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Volume 51, Issue 1
Displaying 1-14 of 14 articles from this issue
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REVIEWS
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Tetsuro Sakai, Kohtaro Kamino2001 Volume 51 Issue 1 Pages 1-18
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSRecently, optical methods for monitoring membrane potential with fast voltage-sensitive dyes have been introduced as a powerful tool for studying cardiac electrical functions. These methods offer two principal advantages over more conventional electrophysiological techniques. One is that optical recordings may be made from very small cells that are inaccessible to microelectrode impalement, and the other is that multiple sites/regions of a preparation can be monitored simultaneously to provide spatially resolved mapping of electrical activity. The former has made it possible to record spontaneous electrical activities in early embryonic precontractile hearts, and the latter has been applied for mapping of the propagation patterns of electrical activities in the cardiac tissue. In this article, optical studies of the electrophysiological function of the vertebrate heart are reviewed.
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George Mchedlishvili, Nobuji Maeda2001 Volume 51 Issue 1 Pages 19-30
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe review article deals with phenomena of the blood flow structure (structuring) in narrow microvessels--capillaries and the adjacent arterioles and venules. It is particularly focused on the flow behavior of red blood cells (RBCs), namely, on their specific arrangements of mutual interaction while forming definite patterns of self-organized microvascular flow. The principal features of the blood flow structure in microvessels, including capillaries, include axial RBC flow and parietal plasma layer, velocity profile in larger microvessels, plug (or bolus) flow in narrow capillaries, and deformation and specific behavior of the RBCs in the flow. The actual blood flow structuring in microvessels seems to be a most significant factor in the development of pathological conditions, including arterial hypertension, brain and cardiac infarctions, inflammation, and many others. The blood flow structuring might become a basic concept in determining the blood rheological properties and disorders in the narrow microvessels. No solid theoretical (biorheological) basis of the blood flow structuring in microvessel has been found, but in the future it might become a foundation for a better understanding of the mechanisms of these properties under normal and pathological conditions in the narrowest microvessels 5 to 25 &mgr;m large. It is also a topic for further biorheological research directed to find the background of actual physiopathological phenomena in the microcirculation.
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Regular Papers
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Shintaro Yamamoto, Tsuguhisa Ehara, Takao Shioya2001 Volume 51 Issue 1 Pages 31-41
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe effects of the activation of cyclic AMP–dependent Cl− current (ICl,cAMP) on cell volume were studied at various [K+]o under isosmotic conditions in guinea-pig ventricular myocytes. The area of the cell image obtained with videomicroscopy was used as an index of cell volume. ICl,cAMP was activated by adrenaline (5.5 μM). Measurements of the membrane potential (Vm) were performed by the gramicidin-perforated patch-clamp method. At 5.4 mM [K+]o with low [Cl−]o, where Vm was negative to the predicted equilibrium potential of Cl− (ECl), adrenaline sizably decreased the cell area. At high [K+]o with normal [Cl−]o, where Vm was positive to ECl, adrenaline increased the cell area; at 145.4 mM [K+]o the cell area was increased to 110% of control on average (n = 22). The cells swollen in this manner shrank when [Cl−]o was reduced to a low level in the presence of adrenaline. The results indicate that the induction of Cl− influxes (outward ICl,cAMP) or effluxes (inward ICl,cAMP) can lead to a cell swelling or shrinkage, respectively. The addition of BaCl2 (1 mm), a blocker of K+ channels, attenuated the adrenaline-dependent cell swelling, supporting the view that Cl− fluxes must be accompanied by cofluxes of K+ ions to affect the cell volume. The adrenaline-dependent cell swelling was inhibited by antagonizing β-adrenergic stimulation with acetylcholine or by blocking ICl,cAMP channels with glibenclamide, confirming the involvement of ICl,cAMP in the adrenaline response. The results show that the activation of ICl,cAMP can shrink or inflate the cardiac cells under isosmotic conditions, depending on Vm and ECl.
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Masaru Sugimachi, Toshiaki Shishido, Kenji Sunagawa2001 Volume 51 Issue 1 Pages 43-51
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSAlthough various investigators have suggested that the left ventricles of aged subjects suffer from high-frequency reflection, arterial reflection is larger in the low-frequency range because of a larger impedance mismatch. It has not been quantified whether high-frequency reflection rather than low-frequency reflection has larger deleterious effects on stroke volume. We used a computer simulation method to evaluate how increases in high- and low-frequency arterial reflections associated with age-related arterial sclerosis affect left ventricular (LV) pump function. Low-frequency reflections derive principally from the total arterial compliance, and high-frequency reflections result from impedance fluctuations in the high-frequency range. We numerically coupled a time-varying elastance LV model with a variety of arterial impedances to quantitatively evaluate the effects of low- and high-frequency reflections on LV pump performance. When we simultaneously increased low- and high-frequency reflections to levels of sclerotic impedance (type A in Murgo et al., Circulation 62: 105–116, 1980), stroke volume decreased by 4.4%. Further increases of the reflections up to 8 times of the type A impedance lowered stroke volume by 15.9%. This trend was clearly seen with selective increases in low-frequency reflections (3.5 and 20.2% decrease in stroke volume, respectively), but not with those in high-frequency reflections (1.0% decrease and 0.9% increase in stroke volume, respectively). Thus we conclude that the detrimental effect of increases in arterial reflections associated with arterial sclerosis on stroke volume is mild and mainly attributable to decreased compliance rather than to increased high-frequency reflections.
