巻号一覧
55 巻, 2 号
選択された号の論文の8件中1～8を表示しています
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Regular Papers
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Takeo Tanaami, Hideyuki Ishida, Hidetaka Seguchi, Yuki Hirota, Toshie ...2005 年 55 巻 2 号 p. 81-91
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/04/28ジャーナル フリーIntracellular [Ca2+] ([Ca2+]i) was imaged in atrial and ventricular rat myocytes by means of a high-speed Nipkow confocal microscope. Atrial myocytes with an absent t-tubule system on 8-di- ANEPPS staining showed an initial rise in Ca2+ at the periphery of the cell, which propagated to the interior of the cell. Ventricular myocytes showed a uniform rise in [Ca2+]i after electrical stimulation, consistent with a prominent t-tubular network. In atrial myocytes, there was a much shorter time between the peak of the [Ca2+]i transient and the peak contraction as compared to ventricular myocytes. A regional release of Ca2+ induced by an exposure of one end of the myocyte to caffeine with a rapid solution switcher resulted in a uniform propagation of Ca2+ down the length of the cell in atrial myocytes, but we found no propagation in ventricular myocytes. A staining with rhodamine 123 indicated a much greater density of mitochondria in ventricular myocytes than in atrial myocytes. Thus the atrial myocytes display a lack of “local control” of Ca2+ release, with propagation after the Ca2+ release at the periphery induced by stimulation or at one end of the cell induced by exposure to caffeine. Ventricular myocytes showed the presence of local control, as indicated by an absence of the propagation of a local caffeine-induced Ca2+ transient. We suggest that this finding, as well as a reduced delay between the peak of the [Ca2+]i transient and the peak shortening in atrial myocytes, could be due in part to reduced Ca2+ buffering provided by mitochondria in atrial myocytes as opposed to ventricular myocytes.
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Tomohiko Takei, Toshihiro Hashimoto, Nobuhiro Hagura, Michikazu Matsum ...2005 年 55 巻 2 号 p. 93-99
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/04/28ジャーナル フリーElectrophysiological studies have shown that cortico-spinal excitability increases during the motor preparation period in reaction time (RT) paradigms. However, there is a line of contradictory evidence with transcranial magnetic stimulation (TMS) showing that its excitability is reduced during the preparation period. In these studies, the subjects can predict the TMS timings. Thus we investigated how the predictability of TMS timing affects cortico-spinal excitability. A single-pulse TMS was delivered to the hand section of the left motor cortex while seven right-handed subjects relaxed their hands in a flexed position. We prepared three conditions: (i) in the semi-PREDICTABLE condition, two visual stimuli at 500 ms interval were presented and the TMS was delivered either 0, 125, 250, 375, or 500 ms after the first stimulus; (ii) in the PREDICTABLE condition, the TMS was provided only at 500 ms after the first stimulus; (iii) in the UNPREDICTABLE condition, no visual cue preceded the TMS. We recorded motor evoked potentials (MEPs) from the wrist flexor and extensor muscles. We found a significant reduction of MEP amplitude in the flexor muscles in both the PREDICTABLE and semi-PREDICTABLE conditions, but not in the UNPREDICTABLE condition. These results showed that the predictability of TMS per se, without the preparation of motor outputs, can reduce cortico-spinal excitability.
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Tomonobu Sakurai, John Hollander, Stacey L. Brickson, Hideki Ohno, Li ...2005 年 55 巻 2 号 p. 101-107
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/04/28ジャーナル フリーThis study investigated the changes in nitric oxide (NO) together with inducible nitric oxide synthase (iNOS) content and enzyme activity at 0, 4, 12, 24, and 48 h following acute muscle stretch injury. A single stretch injury was induced to the tibialis anterior muscle of 30 male New Zealand white rabbits (n = 6 at each time point). Injured and uninjured contralateral sham-operated muscles were harvested and analyzed for NO levels, iNOS content, and iNOS activity at each time point. Furthermore, three animals were used to estimate baseline NO levels and iNOS activity. There was a progressive reduction in NO content in the injured and the sham-operated muscles up to 24 h postoperation and stretch injury (p < 0.05). At 48 h postinjury, however, NO levels were 146% higher in injured muscles than in sham-operated muscles (p < 0.05). iNOS protein content was higher at 4 h and 48 h in injured versus shamoperated muscles (p < 0.05). Similarly, iNOS activity was higher at 4 h (p < 0.05) and at 48 h (p < 0.01) in injured versus sham-operated muscles. These results suggest that NO may play an active role during the postinjury recovery of skeletal muscle modulated by iNOS expression.
