Effects of melittin on isolated papillary muscles of guinea pig.

AIM: To investigate the effect of melittin (Mel) on papillary muscles of guinea pigs. METHODS: Contraction of papillary muscles were examined by conventional method and action potentials (AP) were recorded by standard glass microelectrode technique. RESULTS: Mel (0.5, 3 micromol/L) significantly increased the contractility of guinea pig papillary muscles while 5 micromol/L exerted dual action with a transient decrease followed by an increase of the contractility. Mel shortened the functional refractory period (FRP) at concentrations of 0.5, 3, and 5 micromol/L and increased the automaticity induced by adrenaline (Adr) at 3 and 5 micromol/L. Mel shifted the duration-intensity curve upward at 3 micromol/L. It shortened the action potential duration (APD) of fast action potential (FAP), decreased the action potential amplitude (APA) and resting potential (RP) at 0.5 and 3 micromol/L. As to slow action potential (SAP), Mel 0.8 micromol/L shortened APD20 and APD50, and decreased APA and RP. CONCLUSION: Mel increased the contractility and automaticity of papillary muscles, shortened the FRP, decreased the excitability, shortened the APD, and decreased APA and RP of AP.

Inhibitory effects of vinpocetine on sodium current in rat cardiomyocytes.

AIM: To study the effects of vinpocetine (Vin) on the sodium current (INa) in cardiomyocytes. METHODS: The sodium current in adult rat ventricular myocytes was measured by whole cell patch-clamp technique. RESULTS: The INa in cardiomyocytes was blocked reversibly by Vin, in concentration-dependent and voltage-dependent manner, but not rate- or use-dependent. The INa was attenuated by 13%-75% when the Vin concentration was raised from 10 to 80 mumol.L-1. The IC50 (95% confidence limits) was 36.4 (28.1-47.1) mumol.L-1. When the membrane potential depolarized over the range of -90 mV to +40 mV in 10-mV step, inhibitory effect of Vin on the INa was 39% at first, then maintained at a higher level, about 52% +/- 5%. The maximal depression (57%) reached at about 0 mV. Vin influenced both the activation and inactivation processes of sodium channel, and resulted in attenuation of the window currents (the slowly inactivating sodium currents). CONCLUSION: Vin inhibited sodium currents in rat ventricular myocytes.

Electrophysiological effects of felodipine on guinea pig papillary muscles.

AIM: To determine whether felodipine (Fel) has Ca2+ channel blocking effect in mammalian myocardium in comparison with those of nifedipine (Nif) and verapamil (Ver). METHODS: The action potentials (AP), the slow AP and the inward slow Ca2+ currents of guinea pig papillary muscles were studied using intracellular microelectrodes and voltage-clamp techniques. RESULTS: Fel 1, 3, and 10 mumol.L-1 concentration-dependently shortened APD30, APD50, and APD90 of the AP, while Vmax and APA were not affected. The effect of Fel was not reversible on washout. At 0.1, 1, 3, and 10 mumol.L-1, Fel depressed Vmax, APA, APD30, APD50, and APD90 of the slow AP in a dose-dependent manner. The inward slow Ca2+ currents were reduced by Fel 3 mumol.L-1. APD30, APD50, and APD90 of the first AP after rest were still shortened by Fel. When the stimulation frequency was elevated, the effect of Fel on the AP and slow AP decreased. The effect of Fel 3 mumol.L-1 on the slow AP was abolished in preparation pretreated with trifluoperazine. The threshold concentrations of Nif and Ver for the inhibition of APD50 of the slow AP (P < 0.05) were 0.1 and 1 mumol.L-1, respectively. The effect of Ver 3 mumol.L-1 on the fast AP was not reversible on washout, but that of Nif 3 mumol.L-1 was. When the stimulation frequency was elevated from 0.5 to 2 Hz, the effect of Nif 3 mumol.L-1 on the fast AP was reduced, but that of Ver 3 mumol.L-1 was increased. CONCLUSION: Fel inhibited mainly the resting state of the cardiac Ca2+ channel. The potency of Fel was about the same as that of Nif and about 10 times more potent than that of Ver.

Effects of toquipidine on ionic channels of cultured embryonic Xenopus laevis myoblasts and neurons.

AIM: To study the effects of toquipidine (1-p-methyl-phenyl-2-(alpha-piperidinoacetyl)-1, 2, 3, 4-tetrahydroisoquinoline hydrochloride, Toq), a new anti-arrhythmic agent first synthesized in China, on ionic channels. METHODS: Ionic channel currents were recorded by whole-cell patch clamp technique in cultured embryonic Xenopus laevis myoblasts and neurons. RESULTS: Toq (0.1, 1, 10, and 100 mumol L-1) caused a concentration-dependent inhibition of the Na+ currents with IC50 7.2 mumol L-1 (5.3-9.8 mumol L-1). Toq (10 mumol L-1) also suppressed the high-voltage-activated Ca2+ currents in neurons. But the steady-state outward K+ currents in myoblasts were activated by Toq (10 mumol L-1). CONCLUSION: Toq blocked the Na+ and Ca2+ channels and opened the steady-state outward K+ channels.

Forensic laboratory work in Burma (with special reference to the Office of the Chemical Examiner, Burma).

Burma is a country in Southeast Asia which is slightly smaller than Texas and has a population of 30 million people. The British colonial era brought the Chemical Examiner's laboratory to Burma. This was an all-purpose analytic laboratory. The forensic laboratory evolved within this structure as the need arose. The Medico-legal Division of this laboratory examined trace evidence, drugs, and body fluids of felons and there victims. Various aspects of investigation are discussed.