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Koh-ichi Enomoto, Hiroko Kataoka, Akihiko Hirota2001 Volume 51 Issue 1 Pages 53-61
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe expression levels of seven types of gamma-aminobutyric acid-A (GABA-A) receptor subunits (α1, β2, β3, β4, γ1, γ2, and γ4) were quantified in the embryonic chick brain stem at 2 to 20 d of incubation (E2 to E20) and just after hatching. The expression level of mRNA was measured by using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). When property regions were amplified, two products were observed for each of the β2, β4, and γ2 subunits because of alternative splicing. These were named β2S and β2L, β4S and β4L, and γ2S and γ2L for shorter and longer fragments, respectively. Transcripts of α1, β2L, β2S, β3, β4L, β4S, γ1, and γ2S subunits were first detected from E2 to E5 brain stems. The expression level of each subunit increased gradually with development and reached a plateau at E9 to E12. In contrast, a delay occurred in the appearance of both the γ4 and γ2L subunits, which were not detected until E8 to E10. The absence of γ4 and/or γ2L subunits may explain differences in the pharmacological characteristics of GABA-A receptors at the early stages of development.
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R. Dutta, K. Mukherjee, R. Mathur2001 Volume 51 Issue 1 Pages 63-69
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe ingestion of sucrose (ad libitum) produces an immediate analgesic response to phasic noxious stimuli. The underlying mechanism for the analgesic effect of sucrose is attributed to its palatability, which mediates analgesia probably by the release of β-endorphin in the hypothalamus. The present study was designed to explore the role of ventromedial hypothalamus in the mediation of sucrose-fed analgesia. Adult male albino rats each received (20%) sucrose solution orally through a separate bottle until they had ingested 4–5 ml. Their behavioral responses to tonic noxious stimulus in a formalin test were studied in pre- and postsucrose-fed rats of control and in the VMH lesion groups . The average pain rating of a 60-min session significantly (p < 0.01) decreased after sucrose feeding in control rats, from 1.94 ± 0.13 to 1.45 ± 0.14, but sucrose feeding by the VMH lesion rats did not alter their tonic nociceptive response from a 1.70 ± 0.07 presucrose-fed state to a 1.71 ± 0.08 postsucrose-fed state. VMH lesion per se did not alter the nociceptive response in comparison with controls. The results suggest that sucrose feeding produces analgesia to tonic noxious stimulus, which is abolished by lesion of the VMH, thereby indicating a significant role of VMH in sucrose-fed analgesia.
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Koichi Mori, Tomoyuki Maeda, Yoshimitsu Shiraishi, Yasuaki Kawai2001 Volume 51 Issue 1 Pages 71-79
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe effects of hypothermia on blood flow and neural activity were investigated in rabbit spinal cord during the acute phase of ischemia/reperfusion. Rabbits were exposed to ischemia for 10 or 40 min by occluding the abdominal aorta, using a balloon catheter. The body temperature was maintained either at 38°C (normothermia) or 34°C (hypothermia). Hyperperfusion was observed within 10 min after the cessation of ischemia in all rabbits exposed to ischemia. The magnitude of hyperperfusion in spinal cord blood flow (SCBF) was not significantly different between the 10 and 40 min ischemia rabbits, but the time for 50% recovery from the hyperperfusion was longer in the 40 min ischemia group (26.1 ± 2.5 min) than in the 10 min group (15.1 ± 2.1 min). The amplitude of evoked spinal cord potential decreased during ischemia and recovered to the baseline level during 8 h of reperfusion in the 10 min ischemia group. However, in the 40 min ischemia group, the amplitude was 40 ± 8% of the baseline value after 8 h of reperfusion. Hypothermia prevented the delay of recovery from hyperperfusion and the reduction of evoked spinal cord potential. These results suggest that hypothermia plays a beneficial role in protecting tissue injury in the acute phase of ischemia/reperfusion in the spinal cord by shortening the time for recovery from postischemic hyperperfusion.
