[Results of surgical treatment of scalenus syndrome].
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Adolescent↗
Biomedical subjects
H Sada
Publications and source records attributed to H Sada.
Use of single heart cells from chick embryos for the Na+ current measurements.
To record the fast Na+ current, spheroidal heart cells enzymatically-dispersed from 3 approximately 18-day-old chick embryos were used for voltage clamping. The peak of currents in response to voltage steps of 200 ms long from holding potentials of -90 approximately -105 mV were measured. The current-voltage curves for the peak inward current showed U-shaped relations; the averaged peak current of about -1400 pA was observed at about -30 mV and the current reversed sign at +40 approximately +50 mV. Both the peak current and the reversal potential values showed marked [Na]o-dependence, i.e. reduced by 36% and by 20 mV, respectively, for a halved [Na]o. Tetrodotoxin (TTX) partially (10(-6) M) or completely (10(-5) M) suppressed the current. The steady-state inactivation of the current (h infinity) was characterized by the half inactivation voltage of around -80 mV and the slope factor of -4 approximately -8 mV. The half activation voltage and the slope factor for the steady-state activation (m infinity) were -55 mV and 4-6 mV, respectively. The electrophysiological and pharmacological properties were similar between young (3-day-old) and old (15-18-day-old) embryonic heart cells, excepting the much smaller current and the slower onset of TTX action in young embryonic hearts.
Action Potentials↗
Regulation of the slow Ca++ channels of myocardial cells.
Contraction of the heart is regulated by a number of mechanisms, such as neurotransmitters, hormones, autacoids, pH, intracellular ATP, and Ca++ ions. These actions are mediated, at least in part, by actions on the sarcolemmal slow (L-type) Ca++ channels, exerted directly or indirectly. The major mechanisms for the regulation of the slow Ca++ channels of myocardial cells includes the following. cAMP/PK-A phosphorylation stimulates the slow Ca++ channel activity, whereas cGMP/PK-G phosphorylation inhibits. DAG/PK-C phosphorylation and tyrosine kinase phosphorylation are suggested to stimulate the slow Ca++ channel activity. Intracellular application of Gs alpha protein increases the slow Ca++ currents (ICa(L)). Lowering of intracellular ATP inhibits ICa(L). Acidosis and increase in [Ca]i inhibits ICa(L). A number of changes in the Ca++ channels also occur during development and aging. Thus, it appears that the slow Ca++ channel is a complex structure, including perhaps several associated regulatory proteins, which can be regulated by a number of extrinsic and intrinsic factors, and thereby control can be exercised over the force of contraction of the heart.
Animals↗
Effects of prenylamine on transmembrane action potentials as related to the change in external potassium concentrations in guinea pig papillary muscle.
We studied the effects of 4.8 muM prenylamine on transmembrane potentials in isolated guinea pig papillary muscles using a conventional microelectrode technique and compared them with those of 36.9 microM lidocaine. Prenylamine reduced Vmax at 1 Hz increasingly as the external potassium, [K]o, was increased from 2.7 to 10 mM. The reduction was also increased as the driving rate was increased from 0.25 to 5 Hz. The rate-dependent depression was less in 2.7 and 8.1 mM with 7.2 mM [Ca]o and more in 5.4 and 8.1 mM [K]o with 1.8 mM [Ca]o. Prenylamine produced a marked delay in the recovery of Vmax in premature responses inserted between constant driving stimuli at 0.25 Hz. The delay was also less in the former two, and more in the latter two media. Thus the effects of prenylamine on Vmax were more rate dependent and less [K]o-dependent than those of 36.9 microM lidocaine. At the diastolic interval of 100 ms, prenylamine depressed the overshoot, action potential duration at 0 mV level (APDo) and Vmax in premature responses more markedly than did 36.9 microM lidocaine, the differences of the effects being more significant for the first two. The results are interpreted as representing the calcium-antagonistic property of prenylamine of which lidocaine appears to be devoid.
Action Potentials↗
Actions of the slow channel activator, Bay-K-8644, on the electrical activity of 3-day-old embryonic chick hearts.
In order to assess the effects of Bay-K-8644 on electrical activities of young embryonic chick hearts in which the rising phase of the action potential (AP) depends on tetrodotoxin-insensitive slow Na+ currents, slow AP were recorded in spontaneously beating 3-day-old embryonic chick hearts. Bay-K-8644(10(-6) mol/l) caused increases in the maximum rate of rise, amplitude, and duration of the slow AP; there was a slow increase in the spontaneous firing rate. Thus, Bay-K-8644 stimulates Na+ influx through TTX-insensitive slow channels.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Oxime depression of the fast sodium current in myocardial cells.
Effects of diacetyl monoxime on the fast Na+ current were examined by the whole-cell voltage-clamp method in embryonic chick ventricular myocytes. Diacetyl monoxime (10-20 mM) decreased the duration and amplitude of the action potential and depressed the amplitude of the peak fast inward Na+ current by about 25 (10 mM)-45% (20 mM), without affecting other I-V parameters. Neither the activation and inactivation kinetics of the Na+ channels, such as the time to peak current and the time constant of inactivation, nor the steady state characteristics of the inactivation and activation were affected by diacetyl monoxime. It also did not alter the window conductance and the recovery kinetics from inactivation (reactivation). Hence, diacetyl monoxime suppresses the fast Na+ current, without affecting the time-dependent and voltage-dependent kinetics.
Action Potentials↗