巻号一覧
54 巻, 6 号
選択された号の論文の12件中1～12を表示しています
- |<
- <
- 1
- >
- >|
Invited-Editor Section: Reviews
-
Denis Noble2004 年 54 巻 6 号 p. 509-510
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーPDF形式でダウンロード (44K) -
Bernard Korzeniewski2004 年 54 巻 6 号 p. 511-516
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーA computer model of oxidative phosphorylation was developed in isolated muscle mitochondria [Korzeniewski and Mazat: Biochem J 319: 143-148, 1996] and in intact skeletal muscle [Korzeniewski and Zoladz: Biophys Chem 92: 17-34, 2001]. Within this model the dependence on different metabolite concentrations of the rate of each enzymatic reaction, process and flux is described by an appropriate kinetic equation. The changes of metabolite concentrations over time are described by a set of ordinary differential equations. The model has been very extensively tested by a comparison of computer simulations with a broad set of experimental results concerning various kinetic properties of the oxidative phosphorylation system. Next the model was used for theoretical studies on the regulation of oxidative phosphorylation in intact muscle cells. The model decidedly supports the so-called parallel-activation mechanism or each-step-activation mechanism of adjusting the rate of ATP supply to the current energy demand [Korzeniewski: Biochem J 330: 1189-1195, 1998; Korzeniewski: Biochem J 375: 799-804, 2003]. Because of this mechanism, not only ATP usage, but also the substrate dehydrogenation system and all oxidative phosphorylation complexes (complex I, complex III, complex IV, ATP synthase, ATP/ADP carrier, phosphate carrier) are directly (and not by changes in metabolite concentrations) activated by some intracellular factor(s) related to muscle contraction, probably by calcium ions, during the transition from rest to work. This mechanism is able to account for several kinetic properties of oxidative phosphorylation that cannot be explained by other mechanisms postulated in the literature. Thus the discussed kinetic model of oxidative phosphorylation has appeared to be a very useful research tool.抄録全体を表示PDF形式でダウンロード (123K) -
Satoshi Matsuoka, Hikari Jo, Nobuaki Sarai, Akinori Noma2004 年 54 巻 6 号 p. 517-522
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーThe heart produces and uses ATP at a high rate. Each step involved in ATP metabolism has been extensively studied. However, functional coupling between ATP production and membrane excitation-contraction coupling, which is the main ATP consumption process, is not yet fully understood because of complicated interactions and the lack of quantitative data obtained in vivo. Computer simulation is a powerful tool for integrating experimental data and for solving their complicated interactions. To investigate the mechanisms underlying cardiac excitation-contraction-energy metabolism coupling, we have developed a computer model of cardiac excitation-contraction coupling (Kyoto model) that includes the major processes of ATP production, such as oxidative phosphorylation that was originally developed for skeletal muscle by Korzeniewski and Zoladz [Biophys Chem 92: 17-34, 2001], creatine kinase, and adenylate kinase. In this review, we briefly summarize cardiac energy metabolism and discuss the regulation of mitochondrial ATP synthesis, using the Kyoto model.抄録全体を表示PDF形式でダウンロード (355K) -
Semahat S. Demir2004 年 54 巻 6 号 p. 523-530
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーLittle is known about the ionic mechanisms underlying the action potential heterogeneity in ventricle-associated healthy and disease conditions, even though five decades of histological, electrophysiological, pharmacological, and biochemical investigations exist. The computational modeling in murine ventricular myocytes can complement our knowledge of the experimental data and provide us with more quantitative descriptions in understanding different conditions related to normal and disease conditions. This paper initially reviews the theoretical modeling for cardiac ventricular action potentials of various species and the related experimental work. It then presents the progress of the computational modeling of cardiac ventricular cells for normal, diabetic, and spontaneously hypertensive rats. The paper also introduces recent modeling efforts for the action potential heterogeneity in mouse ventricular cells. The computational insights gained into the ionic mechanisms in rodents will continue to enhance our understanding of the heart and provide us with new knowledge for future studies to treat cardiac diseases in children and adults. Because the dissemination of computational models is very important, we continue to disseminate these models by iCell, the interactive cell modeling resource. iCell (http://ssd1.bme.memphis.edu/icell/) has been developed as a simulation-based teaching and learning tool for electrophysiology and contains JAVA applets that present models of various cardiac cells and neurons and simulation data of their bioelectric activities at cellular level.抄録全体を表示PDF形式でダウンロード (227K) -
Andrew D. McCulloch2004 年 54 巻 6 号 p. 531-539
