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PubMed2005

Effects of long-term administrations of aconitine on electrocardiogram and tissue concentrations of aconitine and its metabolites in mice.

Aconitum alkaloids are well known for their acute and high toxicity, for example, in the causation of severe arrhythmias leading to death. Aconitine, one of the major Aconitum alkaloids, is a highly toxic compound from the Aconitum species. However, there has been no studies reported on the influence of the chronic administration of aconitine. Thus, this study was conducted to investigate the influence of chronic administration of aconitine in experimental animal models. A dose of 1mg/kg per day was administered to the experimental animal models. We determined the concentration of aconitine and its metabolites (benzoylaconine and aconine) in organs and blood with gas chromatography/selected ion monitoring (GC/SIM). In addition, we concurrently recorded the electrocardiogram (ECG). Fifteen minutes after administration on day 0, the early aconitine administered group (acute group) revealed peak organ and blood concentration levels of aconitine with a gradual decrease, thereafter. The concentration of aconitine in organs and blood (from days 0 to 22; 90 min after the last administration of aconitine) gradually decreased according to repeated administration, whereas benzoylaconine and aconine increased. ECG revealed various types of arrhythmias. However, the frequency of arrhythmias remarkably decreased with time and repeated administration of aconitine. These results indicate two possibilities. First, the increase in the activity of aconitine metabolism. Secondly, the decrease of effectiveness to the heart due to long-term (chronic) administration of aconitine.

Aconitine↗
PubMed2003

A new enzyme immunoassay for aconitine and its application to quantitative determination of aconitine levels in plasma.

A reliable enzyme immunoassay (EIA) method was developed for quantitative determination of aconitine with high sensitivity and specificity. The bovine serum albumin (BSA)- and beta-galactosidase (beta-Gal) conjugates as immunogens and enzyme-labeled antigens were prepared by coupling of their proteins with succinic acid (short chain length; n=2, where n represents the number of methylene units) and hexadecanedioic acid (long chain length; n=14) hemiesters of benzoylaconine through the respective N-hydroxysuccinimide esters as intermediates. Two types of the BSA-conjugates with short and long chains were repeatedly injected into rabbits to obtain anti-aconitine antisera (As1 and As2, respectively). All combinations of beta-Gal-labeled antigens LAg1 (n=2) and LAg2 (n=14) with antisera As1 (n=2) and As2 (n=14) showed high sensitivity to aconitine in a range of 0.1-1.0 ng. Although the combination of LAg2 (n=14) with antiserum As1 (n=2) showed high specificity to aconitine, the combination of LAg2 (n=14) and As2 (n=14) was highly specific to both aconitine and mesaconitine. When aconitine was intravenously administered to rats, the aconitine concentration in their plasma remarkably decreased within the first 60 min, and then gradually declined, suggesting a two-compartment pharmacokinetic model in (V(c) 0.41+/-0.09 l/kg, V(dss) 1.7+/-0.4 l/kg, CL(tot) 10+/-2 ml/min x kg, AUC(0-4800) 2055+/-294.3 ng x min/ml). Following oral administration of aconitine to rats at two doses of 0.1 and 1.0 mg/kg b.w., the maximum plasma concentrations (C(max)) were 0.73+/-0.08 and 3.3+/-0.6 ng/ml at times of 45+/-9 and 150+/-52 min, respectively, and the AUC(0-1440) values were 130+/-4 and 1600+/-270 ng x min/ml. The bioavailability (F) of aconitine was determined to be 0.013, where only 1.3% of the aconitine administered orally was absorbed into the body fluid.

Aconitine↗
PubMed1996

A case of aconitine poisoning with analysis of aconitine alkaloids by GC/SIM.

Described here is a fatal case of accidental aconitine poisoning following the ingestion of aconite, Torikabuto, mistaken for an edible grass, Momijigasa. A 61-year-old man developed symptoms of nausea, diarrhea, and discomfort of the body about 2 h after the ingestion and was taken to an emergency room. Resuscitation and antiarrhythmic drugs were ineffective, and ventricular tachycardia and fibrillation developed and lasted for 6 h. He was transferred to a coronary care unit and complete sinus rhythm was obtained on an electrocardiogram 30 h after his admission. The patient fell into a coma and died of brain edema diagnosed by CT on the 6th day. Consent for autopsy was denied by the family but was given for gas chromatography/selected ion monitoring (GC/SIM) to analyze the toxicity of aconitine alkaloids in the blood and the urine. Only a faint amount of jesaconitine was detected, while aconitine, mesaconitine and hypaconitine were not detectable in the blood 24 h after ingestion. On the other hand, aconitine and its related alkaloids such as mesaconitine, jesaconitine, and hypaconitine were clearly detected in the urine.