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Takeshi Hashimoto, Atsushi Sugiyama, Sadayoshi Taguchi2005 年 55 巻 2 号 p. 109-115
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/05/03ジャーナル フリーWe investigated whether the shift of cardiac myosin heavy chain (MHC) isoform observed during exposure to hypoxia is secondary to hypertrophy, or whether it is directly related to the hypoxic stress. Twelve male Wistar-Kyoto rats, 14 weeks old, were randomly assigned to two groups: sea-level control group (CO) and hypoxia group (HX). The CO group was housed 4 weeks at 1,011 hPa, and the HX group was housed for 4 weeks at 701 hPa. The expression of MHC-β was significantly increased (600%) in the HX group as compared to the CO group in the right ventricle (p < 0.01). An increased ventricular mass induced by hypoxic exposure was associated with an increased expression of MHC-β in the right ventricle (p < 0.05). In the left ventricle, the MHC-b expression was significantly increased (295%) in the HX group as compared to the CO group without ventricular hypertrophy (p < 0.01). No differences were observed in the adenylyl cyclase activity or in the phosphodiesterase activities in both ventricles between the CO and HX groups (p > 0.05). Oxidative enzymatic activities (citrate synthase and three-hydroxyacyl-CoA dehydrogenase) were unchanged in both ventricles following 4 weeks of hypoxia (p > 0.05). These findings suggest that, besides cardiac hypertrophy, the hypoxia-induced adaptational change to the MHC-b isoform may be mediated through a specific mechanism related to the stress of hypoxia.
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Effects of Naloxone on Respiratory Sensation before and after a Removal of Severe Respiratory StressTakashi Nishino, Shiroh Isono, Norihiro Shinozuka, Teruhiko Ishikawa2005 年 55 巻 2 号 p. 117-126
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/05/12ジャーナル フリーSevere respiratory stress causes dyspnea, and a sudden release of this stress frequently accompanies a euphoric sensation. We hypothesized that acute severe respiratory stress may result in an elaboration of endogenous opioids within the central nervous system, and that these opioids may play significant roles in relieving dyspnea and generating euphoric sensation after a sudden removal of the stress. To test this hypothesis, we examined the effects of naloxone (0.04 mg/kg, I.V.) and the placebo (normal saline) on changes in respiratory sensation before and after the release of severe respiratory stress in a double-blind, randomized, crossover study in 14 healthy adults. Acute severe respiratory stress was induced by loaded breathing with a combination of resistive loading and hypercapnia. The subjects rated their changes in sensation by using a bidirectional visual analogue scale. Naloxone pretreatment affected neither the ventilation nor the development of dyspneic sensation during loaded breathing. Naloxone pretreatment only slightly attentuated the euphoric sensation developed after the release of severe respiratory stress. These findings suggest a small role of opioids in relieving dyspnea and in generating euphoria before and after a sudden removal of stress.