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーComputational biology is integrative in several ways. Functionally, computational models are valuable for integrating the many interacting processes within biochemical networks and the many interacting physiological subsystems within the cell. Structurally detailed models provide a way of integrating across scales of biological organization from molecule to organism. Data integration across diverse laboratory and clinical measurements is another unique strength of computational biology. We describe examples of all three categories of integration by using recent advances in modeling cardiac excitation-contraction coupling and whole-heart electromechanics in health and disease.抄録全体を表示PDF形式でダウンロード (1187K) -
Nicolas Smith, Peter Hunter2004 年 54 巻 6 号 p. 541-544
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーA computational framework is presented for integrating the electrical, mechanical, and biochemical functions of the heart. The construction of efficient finite element representations of canine and porcine ventricular geometry and microstructure is outlined. Computational techniques are applied to solve large deformation soft tissue mechanics by using orthotropic constitutive laws for myocardial tissue and models of active tension generation embedded at the Gauss points in the finite element mesh. The reaction-diffusion equations governing electrical current flow in the heart are solved on a grid of deforming material points that access systems of ordinary differential equations representing the cellular processes underlying the cardiac action potential. Navier-Stokes equations are solved to predict coronary blood flow in a system of branching blood vessels embedded in the deforming myocardium.抄録全体を表示PDF形式でダウンロード (2036K) -
Eun Bo Shim, Jong Youb Sah, Chan Hyun Youn2004 年 54 巻 6 号 p. 545-553
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーThis work reviews the main aspects of cardiovascular system dynamics with an emphasis on modeling hemodynamic characteristics by the use of a lumped parameter approach. The methodological and physiological aspects of the circulation dynamics are summarized with the help of existing mathematical models. The main characteristics of the hemodynamic elements, such as the heart and arterial and venous systems, are first described. Distributed models of an arterial network are introduced, and their characteristics are compared with those of lumped parameter models. We also discuss the nonlinear characteristics of the pressure-volume relationship in veins. Then the control pathways that participate in feedback mechanisms (baroreceptors and cardiopulmonary receptors) are described to explain the interaction between hemodynamics and autonomic nerve control in the circulation. Based on a set-point model, the computational aspects of reflex control are explained.抄録全体を表示PDF形式でダウンロード (167K)
Regular Papers
-
Tsukasa Tameyasu, Seiko Ogura, Kyoko Ogihara2004 年 54 巻 6 号 p. 555-566
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーTo explore the origin of diarrhea or constipation in human Duchenne muscular dystrophy (DMD), the effect of the inhibition of e- , i-, and n-nitric oxide synthase (NOS) on the motility of proximal and distal segments of colon of muscular dystrophy (mdx) and control mice was studied. The frequency of migrating motor complexes (MMC) was higher in the proximal than in the distal segments in mdx colon (0.56 vs. 0.25 cpm) and in the control colon (0.7 vs. 0.25 cpm), and there was no difference when mdx was compared to control segments. High concentrations of NOS inhibitors, including 1,3-PBIT dihydrobromide (1,3-PBIT) and spermine, inhibited MMC. The dose of spermine required to inhibit MMC was lower for the proximal mdx colon than for the distal mdx or control colon. In the presence of tetrodotoxin, spermine (1 mM) and 1,3-PBIT (5 mM) reduced the magnitude of local, rhythmic contractions (LC) paced by the interstitial cells of Cajal (ICC), but 1,3-PBIT (50 mM) increased their magnitude. There was no difference in the effect of spermine and 1,3-PBIT on the LC between mdx and control colon. The results suggest an inhibition of MMC by high concentrations of e-, i-, and n-NOS inhibitors, modulation of ICC activity by e-NOS, and greater susceptibility of MMC to n-NOS inhibition in the mdx proximal than in the control colon, which is very likely because of a deficit in n-NOS in the mdx smooth muscle affecting the MMC pacemaker. A deficit in the effect of mdx smooth muscle n-NOS on an MMC pacemaker may be the origin of diarrhea or constipation in human DMD.抄録全体を表示PDF形式でダウンロード (511K) -
Mutsuko Matsumoto, Kanji Matsukawa, Jun Murata, Ishio Ninomiya2004 年 54 巻 6 号 p. 567-574