Aconitine↗
PubMed2002

[Determination of aconitine alkaloids in a pesticide--0.25% aconitine alkaloids mixed with emulsion by high performance liquid chromatography].

The raw root of Aconitum, an important Chinese traditional medicine, contains some very toxic alkaloids such as aconitine, mesaconitine and hypaconitine etc. They are usually processed to lower the alkaloid content before used as a drug. The extract of crude drug (aconite) can be made into a plant pesticide by means of mixing with some emulsion. In order to evaluate the quality of the pesticide, we developed a rapid, specific and precise method using high performance liquid chromatography (HPLC) for the separation and quantitation of the alkaloids in the aconite extract and the mixed products (the aconite extract is mixed with emulsion). Before the determination by HPLC, the sample must be acidified with 2% (mass percentage) HCl at first. Extract the acid liquid with CHCl3. Alkalize the extract with ammonia, and add a little of 0.1 mol/L NaHCO3 and 0.1 mol/L Na2CO3 till pH 9. Extract it with CHCl3. Evaporate the extract and add a certain amount of methanol. Add the internal standard into the sample. Inject the combined sample solution onto a column of chemically bonded octadecylsilane phase and develop the chromatogram with MeOH-H2O-CHCl3-triethylamine (68:32:2:0.1, volume ratio). Aconitine, mesaconitine, hypaconitine and medroxyprogesteroni acetas (internal standard) were on base line separated. Quantify the alkaloids by peak area ratio (aconitine alkaloids vs internal standard). This method has high recovery (> 92%) and good reproducibility (RSD < 3.2%).

Aconitine↗
PubMed1983

The positive inotropic effect of aconitine.

1. The inotropic and electrophysiological effects of aconitine were measured in the isolated, isometrically contracting guinea-pig papillary muscle during the prearrhythmic phase of alkaloid action. 2. In muscles stimulated continually at 1 Hz, 1 mumol/l aconitine produced a positive inotropic effect that reached 38 +/- (SEM) 9% immediately before the onset of arrhythmia (n = 3). 3. If aconitine (0.5 mumol/l) was applied to non-stimulated (resting) muscles for 30 min and 1-Hz stimulation resumed thereafter, the arrhythmia occurred after 724 +/- 101 beats. Prolongation of the rest exposure to 2 h did not significantly diminish the number of prearrhythmic beats. Thus, the onset of aconitine action is critically determined by muscle activity (rather than by time), and a 30-min aconitine application to the resting muscle suffices for complete equilibration of the tissue. 4. Using the preequilibration-at-rest procedure, the positive inotropic effect of aconitine (0.25 - 4 mumol) was found (a) to be absent in the rested-state contraction, (b) to grow with both number of subsequent beats and alkaloid concentration, and (c) to reach a similar prearrhythmic maximum at all concentrations. This maximum amounted to about 1/4 of the maximum positive inotropic effect of dihydroouabain. It was not influenced by reserpine pretreatment of the guinea pig. 5. Aconitine (1 mumol/l) delayed the repolarization phase of the action potential by establishing a secondary plateau at approximately -60 mV. This effect paralleled the positive inotropic effect and, like the positive inotropic effect, was abolished by 10 mumol/l tetrodotoxin (TTX). In partially depolarized muscles ([K]0 = 24 mmol/l) aconitine (8 mumol/l) produced a TTX-sensitive increase in amplitude and rate of rise of the rested-state contraction; this indicates a voltage-dependent effect on some resting Na channels. 6. While delaying the late repolarization phase, aconitine markedly shortened the early repolarization at levels positive to -40 mV, reduced the overshoot and decreased the maximum rat of depolarization of the action potential. Slow action potentials ([K]0 = 24 mmol/l; 10 mumol/l TTX) were insensitive to aconitine. 7. We conclude that the well known property of aconitine to prolong the Na influx during the action potential leads to a positive inotropic effect, thus confirming the importance of Na influx for the regulation of myocardial contractility. The exact mechanism of an additional effect by which aconitine reduces the overshoot and shortens the plateau phase of the action potential awaits further study.

