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Volume 53 (2003)
- Issue 6 Pages 389-
- Issue 5 Pages 319-
- Issue 4 Pages 253-
- Issue 3 Pages 157-
- Issue 2 Pages 71-
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Volume 53, Issue 2
Displaying 1-9 of 9 articles from this issue
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Regular Papers
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Naoki Hayama, Tetsuri Kondo, Ichiro Kobayashi, Gen Tazaki, Kenji Eguch ...2003 Volume 53 Issue 2 Pages 71-76
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThis study tested the hypothesis that intrathoracic bronchi intermittently constrict during coughing and attempted to elucidate the effect on explosive flow. The subjects were 21 dogs having undergone tracheostomy. In the first group A (n = 7), the diameter of the fifth-generation bronchus was measured with a balloon-tipped catheter and the change during coughing was analyzed. In the other group (n = 14), the dogs were vagotomized and coughing was simulated by sequential application of positive and negative airway pressures (sham cough). The effects of the bronchial constriction, elicited by the stimulation of vagus efferent fibers, on explosive flow and airway pressure of sham cough were analyzed. The bronchus was constricted in explosive phase of spontaneous coughing in all the dogs of the first group. When cough bouts were repetitively developed, bronchial constriction and phrenic burst developed simultaneously. The intermittent bronchial constrictions fused and virtually acted as tonic constriction. In the second group of dogs the explosive flow of sham cough consisted of two phases; a short bout followed by a near-constant flow. When the bronchus was constricted, the explosive flow was still biphasic in 12 dogs and an exponential decay pattern formed in 2 of them. In these 12 dogs, the peak explosive flow slightly but significantly decreased (mean ± SD, 1.39 ± 0.23 vs. 1.34 ± 0.23 l/s) and airway pressure in the segmental bronchus became smaller (−1.18 ± 0.53 vs. −0.15 ± 0.94 cmH2O). We concluded that intermittent bronchial constrictions act as tonic one during coughing. Bronchial constriction slightly decreased the peak explosive flow and moved the choke point to the proximal airway.
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Aicha Bouhlel, Wissam H. Joumaa, Claude Léoty2003 Volume 53 Issue 2 Pages 77-87
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThe effect of 8 weeks of nandrolone decanoate treatment (15 mg kg−1/week, 5 weeks under normal conditions followed by 3 weeks of unloading) was tested for the voltage-dependence of activation and steady-state inactivation of contraction in isolated small bundles (2–4 cells) of intact slow-twitch skeletal muscle in rats. Twenty-four male rats were divided into three groups (8 rats/group, weight matched) for 8 weeks: (1) control, (2) unloaded, and (3) unloaded-treated. Compared with age-matched control values (unloaded vs. control), suspension induced a shift in the isometric tension characteristics toward fast-twitch types in the soleus muscle. In contrast, nandrolone decanoate treatment of suspended animals reduced unweighting-induced atrophy in the muscle and maintained: (1) the relative amplitude of twitch tension to the maximal Ca2+ activated in saponin-treated fibers (control: 3.6 ± 0.4%, unloaded: 6.9 ± 1.1% and unloaded-treated: 4.6 ± 0.2%), (2) the time to peak tension (control: 130 ± 18 ms, unloaded: 85 ± 12 ms and unloaded-treated: 110 ± 11 ms), (3) the time constant of relaxation (control: 320 ± 12 ms, unloaded: 120 ± 13 ms and unloaded-treated: 349 ± 20 ms), (4) the relative amplitude of K+ contracture tension to the maximal Ca2+ activated in saponin-treated fibers (control: 82.9 ± 3.1%, unloaded: 65.1 ± 2.8%, and unloaded-treated: 91.7 ± 1.9%), (5) the potential at 50% of the activation curve (control: −40.4 ± 1.2 mV, unloaded: −35.5 ± 1.6 mV, and unloaded-treated: −48.4 ± 1.2 mV), and (6) the potential at 50% of the inactivation curve (control: 42.2 ± 1.9 mV, unloaded: −34.5 ± 1.1 mV, and unloaded-treated: −37.9 ± 1.1 mV). This study clearly shows that treatment with anabolic-androgenic steroids can prevent atrophy and functional changes induced by 3 weeks of unweighting in rat skeletal muscles.