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーUrinary bladder distension is known to influence the cardiovascular system under a pathophysiological condition such as spinal cord injury, hypertension, and arteriosclerosis. A reflex due to bladder distension and/or contraction is considered as one reason for the cardiovascular disturbance associated with micturition. However, it has remained unknown how much intravesical pressure (IVP) rises during micturition in daily life and to what extent mean arterial blood pressure (MAP) and heart rate (HR) respond at that time. To answer these questions, we attempted to examine the direct changes in IVP, MAP, and HR during natural micturition in freely moving conscious rats. IVP increased from the baseline value of 4 ± 0.2 mmHg to 14 ± 0.5 mmHg during natural micturition. Although MAP and HR began to increase before micturition, the increases in MAP and HR became significant 1-4 s before its onset. The peak increases in MAP and HR (7 ± 0.8 mmHg and 14 ± 3 beats/min, respectively) were delayed by 2 s from the peak IVP. Following an administration of xylocaine into the urinary bladder, the increases in MAP and HR during micturition were significantly blunted to 5 ± 2 mmHg and 8 ± 3 beats/min, although IVP increased the same as it did during micturition without xylocaine. Moreover, the relationship between IVP and MAP or HR during natural micturition resembled that between IVP and the vesico-cardiovascular reflex responses during isovolumic bladder contraction in anesthetized rats. Therefore it is concluded that natural micturition in freely moving conscious rats accompanies the significant cardiovascular responses despite a limited increase in intravesical pressure, to which a reflex from the urinary bladder may substantially contribute.抄録全体を表示PDF形式でダウンロード (247K) -
Yong-Sam Jung, Dong-Ha Lee, Hong Lim, Kyu Yang Yi, Sung-Eun Yoo, Eunhe ...2004 年 54 巻 6 号 p. 575-583
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーUsing a metabolic inhibition buffer as an ischemic model, we show here that KR-31378, a cardioselective ATP-sensitive potassium channel opener, protects H9c2 cells from chemical hypoxia (CH)-induced cell death. Our previous study showed that CH downregulated caspase activities, but led to differential activation of mitogen-activated protein kinases (MAPKs) in H9c2 cells. The repression of CH-induced c-jun N-terminal kinase (JNK)/p38 MAPK activation resulted in partial protection against CH- induced cell death, implying JNK/p38 MAPK's causative role in CH-induced cell death. This study furthers that research and examines if KR-31378's protective effect came from modulating MAPK activity and/or caspase activity in H9c2 cells. Although KR-31378 did not restore downregulated caspase-3 activity, it did block the activation of JNK and p38 MAPK in a dose-dependent manner. Extracellular signal-regulated kinase activity was not recovered by KR-31378 treatment. CH-induced reactive oxygen species (ROS) generation was suppressed by KR-31378. Thus our results indicate that the cardioprotective effect of KR-31378 in CH is due, at least in part, to the differential inhibition of MAPKs.抄録全体を表示PDF形式でダウンロード (1296K) -
Yudai Takarada, Tomomi Tsuruta, Naokata Ishii2004 年 54 巻 6 号 p. 585-592
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーTo obtain insight into the relative contributions of exercise and occlusive stimuli to these muscular adaptations, the present study investigated the short- and long-term effects of varied combinations of low- intensity exercise and vascular occlusion. The subjects were separated into 3 groups (n = 6 for each group): low- intensity with vascular occlusion (LIO), low-intensity without vascular occlusion (LI), and vascular occlusion without exercise (VO). LIO and LI groups performed bilateral knee extension exercises in seated positions with an isotonic extension machine. In the LIO group, both sides of the thigh were pressure-occluded at the proximal end by means of a tourniquet during the entire session of exercise (˜10 min), whereas only the occlusion with the same pressure and duration was given in the VO group. The mean occlusion pressure was 218 ± 8.1 mmHg (mean ± SE). The exercise session consisted of five sets of exercise at an intensity of 10-20% 1RM and was performed twice a week for 8 wk. After the period of exercise training, isometric and isokinetic strengths at all velocities examined increased significantly in the LIO group (p < 0.05), whereas no significant change in strength was seen in the LI and VO groups. The increase in muscular strength in LIO was associated with a significant increase in the cross-sectional area of knee extensor muscles by 10.3 ± 1.6%. The plasma growth hormone concentration measured 15 min after the session of exercise showed a marked increase only in LIO. The results showed that the low-intensity exercise and occlusive stimuli have cooperative effects in the long-term adaptation of muscle and an acute response to growth hormone.
抄録全体を表示PDF形式でダウンロード (901K)
Short Communication
-
Tetsuro Sakai2004 年 54 巻 6 号 p. 593-599
発行日: 2004年
公開日: 2005/03/12
ジャーナル フリーMultiple-site optical recording of membrane potential activity using a voltage-sensitive dye was employed to monitor action potentials in the rat atrium. Electrical pacing at 1 Hz evoked the events of tachycardia-like excitation (TE). Optical mapping revealed that a coupling of spontaneous and evoked action potentials resulted in the initiation of TE.抄録全体を表示PDF形式でダウンロード (298K)
- |<
- <
- 1
- >
- >|