All issues
Successor
Volume 26 (1976)
- Issue 6 Pages 577-
- Issue 5 Pages 441-
- Issue 4 Pages 345-
- Issue 3 Pages 235-
- Issue 2 Pages 101-
- Issue 1 Pages 1-
Volume 26, Issue 3
Displaying 1-9 of 9 articles from this issue
- |<
- <
- 1
- >
- >|
-
Seiki HORI, Heikichiro IHZUKA, Masashi NAKAMURA1976 Volume 26 Issue 3 Pages 235-244
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSIn an attempt to reconfirm Kuno's observation that changes in sweating reaction during long-term heat acclimatization differ from those during short-term heat acclimatization, Ohara's sweating test was performed in summer in Okinawa on 37 male subjects, including 19 residents born and raised in Okinawa (group O) and 18 residents born and raised on one of the main Japanese islands (group M). Seasonal variation of adaptability to heat was also studied in some subjects of both groups. Group O showed significantly less sweat loss, lower Na concentration in sweat and a longer latent period for onset of sweating than group M. Group O showed no seasonal variation in sweat loss, while group M showed considerably greater sweat loss in summer than in winter. In both groups, lower Na concentration in sweat, lower rise in rectal temperature and lesser increase in heart rate in summer than in winter were observed. Seasonal difference in physiological responses of group O to heat exposure was less than that of group M. In conclusion, it was assumed that acclimatization to heat of group O had advanced further than that of group M and this was the reason for longer latent period of sweating and lesser sweat loss in group O in spite of the same rise in rectal temperature in both groups. Discussions were carried out to explain how the sweating pattern and mechanism of acclimatization in group O were different from those in group M.View full abstractDownload PDF (1129K) -
Miharu MIYAMURA, Tadahiko YAMASHINA, Yoshiyuki HONDA1976 Volume 26 Issue 3 Pages 245-254
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSVentilatory responses to CO2 during rest and exercise were studied in 10 marathon runners and 14 untrained subjects by the rebreathing method.The average responses of the untrained subjects and athletes at rest as measured by the slope of VE-PACO2 curves were 1.86 and 1.12 liters/min·mmHg, the difference being statistically significant (p<0.05). During exercise the slope of VE-PACO2 decreased from 1.86 to 0.62 in the controls, and from 1.12 to 0.62 in the athletes (p<0.01).The mean slope obtained in the athletes, at rest and during exercise, was about 50-60% of that in untrained subjects (p<0.05).The difference in the VE-PACO2 curves between the athlete and the untrained group may be due to a reduced exitability of the respiratory center and/or by a reduced input signal.View full abstractDownload PDF (1021K) -
Yoshimi MIYAMOTO, Takehito NAKABAYASHI, Hiroshi SAJI, Tomohisa MIKAMI1976 Volume 26 Issue 3 Pages 255-266
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSDynamic compliance was determined in patients with 6 chronic obstructive lung diseases, 2 sarcoidosis and in 4 control healthy subjects at several breathing frequencies ranging between 0.2 and 1.3Hz.The compliance exhibited an apparent fall with the increase in frequency of the patients, while it remained unaltered in the controls.A significant correlation was found between the frequency-dependency of compliance and the airway conductance determined plethysmographically.A similar relationship was also found in previous data appearing in the literature. Mathematical simulation based on the time constant theory revealed that the above correlation might be expected when airway obstruction occurred inhomogeneously in the peripheral region of the lungs leaving the central airways intact.View full abstractDownload PDF (1123K) -
Naotoshi MURAKAMI, Yoshiyuki SAKATA1976 Volume 26 Issue 3 Pages 267-278
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSReflex vasodilatation in one ear of a rabbit following radiant heating of the opposite ear was observed by measuring the heat loss by a change in the heat flux when either noradrenaline or procaine hydrochloride was administered locally into various diencephalic or mesencephalic loci in the brain. Hypothalamic cooling resulted in less reflex vasodilatation, while no vasodilatatory effect was observed immediately after an intravenous administration of atropin sulphate (0.5mg). Five μg of noradrenaline injected intrahypothalamically either eliminated or reduced the development of reflex vasodilatation to the same extent as did an injection of procaine hydrochloride (0.5mg).