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Kenji Yawata, Masao Nagata, Akiko Narita, Yasuaki Kawai2001 Volume 51 Issue 1 Pages 81-87
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSATP-induced calcium (Ca2+) mobilization was investigated in rabbit lens epithelial cells that had been cultured in a medium with pH of 7.4 (group 1), 7.2 (group 2), or 7.0 (group 3) for 10 to 21 d. Intracellular free Ca2+ ([Ca2+]i) and pH (pHi) were measured by using fluorescent dyes, fura-2 and BCECF, respectively. The long-term acidification decreased the pHi to 7.15 ± 0.01, from 7.22 ± 0.01, in group 2 and to 7.09 ± 0.01 in group 3. The administration of 10 μmol/l ATP produced an initial peak followed by a sustained increase in [Ca2+]i in the lens cells of group 1. Both the initial peak and the sustained increase in [Ca2+]i were enhanced in groups 2 and 3. The initial peak was abolished by pretreatment with 1 μmol/l thapsigargin, an ER Ca2+ pump inhibitor, but was not affected by the removal of extracellular Ca2+. On the other hand, the sustained increase was suppressed either by the thapsigargin treatment or by the Ca2+ removal. Treatment with only thapsigargin caused a sustained increase in [Ca2+]i that was greater in group 3 than in group 1. These results suggest that (1) the ATP-induced initial peak in [Ca2+]i is due to Ca2+ release from the intracellular stores, (2) the sustained increase in [Ca2+]i is mediated through either Ca2+ influx from the extracellular space or Ca2+ release from the store triggered by the Ca2+ influx, and (3) long-term, moderate acidification enhances both the initial peak and the sustained increase in [Ca2+]i in rabbit lens epithelial cells. One possible mechanism of the ATP-induced Ca2+ influx seems to be a capacitative Ca2+ entry pathway.
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Hiroko Katano, Mika Ishihara, Yoshimitsu Shiraishi, Yasuaki Kawai2001 Volume 51 Issue 1 Pages 89-97
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe effects of aging on the electroretinogram (ERG) during ischemia-reperfusion were investigated in rats. Flash-elicited ERG (a-wave, b-wave, and oscillatory potentials (OPs)) was recorded in young (4 months old) and aged rats (over 18 months old) before, during, and after exposure to 30- or 120-min ischemia induced by increasing intraocular pressure to 80 mmHg. The choroidal blood flow, measured by means of laser Doppler flowmetry, decreased to 40 to 60% of the baseline value during ischemia. Young rats showed no significant difference in the amplitude of each ERG component during ischemia between 30- and 120-min ischemia groups; 78.0 ± 4.9 vs. 76.1 ± 3.6% for a-wave, 63.4 ± 3.1 vs. 60.6 ± 3.0% for b-wave, and 59.6 ± 5.9 vs. 57.5 ± 6.7% for σOP. In aged rats, however, 120-min ischemia caused a greater decrease, to 56.7 ± 3.1% of the baseline value, in the a-wave amplitude than 30-min ischemia did, to 70.8 ± 3.2%. The reduction of each ERG component in both 30- and 120-min ischemia experiments was greater in aged rats than in young rats. The recovery time for the amplitude of each ERG component during reperfusion was longer in aged rats than in young rats. The latency of b-wave and the second component of OPs prolonged during ischemia, and recovery time for the latency was longer in aged rats than in young rats. These results suggest that the electrophysiological function of the retina is less tolerable against ischemia-reperfusion in aged rats than in young rats.
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Hiromi Misawa, Hisaharu Kohzuki, Susumu Sakata, Yoshimi Ohga, Miyako T ...2001 Volume 51 Issue 1 Pages 99-108
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSIn the excised Langendorff-perfused rat whole-heart preparation, a linear relation between left ventricular myocardial oxygen consumption per beat (Vo2) and systolic pressure-volume area (PVA, a total mechanical energy per beat) is obtained from a curved end-systolic pressure-volume relation as in the blood-perfused preparation. The ordinate Vo2 intercept of the Vo2-PVA relation is composed of Vo2 for total Ca2+ handling in the excitation-contraction coupling and basal metabolism. The Vo2 for total Ca2+ handling is mainly consumed by sarcoplasmic reticulum (SR) Ca2+-ATPase. The aim of the present study was to investigate, in terms of left ventricular mechanoenergetics, how an inhibition of SR Ca2+-ATPase by cyclopiazonic acid (CPA; 4 μmol/l) affects Ca2+ handling mechanisms in the excised Langendorff-perfused rat whole-heart preparation. The short-term (for 3 to 6 min after onset of the infusion) CPA infusion decreased Vo2 proportionally to the decrease in PVA. The long-term (for 9 to 12 min after the short-term CPA infusion) CPA infusion gradually increased Vo2 almost to the control level with an increase in PVA. The increases in both Vo2 and PVA during this infusion were completely abolished by a Na+/Ca2+ exchanger inhibitor, 3′9,4′9-dichlorobenzamil, indicating the contribution of Na+/Ca2+ exchanger to the increases in Vo2 and PVA. The O2 cost of left ventricular contractility during the long-term CPA infusion was significantly higher than during the short-term CPA infusion. All these results suggest the possibility of the contribution of greater energy–wasting Ca2+ extrusion processes (such as Na+/K+-ATPase coupled to the Na+/Ca2+ exchanger; its stoichiometry is 1 ATP : 1 Ca2+) to the larger oxygen cost of left ventricular contractility.
