extrathoracic pressure ventilation on left ventricular dimensions and hemodynamics in dogs (1993)
    Springer
    Journal of anesthesia 7 (1993), S. 308-315 
    Details
    ISSN: 1438-8359
    Keywords: Negative pressure ventilation ; Hemodynamics ; Preload ; Transesophageal echocardiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been reported that continuous negative extrathoracic pressure ventilation (CNETPV) depresses cardiac output less than continuous positive pressure ventilation (CPPV) does, and this difference may be related to the different effects of two ventilatory modes on preload. We performed simultaneous measurements of hemodynamics and left ventricular short axis dimensions by transesophageal echocardiography (TEE) to evaluate left ventricular preload and function during CNETPV and CPPV in normal dogs. Hemodynamic measurements and simultaneous TEE recording were performed at 5 successive periods; 1) the first control period of intermittent positive pressure ventilation (IPPV1), 2) CNETPV with negative end-expiratory pressure (NEEP) of −10 cmH2O (CNET10), 3) CNETPV with NEEP of −15 cmH2O (CNET15), 4) the second control period of IPPV (IPPV2), and 5) CPPV with PEEP of 15 cmH2O (CPPV15). Left ventricular end-systolic and end-diastolic dimension (LVESD and LVEDD), ejection fraction (EF) and fractional shortening (FS) were measured from TEE recordings. Both CNET10 and CNET15 induced no significant changes in hemodynamics and left ventricular dimensions, compared with those during IPPV1. However, CPPV15 reduced cardiac output and stroke volume (SV) and increased heart rate significantly, compared with IPPV2. CPPV15 significantly decreased LVEDD compared with IPPV2. Neither EF nor FS showed any significant change throughout the experiment. These results indicate that CNETPV preserved cardiac output because it maintained the preload and the left ventricular function. (Andoh T, Doi H, Kudoh I, et al.: Effects of continuous negative extrathoracic pressure ventilation on left ventricular dimensions and hemodynamics in dogs. J Anesth 7: 308–315, 1993)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054030070308
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of halothane on carotid occlusion in rabbits (1993)
    Springer
    Journal of anesthesia 7 (1993), S. 218-225 
    Details
    ISSN: 1438-8359
    Keywords: Halothane ; Carotid sinus baroreflex ; Reflex control of circulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of halothane on the carotid sinus baroreflex control of circulation were stuied in chronically instrumented rabbits. The carotid sinus baroreflex was evaluated by the hemodynamic responses to bilateral carotid occlusion (BCO). Either 0.5 or 1.0 MAC of halothane inhalation did not alter mean arterial pressure (MAP) or total peripheral resistance (TPR), but significantly increased heart rate (HR). Carotid occlusion produced a significant increase in MAP and HR, and both responses were attenuated dose-dependently by halothane. Halothane depressed the reflex gain of arterial pressure from 3.5 ± 0.3 at conscious state to 1.3 ± 0.2 at 1.0 MAC halothane. Response of cardiac output (CO) to BCO was attenuated significantly only at 1.0 MAC compared with those responses at conscious state and at 0.5 MAC. Response of TPR was attenuated at both 0.5 and 1.0 MAC halothane as compared with at conscious state but no significant defference existed between the two concentrations of halothane. These data suggested that halothane could attenuate the carotid occlusion responses to various degrees in the involved effector componets. 0.5 MAC halothane attenuated MAP response to BCO predominantly by attenuating reflex peripheral vasoconstriction. The reduced CO response was mainly responsible for further attenuation of MAP response at 1.0 MAC halothane. (Sumida T, Ohsumi H, Yamazaki T, et al.: Effects of halothane on carotid occlusion in rabbits. J Anesth 7: 218–225, 1993)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054030070218
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