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Volume 52 (2002)
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Volume 52, Issue 5
Displaying 1-12 of 12 articles from this issue
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Regular Papers
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Eriko Kuwabara, Fujiya Furuyama, Kunihisa Ito, Etsuro Tanaka, Naoichir ...2002 Volume 52 Issue 5 Pages 403-408
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSTail blood flow is crucial for dissipating body heat in rats. Angiographies are convenient tools to evaluate tail circulation. However, conventional angiographies do not have sufficient sensitivity or spatial resolution for small vessels. Recently, we developed a novel microangiographic system using monochromatic synchrotron radiation and a high-definition video camera system. Here, we report an evaluation of rat tail circulation under heat stress using the synchrotron radiation microangiographic system. We performed an experiment using the microangiography of the caudal artery before and after heating up WKAH/HkmSlc rats to rectal temperature of 39°C. The images were digitized and temporal subtraction was performed, and the diameters of caudal arteries were evaluated. After heating, the medial caudal artery was markedly dilated (320 ± 53 to 853 ± 243 μm in diameter, plt;0.001), while no significant change was observed in the lateral caudal arteries (139 ± 42 to 167 ± 73 μm) and segmental anastomosing vessels. The heat stress allowed for visualization of the superficial caudal arteries with a diameter of approximately 60 μm, not visible prior to heating. Thus, synchrotron radiation microangiography demonstrated that the rat tail possessed dual sets of arteries; one set was highly sensitive to heat-induced vasodilation (medial caudal artery and superficial caudal arteries) and the other set was less sensitive (lateral caudal arteries and segmental anastomosing vessels).
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Junichi Suzuki2002 Volume 52 Issue 5 Pages 409-419
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThis study was designed to examine the changes in capillary geometry, especially the distribution of arteriolar and venular capillaries, in the skeletal muscles of female Wistar rats after endurance training with and without chronic CoCl2 administration. Four groups of rats were used: non-treated sedentary, non-treated training, Co2+-treated sedentary, and Co2+-treated training. Exercise training by running lasted for 5 weeks at 25 m/min on a 20% gradient, 10–60 min/d, 5 d/week. The Co2+-treated rats drank water containing 0.01% CoCl2 for 5 weeks. Morphological findings were obtained from the soleus (SOL), deep (PLd) and superficial (PLs) portions of plantaris, and diaphragm (DIA) muscles. Co2+ administration significantly increased the blood hemoglobin concentration by approximately 25% with and without training. Only in DIA, the Co2+ treatment alone significantly increased total capillary density and the capillary-to-fiber ratio (C : F) (plt;0.05). Both training groups with and without Co2+ administration showed a significant increase in the C : F in SOL and PLd (plt;0.05). In PLd, the increase was significantly greater in the Co2+-treated training group than in the non–Co2+-treated training group (plt;0.05). Training significantly increased the proportion of arteriolar capillaries while it decreased that of venular capillaries in both SOL and PLd (plt;0.05). These changes were also observed in PLd after training with Co2+. The densities of VEGF-positive and TGF-β1–positive capillaries remained unchanged in all muscle portions examined after either Co2+ administration or exercise training. These results suggest that chronic Co2+ administration causes adaptive changes in the oxygen transport system in respiratory muscle and facilitates exercise-induced angiogenesis in hind-leg muscles.
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Yutaka Endo, Katsuya Yamauchi, Yuka Tsutsui, Zenzaburo Ishihara, Fumio ...2002 Volume 52 Issue 5 Pages 421-427
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSTo investigate the possible involvement of the sympathetic nervous system in pressor response during water drinking, muscle sympathetic nerve activity (MSNA), blood pressure (BP), and heart rate (HR) were continuously measured in healthy young volunteers throughout the experiments of a 5-min control, 2 min of drinking 500 ml water, and a 28-min recovery. To avoid the effects of water passing through the oropharyngeal and esophageal regions and/or effects of swallowing, an equal amount of water was directly infused to the stomach through a stomach tube for 2 min. Water drinking caused a transient increase in mean arterial pressure (MAP) and HR immediately after drinking (ΔMAP, 12.6 ± 2.1 mmHg; ΔHR, +19.9 ± 1.7 beats/min at the peak). An abrupt decrease of MSNA was observed directly during water drinking (Δburst rate, −6.9 ± 1.3 bursts/min; Δtotal activity, −2,606 ± 491 U/min), and it increased to the baseline level thereafter. Gastric infusion had little or no effect on MAP, HR, and MSNA. The present study demonstrated that a pressor response during water drinking was associated with the attenuation of MSNA and not generated by gastric infusion of water at the same rate as in this drinking manner. In conclusion, the rapid rise in BP might be caused through stimulations from the oropharyngeal region, swallowing-induced factors, and/or a feedforward mechanism by a central descending signal from the higher brain centers.
