The Journal of Physiological Sciences
Online ISSN : 1880-6562
Print ISSN : 1880-6546
ISSN-L : 1880-6546
Volume 56, Issue 4
Displaying 1-9 of 9 articles from this issue
Regular Papers
  • Juichiro Shimizu, Satoshi Mohri, Haruo Ito, Hiroki Yamaguchi, Shunji S ...
    2006 Volume 56 Issue 4 Pages 269-274
    Published: 2006
    Released on J-STAGE: September 15, 2006
    Advance online publication: July 13, 2006
    JOURNAL FREE ACCESS
    We analyzed the frequency distribution of the left ventricular (LV) mechanical efficiency of individual arrhythmic beats during electrically induced atrial fibrillation (AF) in normal canine hearts. This efficiency is the fraction of the external mechanical work (EW) in the total mechanical energy measured by the systolic pressure-volume area (PVA). The mean, median, and mode of this efficiency (EW/PVA) were as high as 78%, 80%, and 81%, respectively, on average in six hearts. These high efficiencies were comparable to that of the regular beats in these hearts. The frequency distribution of the EW/PVA during AF tended to skew to the higher side in all the hearts. Since the EW/PVA is directly related to both the ventriculo-arterial (or afterload) coupling ratio (Ea/Emax; Ea = effective arterial elastance, Emax = end-systolic ventricular elastance) and the ejection fraction on a per-beat basis, we also analyzed their frequency distributions. We found them to skew enough to account for the rightward skewed frequency distribution of the EW/PVA during AF with the unexpectedly high mean EW/PVA. These results indicate that the LV arrhythmia during AF per se does not directly suppress the mean level of LV mechanical efficiency in normal canine hearts.
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  • Junhong Gao, Weixing Fu, Zhigao Jin, Xiaochun Yu
    2006 Volume 56 Issue 4 Pages 275-279
    Published: 2006
    Released on J-STAGE: September 15, 2006
    Advance online publication: July 27, 2006
    JOURNAL FREE ACCESS
    The purpose of this study was to determine the cardioprotective effects of the repetitive pretreatment of acupuncture in rats with myocardial ischemia and reperfusion (MIR). Experimental MIR was produced by ligating and reperfusing the left anterior descending coronary artery in the rats. The elevated ST segments of electrocardiogram (ECG), cardiac arrhythmias, and ratio of infarct size/risk zone were compared among the normal control (NC), ischemia and reperfusion (IR), electro-acupuncture (EA), electro-acupuncture plus propranolol (EAP), and EA at nonacupoint (EAN) groups. Before the experiment, EA was applied at bilateral Neiguan acupoints (PC6) in the forelimbs in EA and EAP groups for 30 min once a day for 3 consecutive days. In the EAN group, the same EA treatment was administered at bilateral nonacupoints in the hind limbs. In the EAP group, propranolol, a nonspecific antagonist of β-adrenoceptors, was administered intraperitoneally 15 min before each EA pretreatment. The results showed that the elevated ST segment of ECG, cardiac arrhythmia score, and ratio of infarct size/risk zone were significantly attenuated in the EA group when compared with those in the IR group (P < 0.05), indicating a cardioprotection of EA pretreatment. When propranolol was given before each EA pretreatment in the EAP group, the cardioprotective effect of EA pretreatment was abolished, showing an involvement of β-adrenoceptors in mediating the effect of EA pretreatment. There was no significant cardioprotective effect observed in the EAN group. The results suggest that pretreatment may be a better way to apply acupuncture in the prevention and treatment of coronary heart disease.
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  • R.A. Krasnoperov, S.V. Grachev, V.A. Glumova, A.N. Gerasimov, S.N. Rya ...
    2006 Volume 56 Issue 4 Pages 281-286
    Published: 2006
    Released on J-STAGE: September 15, 2006
    Advance online publication: August 01, 2006
    JOURNAL FREE ACCESS
    This paper studies calcitonin (CT) transport across the C-cell–blood (CCB) barrier in normal rats. The efficiency of this transport is expressed as endogenous calcitonin bioavailability (FCT), i.e., that portion of CT molecules extruded by the thyroid C-cell basal pole that enters the circulating blood. Because currently FCT cannot be estimated directly, a novel methodology was used for its estimation. The essence of this methodology is to assess the CT level before and after the CCB barrier, to study these input-output CT relationships mathematically, and to find the FCT range allowed by the relationships. In this context, the subplasmalemmal granule numerical density in the C-cell basal pole (X) and the CT concentration in the right ventricular blood (Y) were found to be highly correlated: rxy = 0.922, P < 0.001; the covariance coefficient ρxy = 0.9980, P < 0.0001. Clearly, the overall variance of these input-output relationships in the covariance model (√(Varxy) = 6.32) is explained, specifically, by CT retention (RCT) variability at the CCB transport stages. The greater the RCT mean value in the studied rats, the greater is the impact of RCT variability on Varxy. The estimated variance caused by RCT (VarCCBR) makes it possible to determine RCT and FCT (FCT = 100% − RCT). Thus we estimated VarCCBR as VarCCBR < VarxyCVRIA2, where CVRIA2 is CT assay variance: √(VarCCBR) = 6.00% (P ≥ 0.95). We then estimated FCT as the value range that does not contradict the VarCCBR obtained: 62% < FCT < 100% (P ≥ 0.95).