On the other hand, the magnitude of the reflex vasodilatation increased markedly with an injection of either procaine hydrochloride (1.5mg) or noradrenaline (10μg) into the reticular formation of the midbrain. Increased reflex vasodilatation was also obtained with a localized administration of procaine hydrochloride into the medial forebrain bundle of the hypothalamus. These results suggest that the noradrenaline in the preoptic/anterior hypothalamic (PO/AH) area and the midbrain reticular formation exerted an inhibitory effect on the action of the neural structure in connection with the heat dissipation system.View full abstractDownload PDF (1193K) -
Masashi KURAHASHI, Akihiro KUROSHIMA1976 Volume 26 Issue 3 Pages 279-288
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSMechanism of thyroid-induced creatinuria was investigated in rats. The rats were injected with triiodothyronine (T3)(100μg/100 g, sc) at 9.00 hr. Oxygen consumption increased 12 hr after T3 injection, reaching peak value 48 hr after the injection and decreasing to the pre-injection level at 96 hr. Urinary creatine excretion also increased during the first 10 hr after the injection, approaching maximal value 34-48 hr after the injection, and decreasing to the pre-injection level 72-82 hr after the injection. Throughout the experimental period, urinary creatinine decreased with time after the injection, although the difference between the groups was not significant. A decreased creatine tolerance was also observed after T3 injection.β-Guanidinopropionic acid (β-GPA), a competitive inhibitor of creatine transport into skeletal muscle, as well as partial hepatectomy, causing inhibition of creatine synthesis, were without effect on the difference in urinary creatine excretion between T3-treated and control animals. T3 increased the plasma creatine level both in bilateral nephrectomized and in bilateral nephrectomized plus β-GPA administrated groups. These results suggest that increased creatine loss from skeletal muscle in addition to decreased creatine uptake of skeletal muscle rather than increased hepatic synthesis of creatine play an important role in T3-induced creatinuria.View full abstractDownload PDF (936K) -
Takashi AKASU, Kyozo KOKETSU1976 Volume 26 Issue 3 Pages 289-301
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSEffects of adrenaline on K+-activated hyperpolarization of bullfrog sympathetic ganglion cells, preganglionic nerve axons and splanchnic nerve axons were studied.The K+-activated hyperpolarization recorded from ganglion-postganglionic nerve preparations by the sucrose-gap method was augmented in the presence of adrenaline (0.3mM).On the other hand, the K+-activated hyperpolarization of postganglionic, preganglionic nerve axons and splanchnic nerve axons was not affected under the same experimental conditions.The facilitatory effect of adrenaline on the K+-activated hyperpolarization was gradually intensified when the application of adrenaline was sustained for up to 60min.The effect was reversible.The K+-activated hyperpolarization recorded from ganglion cell-bodies by intracellular microelectrodes was similarly augmented by adrenaline (0.1mM).Adrenaline in this concentration, however, caused no significant changes of the membrane potential and conductance in the presence of ouabain (0.002mM) which completely and reversibly inhibited K+-activated hyperpolarization. Noradrenaline showed similar but less effect and isoproterenol showed no significant effect on the K+-activated hyperpolarization.The facilitatory effect of adrenaline was inhibited in the presence of phentolamine but not of DCI. These results suggested that the intraganglionic membrane of ganglion cells possessed some kind of adrenergic α-receptors and the electrogenic Na+pump of ganglion cells was accelerated by some unknown mechanism when adrenaline reacted to these receptors.View full abstractDownload PDF (1514K) -
Hikaru SUZUKI, Kyoko MORITA, Hirosi KURIYAMA1976 Volume 26 Issue 3 Pages 303-320
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSThe membrane potential of dog tracheal muscle was stable at -59.2mV. The length constant of the muscle tissue was 3.2mm and the time constant of the membrane was 449msec. Outward current pulses could not evoke a spike and showed marked rectification of the membrane.Tetraethylammonium, TEA, depolarized the membrane, suppressed the rectification of the membrane, and increased the membrane resistance, and in the presence of TEA outward current pulses could evoke a spike. Acetylcholine and histamine depolarized the membrane but could not evoke a spike. Mechanical response could be evoked by field stimulation via either nerve stimulation or direct muscle stimulation. The mechanical response induced by nerve stimulation was markedly suppressed by atropine. Phentolamine suppressed the contraction which was produced in the presence of atropine, and propranolol suppressed the relaxation. It is unlikely that nonadrenergic-non-cholinergic inhibitory nerves played an important role in the mechanical response. It is concluded regarding the neural actions to the dog trachea that a constriction is induced by cholinergic and adrenergic α-action and a dilation is induced by adrenergic β-action.The relationship between the membrane potential and tension was measured in various [K]O. The mechanical response was triggered by only 5mV depolarization. The physiological evidence and histological finding were compared in relation to nerve activity on the tracheal muscle activity.View full abstractDownload PDF (10171K) -
P. Y. D. WONG1976 Volume 26 Issue 3 Pages 321-331
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSThe rate of 22Na uptake into isolated rat seminiferous tubules has been studied in vitro. The intracellular sodium exchanged rapidly with the outside sodium and within 26 min exposure to radiosodium, isotopic equilibrium was reached. The relationship between sodium influx at 2min and external sodium concentrations was found to be linear suggesting that the entry of sodium into the seminiferous tubules is by simple diffusion. The intracellular Na+ concentration as measured by the 22Na taken up into the tubules at equilibrium condition was elevated in the absence of peritubular K+ and Cat2+ ions and treatment of the tubules with ouabain. No effects of amiloride and acetazolamide on the intracellular Na+ concentration were found. The significance of the 22Na uptake in relation to fluid secretion in the isolated seminiferous tubules was discussed.View full abstractDownload PDF (1107K) -
ROLE OF T-TUBULES IN ELECTROCHEMICAL COUPLINGYoshimichi YAMAMOTO, Yasuhiro HASEGAWA, Ken HOTTA1976 Volume 26 Issue 3 Pages 333-343
Published: 1976
Released on J-STAGE: June 07, 2011
JOURNAL FREE ACCESSResponse of skeletal muscle fibers upon intracellular stimulation was investigated to elucidate the role of the T-system in the electrochemical coupling process.
Upon stimulation, the fiber generates twitch and tonic tension which is independent of the excitation of the membrane (not inhibited by TTX). The fiber placed in low Ca2+ medium (10-7M, controlled by EGTA-Ca) for more than ten minutes, exhibited explosive contraction; this phenomenon was not observed in Na-free choline Ringer or glyceroltreated (T-tubule disrupted) fibers. Injection of a small amount of Mn2+ into the muscle cells produced strong, long lasting contraction without excitation of the membrane.Glycerol-treated fibers failed to respond to the stimulus using a Mn2+ electrode.
These facts suggest that Ca2+ release or entry which probably caused by depolarization of T-tubule membrane in the presence of Na+, may be essential for the initiation of Ca2+ release from sarcoplasmic reticulum.View full abstractDownload PDF (1051K)
- |<
- <
- 1
- >
- >|