Aconitine↗
PubMed2005

Effects of chronic administrations of aconitine on body weight and rectal temperature in mice.

Aconitine, a major Aconitum alkaloid, is well known for its high toxicity that induces severe arrhythmias leading to death. However, aconitine has been used as one of the most popular compounds in Shino-Japanese traditional herbal medicine. Little has been reported concerned with the long-term effects of aconitine. Therefore, the authors investigated the physiological effects of chronic administrations of aconitine by determining the changes in body weight and rectal temperature of mice, compared with the concentrations of aconitine and its metabolites (benzoylaconine and aconine) in the liver and kidneys. The concentration ratio of aconitine to the total Aconitum alkaloids (from day 0 to 22; 90 min after the last administration) gradually decreased, whereas its metabolites increased until day 22. The body weight gain in aconitine-administered group was less than that of the control group until day 22. Transient rectal hypothermia occurred within 30 min after the last administration of aconitine. Then the rectal temperature gradually increased to normal level in respect to time. This study might reveal the possibilities that the drug metabolism of aconitine increased and the toxicity of aconitine decreased due to long-term administrations of aconitine.

Aconitine↗
PubMed2004

Increased susceptibility of ventricular arrhythmias to aconitine in anaesthetized rats is attributed to the inhibition of baroreflex.

1. Aconitine is widely used to produce ventricular arrhythmias in anaesthetized rats. The present work was designed to test the hypothesis that anaesthesia may increase the susceptibility of ventricular arrhythmia to aconitine due to the inhibition of arterial baroreflex. In addition, the susceptibility of ventricular arrhythmia to aconitine at different times during the course of a whole day was also investigated. 2. Male Sprague-Dawley rats were used. Arrhthymias were induced by aconitine infusion at six time points (01.00, 05.00, 09.00, 13.00, 17.00 and 21.00 h) with rats in both anaesthetized and conscious states. In sinoaortic-denervated (SAD) rats, ventricular arrhythmias were induced by aconitine infusion between 09.00 and 13.00 h. 3. There was a significant difference in the lethal dose of aconitine between anaesthetized and conscious rats (99.6 +/- 30.1 vs 58.2 +/- 14.7 micro g/kg; P < 0.001). Anaesthesia did increase the susceptibility of rats to ventricular arrhythmias following aconitine. 4. In SAD rats, the lethal dose of aconitine was less than that for baroreflex-intact rats when determined in the conscious state. The difference in the lethal dose of aconitine between SAD and baroreflex-intact rats disappeared when it was determined in anaesthetized rats. 5. The time of day did not affect the susceptibility of either anaesthetized or conscious rats to ventricular arrhythmias following aconitine, except for a difference in the ventricullar fibrillation threshold dose between 13.00 and 17.00 h in anaesthetized rats. 6. In conclusion, anaesthesia may increase the risk of ventricular arrhythmias following aconitine. Intact arterial baroreflex function is necessary to prevent drug-induced ventricular arrhythmias.

Aconitine↗
PubMed2002

Aconitine facilitates spontaneous transmitter release at rat ventromedial hypothalamic neurons.

The effects of aconitine, an Aconitum alkaloid, on spontaneous inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs respectively) were investigated in the mechanically dissociated rat ventromedial hypothalamic (VMH) neurons in which native presynaptic nerve terminals remained intact. Under current-clamp conditions, aconitine (3 x 10(-6) M) depolarized the neuron with generating the action potentials. The aconitine-induced depolarization was markedly suppressed in the presence of CNQX but it was facilitated in the presence of bicuculline, suggesting that release of excitatory and inhibitory neurotransmitters may be involved in the aconitine action in addition to its direct action on postsynaptic membrane. Under the voltage-clamp conditions, aconitine reversibly increased the frequency of spontaneous IPSC and EPSC frequency, but it did not alter their amplitude distribution. Tetrodotoxin (TTX, 3 x 10(-7) M) completely abolished the aconitine action on spontaneous IPSC frequency. Likewise removal of extracellular Na(+) completely suppressed the aconitine action. Both Ca(2+)-free external solution or addition of 10(-4) M Cd(2+) to normal solutions eliminated the facilitatory effect of aconitine on the IPSC frequency. Overall these results suggest that aconitine depolarizes the presynaptic membrane by activating voltage-dependent Na(+) channels. Increase of intraterminal Ca(2+) concentration via an activation of voltage-dependent Ca(2+) channels in turn enhances the spontaneous transmitter release from presynaptic nerve terminals. The presynaptic action of aconitine may play a crucial role for membrane excitability of rat VMH neurons.