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Hironori Miyoshi, Yasuo Takayama, Teruhiro Tamura, Shuji Kitashiro, To ...2001 Volume 51 Issue 1 Pages 109-114
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSThe importance of the mitral apparatus to the global left ventricular (LV) function has been suggested in several clinical studies. One recent study reported that chordal transsection induced an unloading of myocardium at the papillary muscle insertion site. We hypothesized that the regional response for afterloading at this site with intact mitral apparatus was different from that at the free wall. We investigated the end-systolic pressure–regional segment length relations (ESPLR) in two anterior LV sites, free wall (FREE) and the papillary muscle insertion site (PAP), during an increasing afterload by aortic occlusion in 7 anesthetized open-chest dogs. To measure the regional segment length at FREE and PAP, two sets of the pair of sonomicrometer crystals were implanted in the same midwall depth at the same circumferential hoop by using an echocardiographic guide. ESPLR both at FREE and PAP were always highly linear in a physiological range (r ≥ 0.9). The slope of this relation at FREE (274 ± 164 mmHg/mm) was significantly steeper than that at PAP (157 ± 118 mmHg/mm) for each dog (p < 0.05). These data indicate that the regional response for afterloading at PAP loaded by chordal tension is different from that at FREE in the same heart.
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Short Communications
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Masanori Sunagawa, Mariko Nakamura, Tadayoshi Kosugi, Franz Hofmann, N ...2001 Volume 51 Issue 1 Pages 115-119
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSTyrosine protein kinase (Tyr-PK) regulation of L-type Ca2+ channel (CaL) current was studied in COS-7 cells expressing vascular smooth muscle-type α1C-b with no auxiliary subunit by using a whole-cell voltage clamp. The averaged peak amplitude of CaL currents was −0.33 ± 0.03 at holding potential of −60 mV. Na3VO4, genistein and phosphorylated p60c-src peptide had no effect on the current. Thus the α1C-b subunit may not be involved in Tyr-PK regulation of CaL current.
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Hideki Sakai, Masashi Ukai, Akira Ikari, Shinji Asano, Noriaki Takeguc ...2001 Volume 51 Issue 1 Pages 121-125
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSAn expression of mRNA coding the calcium-activated Cl− channel-1 (CLCA1) in rabbit gastric parietal cells was examined to verify the possibility that the CLCA1 mediates housekeeping Cl− channels in the basolateral membrane. In whole-cell voltage-clamp experiments of rabbit parietal cells, A23187 (2 μM), a Ca2+ ionophore, activated the basolateral Cl− channels. The partial cDNA fragment of rabbit CLCA1 could be amplified from the total RNA of tracheal epithelium. A Northern blot analysis showed that rabbit CLCA1 mRNA of 3.4 kb is highly expressed in the tracheal epithelium, but not in the gastric parietal cells. Even in a more sensitive detection of rabbit CLCA1 mRNA by RT-PCR, no signal could be observed in the gastric parietal cells. These results suggest that the CLCA1 protein may not be a subunit of the housekeeping Ca2+-dependent Cl− channel in the basolateral membrane of rabbit gastric parietal cells.
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Masato Konishi, Toshikazu Yamashita, Shinsuke Nakayama, Shinichiro Kok ...2001 Volume 51 Issue 1 Pages 127-132
Published: 2001
Released on J-STAGE: June 22, 2004
JOURNAL FREE ACCESSIn rat ventricular myocytes chemically skinned with saponin, a local rise of [Ca2+] was achieved by two-photon excitation photolysis (TPP) of the caged Ca2+ compound 1-(2-nitro-4,5-dimethoxyphenyl)-N,N,N′9,N′9-tetrakis[(oxycarbonyl)methyl]-1,2-ethanediamine (DM-nitrophen). Confocal Ca2+ images, by use of fluo-3, were simultaneously collected. TPP of DM-nitrophen induced Ca2+ waves propagating over the myocyte, and the local rise of [Ca2+] at the site of photolysis sustained for 50–60 ms. These TPP-induced Ca2+ events were completely suppressed by ryanodine (10 μM), suggesting that Ca2+ release resulting from TPP of DM-nitrophen triggered regenerative Ca2+ release from the neighboring sarcoplasmic reticulum. The present techniques should be useful to investigate the interaction of elementary Ca2+ events, the process leading to global Ca2+ movements, in cardiac myocytes and other types of cells.
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