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  • Takashi Ishiguro, Michiko Iwase, Mitsuko Kanamaru, Masahiko Izumizaki, ...
    2006 Volume 56 Issue 4 Pages 287-295
    Published: 2006
    Released on J-STAGE: September 15, 2006
    Advance online publication: August 01, 2006
    JOURNAL FREE ACCESS
    Histaminergic neurons in the hypothalamus are well documented as being involved in the control of autonomic functions, such as the balance of energy metabolism and circadian rhythm. We tested the hypothesis that an activation of the histamine type-1 (H1) receptor is required for the control of ventilation during the course of a day in free-moving mice. Ventilation, aerobic metabolism, and electroencephalogram were measured by a whole-body-plethysmograph, a magnetic-type mass spectrometry system, and a telemetry system, respectively, in H1 receptor-knockout (H1RKO) and wild-type mice. Both genotypes showed daily oscillations in minute ventilation (VE) and oxygen consumption (Vo2), with greater values during the dark period compared to the light period. In the latter, H1RKO mice showed increased VE and CO2 excretion (Vco2) relative to wild-type mice, and VE was comparable to the Vco2 increase. However, there was no change in Vo2 in H1RKO mice, suggesting that differences in Vco2 between genotypes are responsible for differences in VE during the light period. During the dark period, Vco2 was elevated in H1RKO mice compared with WT mice. Because there was no difference in VE, the ratio of VE to Vco2 was reduced in H1RKO mice. Electroencephalogram results suggested that this might be due to a depressed arousal state in H1RKO mice because the ratio of delta to theta band power spectrum densities was greater in H1RKO mice than in wild-type mice. We concluded that histamine modulates ventilation by affecting metabolism and arousal state via H1 receptors.
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  • Shuta Hirano, Yoichiro Kusakari, Jin O-Uchi, Satoshi Morimoto, Makoto ...
    2006 Volume 56 Issue 4 Pages 297-304
    Published: 2006
    Released on J-STAGE: September 15, 2006
    Advance online publication: August 04, 2006
    JOURNAL FREE ACCESS
    Alpha1-adrenoceptor stimulation (α1ARS) shows a positive inotropic effect in most mammalian myocardium. In mouse myocardium, however, α1ARS showed the negative inotropic effect, of which intracellular mechanisms are not fully clarified. The purpose of this study is to investigate the intracellular mechanism of the negative inotropic effect by α1ARS in C57BL/6 mouse myocardium. We used isolated ventricular papillary muscles of C57BL/6 strain mouse which is widely used for genetic manipulation. We simultaneously measured isometric tension and intracellular Ca2+ concentration ([Ca2+]i) using the aequorin method. In twitch contraction, phenylephrine concentration-dependently (1–100 μM) decreased tension without significant changes in the Ca2+ transient, and these effects were completely blocked by prazosin (3 μM) or calphostin C (a PKC inhibitor, 1 μM). Phorbol 12-myristate 13-acetate (PMA) (a PKC activator, 1 μM) decreased tension as observed in phenylephrine. After PMA application, the negative inotropic effect of phenylephrine disappeared. To estimate the Ca2+ sensitivity, tetanic contraction was produced, and the relation between [Ca2+]i and tension at a steady state was measured. Phenylephrine (10 μM) decreased the Ca2+ sensitivity, and PMA showed a similar Ca2+ desensitizing effect. These results suggest that the negative inotropic effect of phenylephrine in mouse myocardium can be explained by the decrease in the Ca2+ sensitivity through the activation of PKC. The present result indicates that the effect of α1ARS differs among species and strains of experiment animals. Thus, we should be careful about using the results of mouse myocardium to understand the functions of the human heart.
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  • Junghoon Kim, Edward B. Arias, Gregory D. Cartee
    2006 Volume 56 Issue 4 Pages 305-312
    Published: 2006
    Released on J-STAGE: September 15, 2006
    Advance online publication: August 26, 2006
    JOURNAL FREE ACCESS
    The purpose of this study was to characterize the effects of prior swim exercise on glucose uptake in isolated skeletal muscles of mice. Male and female mice (C57BL/6) performing 180 min of swimming had significantly decreased glycogen concentration compared to resting controls in soleus, extensor digitorum longus (EDL), and epitrochlearis muscles, regardless of gender. Glucose uptake by isolated muscles was measured using [3H]-2-deoxyglucose without insulin or with 180 pmol/l insulin (20, 75, or 200 min post-exercise and sedentary) or 12,000 pmol/l (20 or 200 min post-exercise and sedentary) in the soleus and EDL and without insulin or with 12,000 pmol/l insulin (20 or 200 min post-exercise and sedentary) in the epitrochlearis. Glucose uptake was higher (P ≤ 0.01) for female versus male mice at each insulin concentration in the soleus and EDL, but not the epitrochlearis. Although prolonged (180 min) swim exercise did not alter subsequent glucose uptake, a shorter duration exercise protocol (60 min) tested in male mice (20 min post-exercise) led to a 1.5-fold increase in insulin-independent glucose uptake in EDL muscles. However, insulin-stimulated (180 pmol/l) glucose uptake was not altered by 60 min exercise in EDL or soleus. In light of these results, swim exercise is not recommended to evaluate the exercise-induced improvement in insulin-stimulated glucose uptake of muscles of C57BL/6 mice.
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