Aconitine↗
PubMed1993

R 56 865, a Na+/Ca(2+)-overload inhibitor, protects against aconitine-induced cardiac arrhythmias in vivo.

Disturbances in cellular Na+/Ca2+ homeostasis may play a central role in the pathogenesis of ventricular arrhythmias and cell damage induced by the alkaloids veratridine and aconitine in vitro. To test this hypothesis in vivo, the effects on aconitine-induced arrhythmias of intravenous (i.v.) pretreatment with R 56 865 (a Na(+)- and Ca(2+)-overload inhibitor) were compared with those of lidocaine, verapamil, and tetrodotoxin (TTX) in anesthetized rats (n = 10 for each compound). The i.v. bolus injection of aconitine (6.2, 12.5, or 25 micrograms/kg) induced ventricular premature beats (VPBs), ventricular tachycardia (VT), ventricular fibrillation (VF), and mortality in a dose-dependent manner. Because aconitine at a dose of 12.5 micrograms/kg i.v. resulted in a high incidence of ventricular arrhythmias as well as mortality, this dose was used in further tests. Pretreatment of rats with R 56 865 (1.25 mg/kg) significantly reduced the incidences of aconitine-induced VT and VF, as well as mortality, relative to the saline control group. Pretreatment with verapamil (0.32 mg/kg), was ineffective against aconitine-induced ventricular arrhythmias and mortality. Pretreatment with lidocaine (10 mg/kg) significantly reduced the incidence of VT and caused low but not significant reductions in the incidences of VF and mortality induced by aconitine. Pretreatment with a selective sodium channel blocker TTX (4 micrograms/kg) also significantly reduced the incidences of VT, VF, and mortality elicited by aconitine. These results suggest that intracellular Na+ loading plays an important role in aconitine-induced ventricular arrhythmias; the Ca(2+)-overload after Na+ loading elicited by aconitine is not likely to be mediated by increased Ca2+ influx through a slow channel.

Aconitine↗
PubMed1996

Electrophysiological effects of aconitine in rat hippocampal slices.

The electrophysiological effects of aconitine were investigated in the rat hippocampal slice and compared with those of veratridine. Both alkaloids are known to bind at site 2 of sodium channels and to block its inactivation. Extracellular recordings revealed that aconitine and veratridine exert inhibitory effects on neuronal excitability. Aconitine slowly and reversibly decreased the population spike recorded in the CA1 pyramidal cell layer. The reduction of the spike amplitude was similar whether orthodromically or antidromically activated. The aconitine-induced inhibition did not differ from that of veratridine. However, following washout of aconitine, the amplitude of the antidromic spike was increased compared to the control amplitude. The veratridine-induced inhibition was only partially reversible. This inhibition was also observed during suppression of synaptic transmission by a low Ca2+/high Mg2+-medium, indicating an inhibition of axonal conductance. The results show that in the absence of synaptic transmission the antidromic (alvear) spike is more sensitive to the inhibitory action of aconitine than the presynaptic fiber spike elicited by stimulation of the Schaffer collaterals. Furthermore, it is shown that aconitine acts in an activity-dependent manner, in that the latency of onset of the inhibition is prolonged when the stimulation frequency is decreased. Field excitatory postsynaptic potentials were also suppressed by aconitine, whereas excitatory postsynaptic currents recorded by the patch clamp technique were not influenced by aconitine when cells were held at -60 mV.

Aconitine↗
PubMed1999

Interaction of the structurally related aconitum alkaloids, aconitine and 6-benzyolheteratisine, in the rat hippocampus.