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Toru Ide, Yuko Takeuchi, Takaaki Aoki, Toshio Yanagida2002 Volume 52 Issue 5 Pages 429-434
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSIn recent years, the single-molecule imaging technique has proven to be a valuable tool in solving many basic problems in biophysics. The technique used to measure single-molecule functions was initially developed to study electrophysiological properties of channel proteins. However, the technology to visualize single channels at work has not received as much attention. In this study, we have for the first time, simultaneously measured the optical and electrical properties of single-channel proteins. The large conductance calcium-activated potassium channel (BK-channel) labeled with fluorescent dye molecules was incorporated into a planar bilayer membrane and the fluorescent image captured with a total internal reflection fluorescence microscope simultaneously with single-channel current recording. This innovative technology will greatly advance the study of channel proteins as well as signal transduction processes that involve ion permeation processes.
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Gulzade Donmez, Ulver Derici, Deniz Erbas, Turgay Arinsoy, Ayhan Onk, ...2002 Volume 52 Issue 5 Pages 435-440
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSSeveral recent studies have shown that essential hypertension is associated with increased oxidative stress, which may cause hypertension via enhanced oxidation and inactivation of nitric oxide. In this study, we investigated the malondialdehyde, nitric oxide, and glutathione levels in newly diagnosed essential hypertensive patients and whether or not there was any effect of antihypertensive treatment with angiotensin II type 1 receptor antagonist, losartan or angiotensin converting enzyme inhibitor, enalapril on plasma malondialdehyde, nitric oxide, and glutathione values. We selected 17 patients (F/M: 10/7, mean age: 46.12 ± 9.2 years) for enalapril therapy (10–20 mg/d) and 14 patients (F/M: 8/6, mean age: 47.7 ± 7.5 years) for losartan therapy (50–100 mg/d), and compared them with 12 normotensive controls. At the beginning of the study, both treated groups showed significantly higher plasma malondialdehyde and lower glutathione and nitric oxide in exhaled air compared to the control group. After 9 weeks of enalapril and losartan treatment, both systolic and diastolic pressure were significantly reduced. Both enalapril and losartan produced a significant decrease in plasma malondialdehyde and a significant increase in plasma glutathione levels and nitric oxide in exhaled air after 9 weeks. Initial values of plasma nitrate levels in patient groups were similar to the control group and increased significantly after the treatment period. In conclusion, both losartan and enalapril may be regulators between oxidant stress and the antioxidant system.
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Tatsuhiko Shibata, Fumitaka Ikomi, Toshio Ohhashi2002 Volume 52 Issue 5 Pages 441-448
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSWe examined the effects of plasma on contractile responses of isolated dog external jugular veins to a thromboxane A2 analog, U46619, and noradrenaline. Pretreatment with 1.0% plasma in Krebs-bicarbonate solution, but not 0.1%, caused a significant left and upward shift in the concentration–contractile response curve for U46619. The plasma-mediated potentiation of the response to U46619 was found in the venous segments without intact endothelium. The administration of 2×10−5 M lysophosphatidylcholine in Krebs-bicarbonate solution with no plasma also produced a significant left and upward shift of the concentration–contractile response curve for U46619, the shift being quite similar to that obtained with 1.0% plasma. In contrast, pretreatment with 1.0% plasma or 2×10−5 M lysophosphatidylcholine produced no significant effect on the noradrenaline-mediated contractions in the venous segments. Pretreatment with 10−4 M L-ascorbate or 0.1 mg/ml α-tocopherol in the presence of 1.0% plasma caused a significant reduction in the plasma-mediated potentiation of the contractile responses to U46619. These findings suggest that lysophosphatidylcholine, a major phospholipid component of oxidized low-density lipoproteins, may contribute, in part, to the plasma-mediated potentiation of contractile responses of the isolated veins to U46619, and that the antioxidant vitamin, L-ascorbate, or α-tocopherol significantly reduces the plasma-mediated potentiation of the contractile responses to U46619, which may be related to inhibiting the production of lysophosphatidylcholine in plasma.