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Does Chronic Experimental Head-Down Tilt Alter Intramural Innervation Density of Limb Blood Vessels?M. Lóránt, G. Raffai, G. Nádasy, E. Fehér, ...2005 年 55 巻 2 号 p. 127-134
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/05/14ジャーナル フリーEarlier, substantial increases in the intramural sympathetic innervation density of rat hind-limb blood vessels were found after 2 weeks of experimental orthostasis with tubular 45° head-up tilt cages. In the present study, we presumed that chronic head-down tilting induces opposite changes in the innervation density. Tilted rats were kept 45° head-down in long tubular cages for either 2 or 4 weeks (HDT2, HDT4), and the control animals were maintained in horizontal tilt cages for the same period (HOR2, HOR4). Segments of the saphenous and brachial veins and arteries were used for quantitative electron microscopic examinations. Intramural innervation density was defined by nerve terminal density (NTD) and synaptic microvesicle count (SVC) within the vascular adventitia. Neither HDT2 nor HDT4 resulted in a decrease of NTD or SVC of the saphenous and brachial veins or arteries; instead, a tendency to increase was observed in some cases. Thus in contrast to the large increases we found earlier in hind-limb vascular innervation density after 2 weeks of head-up tilting, head-down tilting of the same duration—or even twice as long—did not decrease the adventitial innervation density in our model. We assume that the quasi-free locomotor exercise the tilted animals in the long tubular cages were allowed may counteract a possible suppressive effect of chronic head-down tilt on hind-limb vascular innervation density.
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Juichiro Shimizu, Satoshi Mohri, Gentaro Iribe, Haruo Ito, Terumasa Mo ...2005 年 55 巻 2 号 p. 135-142
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/05/19ジャーナル フリーLeft ventricular (LV) O2 consumption (Vo2) per minute is measurable for both regular and arrhythmic beats. LV Vo2 per beat can then be obtained as Vo2 per minute minute divided by heart rate per minute minute for regular beats, but not for arrhythmic beats. We have established that Vo2 of a regular stable beat is predictable by Vo2 = a PVA + b Emax + c, where PVA is the systolic pressure-volume area as a measure of the total mechanical energy of an individual contraction and Emax is the end-systolic maximum elastance as an index of ventricular contractility of the contraction. Furthermore, a is the O2 cost of PVA, b is the O2 cost of Emax, and c is the basal metabolic Vo2 per beat. We considered it theoretically reasonable to expect that the same formula could also predict LV Vo2 of individual arrhythmic beats from their respective PVA and Emax with the same a, b, and c. We therefore applied this formula to the PVA - Emax data of individual arrhythmic beats under electrically induced atrial fibrillation (AF) in six canine in situ hearts. We found that the predicted Vo2 of individual arrhythmic beats highly correlated linearly with either their Vo2 (r = 0.96 ± 0.01) or Emax (0.97 ± 0.03) while both also highly correlated linearly with each other (0.88 ± 0.04). This suggests that the above formula may be used to predict LV Vo2 of absolute arrhythmic beats from their Emax and PVA under AF.
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Short Communication
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Toshishige Shibamoto, Sen Cui, Zonghai Ruan, Yasutaka Kurata2005 年 55 巻 2 号 p. 143-148
発行日: 2005年
公開日: 2005/07/12
[早期公開] 公開日: 2005/04/29ジャーナル フリーMice have frequently been used for a variety of physiological studies because of the development of genetic engineering. However, the characteristics of hepatic vessels such as the vascular resistance distribution and the reactivity to various vasoconstrictors are not known in mice. We therefore determined the basal levels of segmental vascular resistances and the effects of histamine and norepinephrine on the vascular resistance distribution of mice. The liver of male non-inbred ddY mice was excised and perfused via the portal vein with 5% bovine albumin-Krebs solution at a constant flow rate. The sinusoidal pressure was measured by the double occlusion pressure and used to determine the presinusoidal (Rpre) and postsinusoidal (Rpost) resistances. The basal Rpost comprised 53 ± 1% of the total hepatic vascular resistance. The norepinephrine and histamine increased Rpre in a greater magnitude than Rpost with liver weight loss. However, the response to histamine was weaker than that to norepinephrine. Moreover, histamine-induced vasoconstriction showed tachyphylaxis. In conclusion, the presinusoidal and postsinusoidal resistances of mouse livers were similar in magnitude. The presinusoidal vessels predominantly contract in response to norepinephrine and histamine in mouse livers.
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