Aconitine is a highly toxic diterpenoid alkaloid occurring in plants of the Aconitum genus. Aconitine is known to shift the voltage-dependence of the voltage-dependent Na(+) channel towards hyperpolarized direction, thereby leading to a permanent activation of the channel. 6-benzoylheteratisine is a plant alkaloid which is structurally related with aconitine. The aim of the present study was to investigate the interaction of aconitine and 6-benzoylheteratisine in the rat hippocampus. The experiments were carried out as extracellular recordings of stimulus evoked population spikes and field excitatory postsynaptic potential (EPSP) in rat hippocampal slices. Aconitine (10-100 nM) exerted a concentration-dependent decrease in the amplitude of the orthodromic population spike. When aconitine was applied in presence of 6-benzoylheteratisine (3 microM), the concentration-response curve was shifted to the right. Furthermore, the complete suppression of the population spike evoked by 100 nM aconitine was reversed by 10 microM 6-benzoylheteratisine. The closely related alkaloid heteratisine (3 and 30 microM), however, was not capable to antagonize the aconitine action. 6-benzoylheteratisine shifted the input-output relationship of the presynaptic fiber spike as function of the stimulation intensity and the input-output relationship of the field EPSP as function of the presynaptic fiber spike to the right. Thus, electrophysiologically this alkaloid seems to inhibit predominantly the excitability of the afferent fibres and, in consequence, neurotransmission between Schaffer collaterals and the CA1 neurons, thereby suppressing the firing of the latter. Spontaneously occurring epileptiform activity in area CA3 elicited by omission of Mg(2+) and elevation of K(+) was attenuated by 6-benzoylheteratisine (1 and 10 microM). Patch clamp studies performed on cultured rat hippocampal pyramidal cells revealed an inhibitory action of 6-benzoylheteratisine on whole cell Na(+) currents. It is concluded that the inhibitory and antiepileptiform effect of ajacine and lappaconitine is mediated by an inhibition of the voltage-dependent Na(+) channel which might be important for filtering high frequency bursts of action potentials characteristic for epileptiform activity in the hippocampus. Thus, 6-benzoylheteratisine seems to be a naturally occurring antagonist of the Na(+) channel activator aconitine.

Aconitine↗
PubMed1983

Gating and selectivity of aconitine-modified sodium channels in neuroblastoma cells.

Currents through normal and aconitine-modified sodium channels in perfused neuroblastoma cells were measured under voltage-clamp conditions. Aconitine is shown to induce changes in channel selectivity so that channels become more permeable to NH4+ than to Na+. Aconitine induces the shift of voltage dependence of channel activation toward more negative potentials by about 20 mV. Aconitine-modified channels inactivate practically completely with a time-course similar to that for normal channels. Aconitine is effective when applied to either side of the membrane. Steady-state characteristics of the gating machinery of aconitine-modified channels are discussed in terms of three-state model. According to the model, aconitine increases the probability of finding the channel in open state, which is reflected in negative shift of the voltage dependence of activation. The model predicts that the larger this shift, the higher is the level of steady-state sodium conductance. The comparison of respective properties of aconitine-modified channels in neuroblastoma cell and frog nerve confirms this prediction. Aconitine is assumed to reach its receptor through the lipophilic part of the membrane.

Aconitum↗
PubMed1997

Calcium-dependent, sustained enhancement of excitability during washout of aconitine in rat hippocampal slices.

Extracellular recording of the stimulus-evoked population spike was performed in the CA1 area of rat hippocampal slices in order to investigate delayed effects of the plant alkaloids aconitine and veratridine. Veratridine (1 microM and 10 microM) suppressed the orthodromic and antidromic population spike. After washout of the drug, only a partial recovery was obtained. Aconitine (1 microM) exerted the same inhibitory action as veratridine. However, after washout, the spike amplitude was enhanced compared with the control. This enhancement of the spike amplitude was dependent on the concentration of aconitine and was maintained during the observation period of at least 2 h. Lowering the Ca2+ concentration of the bathing medium from 2.5 mM to 1.25 mM during application of aconitine attenuated recovery and prevented the enhancement observed during washout of the drug. Application of aconitine in the presence of CdCl2 as well as in the presence of inhibitors of protein kinase C and Ca2+/calmodulin-dependent protein kinase II prevented the increase in spike amplitude during washout with standard artificial cerebrospinal fluid. In contrast, the N-methyl-D-aspartate (NMDA) receptor antagonists D-AP5 and MK-801 as well as the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione were ineffective in abolishing the aconitine-induced enhancement. These data support the conclusion that different modes of action are involved in the effects of aconitine but not veratridine. It is concluded that the aconitine-induced increase in neuronal activity is mediated by intracellular Ca2+-dependent mechanisms leading to an activation of Ca2+-dependent protein kinases. This effect is independent of Ca2+ entrance through NMDA and non-NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1996

Potentiation by higenamine of the aconitine-induced positive chronotropic effect in isolated right atria of mice: the effects of cholera toxin, forskolin and pertussis toxin.