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Tsukasa Tameyasu, Megumi Ohta, Midori Tanaka, Kyoko Ogihara, Saeko Tak ...2002 Volume 52 Issue 5 Pages 449-456
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThe effect of zinc-carnosine complex (Z-103) on muscle function in dystrophin-deficient (mdx) mice was examined using several different courses of repetitive administration. Z-103 at a dose of 100 mg/kg increased the load resistant time (LRT), during which an animal bearing a load holds himself upright on a wire net, in mdx mice when administered at an age of less than about 4 months. The effect of Z-103 on LRT was independent of sex when given by intraperitoneal (I.P.) administration between 4 and 8 weeks of age. Administration of Z-103 from the age of 4 to 9 weeks had no significant effect on wet weight, magnitude or rate of rise of twitch force, or rate of decay of twitch force over time with twitch elicited by 0.5 Hz of electricity in the extensor digitorum longus muscle or calcium content in the gastrocnemius muscle, while it increased the magnitude of twitch force in the soleus muscle. These results suggest that Z-103 reduces fatigability of the whole body in mdx mice, possibly by increasing the contractility of slow fibers.
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Tamotsu Mitsuiye, Akinori Noma2002 Volume 52 Issue 5 Pages 457-469
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSInactivation of the cardiac Na+ channel was analyzed by recording channel currents from a cell-attached patch containing only one functional Na+ channel in guinea-pig ventricular myocytes. A two-step test pulse, first to variable levels (Pulse 1) and then to −30 mV (Pulse 2) was applied from a holding potential of −140 mV. When a cumulative histogram was determined for the latency of first opening, the histogram was well fitted with a single exponential function at −70 to −30 mV of Pulse 1. The activation time course of ensemble average was virtually single exponential. Although the ensemble average of 500 sweeps showed various extents of inactivation during Pulse 1, the saturation level of the cumulative first-latency histogram at the end of the two-step pulse was almost constant (0.7–0.8), irrespective of Pulse 1. Even when the interval between successive test pulses was prolonged from 70 to 970 ms, the saturation level of the histogram was not modified. These findings are consistent with inactivation only through the open state. Thus, the apparent "blank sweep inactivation" does not necessarily indicate direct inactivation from closed states. These findings support the hypothesis that the inactivation of cardiac Na+ channel occurs exclusively through the open state.
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Yasuaki Yashiro, Toshio Ohhashi2002 Volume 52 Issue 5 Pages 471-477
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSCilostazol, a potent inhibitor of guanosine 3′:5′-cyclic monophosphate (cGMP)-inhibited adenosine 3′:5′-cyclic monophosphate (cAMP) phosphodiesterase (PDE3), has been used clinically for the treatment of chronic peripheral arterial occlusive disease. The beneficial effect of cilostazol is attributed to both anti-platelet aggregating activity and vasodilation. However, the effect of cilostazol on resistance-sized vasculature is not well documented. Furthermore, mechanisms of vasodilation and influence on endothelium function are not fully understood. Thus, we investigated the vasodilator action of cilostazol using isolated, pressurized rabbit spinal arterioles with special reference to the functional endothelium. Cilostazol, acetylcholine (ACh), isocarbacyclin (prostacyclin analogue), and sodium nitroprusside (SNP) all produced concentration-dependent vasodilations of isolated spinal arterioles with endogenous myogenic tone. The order of potency of these agonists was isocarbacyclin>ACh>SNP>cilostazol. Indomethacin (10 μM, a cyclo-oxygenase inhibitor), Nω-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor, 30 μM), or chemical denudation of the endothelial cells did not significantly alter the cilostazol-induced arteriolar dilation. Furthermore, stimulating the release of endothelium-derived relaxing factors by administering ACh (100 nM), or treating with isocarbacyclin (1 nM) or SNP (3 nM) did not significantly modify the cilostazol-induced vasodilation. These results suggest that cilostazol produces the vasodilation of isolated, pressurized rabbit spinal arterioles independent of the functional endothelium. We infer that the vasodilator action of cilostazol in the spinal arterioles may be attributed to a yet unknown mechanism that is independent of the PDE3 inhibition.