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Yumiko Doi, Junichi Araki, Waso Fujinaka, Takahiko Kiyooka, Yu Oshima, ...2003 Volume 53 Issue 2 Pages 89-96
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThe recirculation fraction of intramyocardial Ca2+ (RF) has conventionally been obtained from the monotonic decay of postextrasystolic potentiation (PESP). The used assumption is that the decay is exponential. However, we have found that PESP usually decays in alternans even at spontaneous heart rates (>100 beats/min) in excised, cross-circulated canine heart preparations under normal coronary perfusion and normothermia. We have already devised a means of extracting the exponential decay component for RF calculation by subtracting the oscillatory component from the alternans PESP decay by a curve-fitting method. Using mathematics, we assessed the possible error in estimated RF when an exponential curve was naively fit to the alternans PESP decay. We obtained results showing that the exponential assumption may considerably underestimate RF even when the alternans is trivial with the oscillatory component of only 10% of the exponential component.
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Hidehiko Komine, Kanji Matsukawa, Jun Murata, Hirotsugu Tsuchimochi, K ...2003 Volume 53 Issue 2 Pages 97-103
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThe aim of this study was to examine whether or not stimulation of the hypothalamic defense area is capable of inducing sympathetic vasodilatation of the forelimb vascular bed in anesthetized cats. When the hypothalamic defense area was electrically stimulated, brachial blood flow velocity (brachial BFV) and vascular conductance were increased as well as femoral BFV and vascular conductance. Brachial BFV and vascular conductance increased by 110–139% during hypothalamic stimulation. These increases were blunted to approximately one-fifth of the control responses following i.v. injection of a synthesis inhibitor of nitric oxide, Nω-nitro-L-arginine methyl ester (L-NAME). The attenuating effect of L-NAME on forelimb vasodilatation evoked by hypothalamic stimulation was greater than that on hindlimb vasodilatation. The combined administration of L-NAME and atropine sulfate eliminated nearly all of the increases in brachial BFV and vascular conductance during hypothalamic stimulation. From the present results, we conclude that stimulation of the hypothalamic defense area is able to induce neurogenic vasodilatation of the cat forelimb vascular bed, which is greatly mediated with a nitric oxide mechanism. The contribution of nitric oxide to neurogenic vasodilatation seems to be greater in the forelimbs than hindlimbs.
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Satoshi Matsuoka, Nobuaki Sarai, Shinobu Kuratomi, Kyoichi Ono, Akinor ...2003 Volume 53 Issue 2 Pages 105-123
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSIndividual ion channels or exchangers are described with a common set of equetions for both the sinoatrial node pacemaker and ventricular cells. New experimental data are included, such as the new kinetics of the inward rectifier K+ channel, delayed rectifier K+ channel, and sustained inward current. The gating model of Shirokov et al. (J Gen Physiol 102: 1005–1030, 1993) is used for both the fast Na+ and L-type Ca2+ channels. When combined with a contraction model (Negroni and Lascano: J Mol Cell Cardiol 28: 915–929, 1996), the experimental staircase phenomenon of contraction is reconstructed. The modulation of the action potential by varying the external Ca2+ and K+ concentrations is well simulated. The conductance of ICaL dominates membrane conductance during the action potential so that an artificial increase of Ito, IKr, IKs, or IKATP magnifies ICaL amplitude. Repolarizing current is provided sequentially by IKs, IKr, and IK1. Depression of ATP production results in the shortening of action potential through the activation of IKATP. The ratio of Ca2+ released from SR over Ca2+ entering via ICaL (Ca2+ gain = ∼15) in excitation-contraction coupling well agrees with the experimental data. The model serves as a predictive tool in generating testable hypotheses.
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Nobuaki Sarai, Satoshi Matsuoka, Shinobu Kuratomi, Kyoichi Ono, Akinor ...2003 Volume 53 Issue 2 Pages 125-134
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThis paper discusses the development of a cardiac sinoatrial (SA) node pacemaker model. The model successfully reconstructs the experimental action potentials at various concentrations of external Ca2+ and K+. Increasing the amplitude of L-type Ca2+ current (ICaL) prolongs the duration of the action potential and thereby slightly decreases the spontaneous rate. On the other hand, a negative voltage shift of ICaL gating by a few mV markedly increases the spontaneous rate. When the amplitude of sustained inward current (Ist) is increased, the spontaneous rate is increased irrespective of the ICaL amplitude. Increasing [Ca2+]o shortens the action potential and increases the spontaneous rate. When the spontaneous activity is stopped by decreasing ICaL amplitude, the resting potential is nearly constant (−35 mV) over 1–15 mM [K+]o as observed in the experiment. This is because the conductance of the inward background non-selective cation current balances with the outward [K+]o-dependent K+ conductance. The unique role of individual voltage- and time-dependent ion channels is clearly demonstrated and distinguished from that of the background current by calculating an instantaneous zero current potential ("lead potential") during the course of the spontaneous activity.