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Wissam H. Joumaa, Aicha Bouhlel, Claude Léoty2002 Volume 52 Issue 5 Pages 479-487
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSThe post-effects of nandrolone decanoate treatment (15 mg·kg−1·week−1) were studied on contractile responses of isolated small bundles of intact slow-(soleus) and fast-(extensor digitorum longus, edl) twitch fibers in rat. Five weeks of treatment induced, in edl, an increase in the amplitude of twitch (55%) and K+ contracture (32%) without significant change in the time constant of relaxation and caffeine contracture. In soleus, an increase in the amplitude of twitch (35%) and caffeine contracture (0.2 mM: 218%, 0.5 mM: 88%, 5 mM: 28%, and 10 mM: 25%) was observed without change in K+ contracture characteristics. In addition to these effects, 10 weeks of drug treatment increased the amplitude of soleus K+ contracture (29%) and edl caffeine contracture (0.2 mM: 247%, 0.5 mM: 170%, 5 mM: 29%, and 10 mM: 45%), and reduced the 50% recovery time for K+ contracture (EC50) (soleus: 37%, edl: 12%). After 5-week treatment followed by 5-week arrest, as compared to the control group, no change in the amplitude of twitch, K+ or caffeine contractures was found in edl. In soleus, although no significant difference was observed in the amplitude of twitch, the amplitude of K+ (35%) and caffeine contractures (0.2 mM: 227%, 0.5 mM: 128%) remained greater than the control group. Moreover, the EC50 values were prolonged (46%) in soleus, whereas no significant difference was observed in edl. The present work suggests that nandrolone decanoate treatment induced differential post-effects on contractile responses developed in slow- and fast-twitch skeletal muscles by acting differently on the different steps of the excitation-contraction coupling mechanism.
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Masahiro Itoh, Yoshiyuki Fukuoka, Bruno Grassi, Claudio Marconi, Paolo ...2002 Volume 52 Issue 5 Pages 489-496
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSWe designed two experiments to investigate the relationship between ventilation (V˙E) and CO2 output (V˙CO2) during exercise under the conditions of exercising different limbs, the arms as opposed to the legs (experiment 1), and of different physical training states after undergoing standard exercise training for 90 d (experiment 2). Six healthy young subjects underwent submaximal ramp exercise at an incremental work rate of 15 W/min for the arm and leg, and 11 healthy middle-aged subjects underwent an incremental exercise test at the rate of 30 W/3 min before and after exercise training. We measured pulmonary breath-by-breath V˙E, V˙CO2, oxygen uptake (V˙O2), tidal volume (VT), breathing frequency (bf), and end-tidal O2 and CO2 pressures (PETO2, PETCO2) via a computerized metabolic cart. In experiment 1, arm exercise produced significantly greater V˙E than did leg exercise at the same work rates, as well as significantly higher V˙O2, V˙CO2, and bf. The slopes of the regression lines in the V˙E–V˙CO2 relationship were not significantly different: the values were 27.8 ± 2.1 (SD) during the arm exercise, and 25.3 ± 3.9 during the leg exercise, with no differences in their intercepts. In experiment 2, the V˙O2, V˙CO2, and V˙E responses at the same work rates were similar in both before and after the 90-d exercise training, whereas the heart rate (HR) and mean blood pressure (MBP) were significantly reduced after training. Exercise training did not alter the V˙E–V˙CO2 relationship, the slope of which was 31.9 ± 4.9 before exercise training and 34.2 ± 4.4 after exercise training. We concluded that the V˙E–V˙CO2 relationship during exercise is unaltered, independent of not only working muscle regions but also exercise training states.
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Kazunori Uemura, Masaru Sugimachi, Toshiaki Shishido, Toru Kawada, Mas ...2002 Volume 52 Issue 5 Pages 497-503
Published: 2002
Released on J-STAGE: June 19, 2004
JOURNAL FREE ACCESSConventional conductance volumetric systems require ex-vivo calibrations for blood conductivity and parallel conductance. It is often impractical to repeat blood sampling and hypertonic saline infusion for these calibrations. To overcome these limitations, we developed a useful, self-calibrating conductance volumetric system that does not require ex-vivo calibrations. On a conventional 6-electrode catheter, we added an extra electrode close to one of the recording electrodes to estimate blood conductivity. These two electrodes were placed close (0.5 mm) enough so that conductance between them reflected only blood conductivity regardless of cardiac volume. We estimated parallel conductance by the dual-frequency excitation (2 and 20 kHz) method. In 18 anesthetized rabbits, blood conductivity (σest) thus estimated agreed well with that (σconv) measured by the conventional ex-vivo blood sampling method (σest = 1.04σconv−0.25, R2 = 0.98, SEE = 0.01 mS/cm, 1.2% error). Parallel conductance (Gp est) estimated by dual-frequency excitation also agreed well with that (Gp conv) estimated by the saline injection method (Gp est = 0.95Gp conv+4.25, R2 = 0.87, SEE = 4.0 mS, 6.0% error). Estimated ventricular volume (Vest) by our system agreed reasonably well with that (Vconv) by the conventional method (Vest = 0.93Vconv+0.01, R2 = 0.86, SEE = 0.22 ml, 14.7% error). The fact that this self-calibrating conductance volumetric system drastically simplifies volume measurement makes it an attractive tool for the assessment of cardiac function where significant changes in blood conductivity and parallel conductance are inevitable, such as in cardiac surgery.
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