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Koji Kashihara, Yousuke Takahashi, Kaori Chatani, Toru Kawada, Can Zhe ...2003 Volume 53 Issue 2 Pages 135-143
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSAlthough the elevation of angiotensin II (Ang II) associated with cardiovascular diseases has been considered to suppress the arterial baroreflex function, how Ang II affects dynamic arterial pressure (AP) regulation remains unknown. The aim of the present study was to elucidate the acute effects of Ang II on dynamic AP regulation by the arterial baroreflex. In seven anesthetized Japanese white rabbits, we randomly perturbed intra-carotid sinus pressure (CSP) according to a binary white noise sequence while recording renal sympathetic nerve activity (RSNA) and AP. We estimated the neural arc transfer function from CSP to RSNA and the peripheral arc transfer function from RSNA to AP before and after 30-min intravenous administration of Ang II (100 ng/kg/min). Ang II increased mean AP from 75.7 ± 3.1 to 95.5 ± 5.1 mmHg (p < 0.01), while it did not affect mean RSNA (from 5.9 ± 1.3 to 5.7 ± 1.2 a.u.). The neural arc transfer functions did not differ before or after Ang II administration (dynamic gain: −0.94 ± 0.04 vs. −0.94 ± 0.13, corner frequency: 0.06 ± 0.01 vs .0.06 ± 0.01 Hz, pure delay: 0.16 ± 0.01 vs. 0.17 ± 0.02 s). The peripheral arc transfer function did not differ before or after Ang II administration (dynamic gain: 1.18 ± 0.05 vs. 1.06 ± 0.11, natural frequency: 0.07 ± 0.01 vs. 0.08 ± 0.01 Hz, damping ratio: 1.19 ± 0.06 vs. 1.24 ± 0.19, pure delay: 0.83 ± 0.06 vs. 0.78 ± 0.05 s). Intravenous Ang II hardly affects the dynamic characteristics of neural and peripheral arc around the physiological operating pressure.
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K. I. Wada, S. Katsuta, H. Soya2003 Volume 53 Issue 2 Pages 145-150
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSIt has been shown that changes in the nuclear number in myofibers are synchronized with myofiber size. Therefore, under some conditions, the myonuclear number is thought to be a determinant factor of myofiber size. However, we have clearly shown that denervation-induced fiber atrophy occurs without any decrease in myonuclear number, indicating that the myonuclear number is not always an important determinant factor of myofiber size. However, this was an event found under experimental conditions. In the present study, we examined the morphological features of single myofibers under normal conditions throughout the lifespan of normal mice. We discovered that the C/N ratio (cell volume/nucleus) greatly increases during the growth period and clearly decreases during the aging period. From 5 weeks to 6 months old, the myofibers undergo fiber hypertrophy accompanied by a decrease in myonuclear number. In muscle at 18 months, we found no correlation between myonuclear number and fiber cross-sectional area. These results suggest that, even under normal physiological conditions, the myonuclear number is not always a determinant factor of the myofiber size.
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Short Communication
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Hironobu Morita, Nobuhiro Fujiki, Taro Gotoh, Tomoko Matsuda, Gao Shua ...2003 Volume 53 Issue 2 Pages 151-155
Published: 2003
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSTo test the hypothesis that the aortic wall is stretched without increasing aortic pressure (AP) during microgravity (μG), the AP, intrathoracic pressure (ITP), and aortic diameter (AD) were measured in anesthetized Sprague-Dawley rats during 4.5 s of μG produced by freefall. A smooth and immediate reduction in gravity (G) occurred during freefall, μG being achieved 100 ms after the start of the drop. Acute μG elicited an immediate increase in AD, which was not accompanied by an increase in AP. However, the ITP decreased during μG resulted in an increase in the calculated transmural pressure (TP = AP−ITP) of the aortic wall. A simple linear regression analysis showed that the slopes of the plot of AP vs. AD differed at 1 G and μG, whereas those for the plot of TP vs. AD did not. Thus, the increase in AD during μG was accounted for by the increase in TP. These results suggest that a decrease in ITP, resulting in an increase in TP of the aorta, is a key issue in understanding cardiovascular responses to μG.
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