Aconitine and higenamine are the major cardioactive compounds obtained from processed aconite. The chronotropic interaction between these two compounds was investigated in isolated right atria of mice. Both aconitine and higenamine potentiated the action of the other. Practolol (1 nM), a selective beta 1-adrenergic antagonist, but not butoxamine (1 microM), a beta 2-adrenergic antagonist, blocked the potentiation by higenamine (5 nM) of the aconitine-induced positive chronotropic effect and, at high concentrations (30 and 300 nM) also shifted the aconitine concentration-response curves to the right. The potentiating interaction between aconitine and higenamine was reversed by pretreating with cholera toxin (CTX) and forskolin. In CTX (100 nM, 1 h)- and forskolin (30 and 100 nM)-treated atria, higenamine significantly depressed the aconitine-induced response, which was abolished by pertussis toxin (PTX, 150 micrograms/kg, i.p., 3 d). Neither CTX (50 and 100 nM) nor forskolin (15-100 nM) significantly affected the aconitine-induced positive chronotropic effect, while PTX (150 micrograms/kg) depressed it. These results suggest that the potentiating interaction between aconitine and higenamine involves "cross-talk" between the beta 1-adrenergic signalling pathway and Gi-protein.

Aconitine↗
PubMed1987

Aconitine-induced delayed afterdepolarization in frog atrium and guinea pig papillary muscles in the presence of low concentrations of Ca2+.

Aconitine will induce arrhythmias after the fiber has been completely repolarized. This arrhythmia is generally facilitated in the presence of high Ca2+ solution, yet the aconitine-induced arrhythmia occurs even in the presence of low Ca2+ solutions. We studied aconitine-induced arrhythmia (particularly the amplitude of delayed afterdepolarization) in the frog atrium or guinea-pig papillary muscles in Ca2+-free solution, in the presence or absence of Ca2+ channel blocking agents. In Ca2+-free solution, aconitine (10(-5) g/ml) decreased the resting potential, overshoot, Vmax, and shortened the duration of the 90% action potential, before the onset of delayed afterdepolarization in frog atrial preparations. Tetrodotoxin (TTX) (2 X 10(-7) g/ml) blocked these aconitine-induced electrical changes. Verapamil (10(-6) g/ml) in nominally Ca2+-free solution blocked neither the generation of delayed afterdepolarization nor the triggered activity, while LaCl3 (0.5 mM) or TTX halted it. Delayed afterdepolarization appeared following the aconitine-induced transient increase in twitch tension. This transient increase in twitch tension was blocked by LaCl3 and TTX but not by verapamil. Delayed afterdepolarization in Ca2+-free solution demonstrated the voltage dependence of a U shape between -40 and -80 mV and was inhibited by low Na+ and high K+. Under the influence of aconitine in the guinea pig papillary muscle exposed to the Ca2+-free solution, depolarizing clamp pulses produced a transient inward current, and here the sigmoid time- and voltage-dependent characteristics were similar to those seen in the case of digitalis intoxication. These results suggest that intracellular Na+ loading plays an important role in the aconitine-induced delayed afterdepolarization and transient inward currents in low Ca2+ solution.

Aconitine↗
PubMed2005

[Separation and determination of aconitine in medicine wine by reversed-phase high performance liquid chromatography].

OBJECTIVE: For the purpose of more accurate and rapid analysis of aconitine in medicine wine, a reversed-phase High Performance Liquid Chromatography (HPLC) method was developed. METHODS: Standard aconitine was added to the blank wine when the wine sample was pretreated. The pretreatment method of samples, the linear range, the precision, the recoveries in the plasma were investigated by using of white wine plasma spiked with standard aconitine. RESULTS: The linear range was 0.45 approximately 9.0 microg x mL(-1), r=0.998 8. The detective limit was 0.45 microg x mL(-1), The intra and inter-day precision of assay for aconitine were less than 3.1% and 4.7% (n=5) in wine respectively. The recoveries of aconitine were more (97.3+/-2.8)% in medicine wine. The HPLC method has been used to investigate the concentration of aconitine in one forensic medicine case. CONCLUSION: The HPLC method of quantitative analysis aconitine is rapid and sensitive. It is only in the 2.0 h that determination of aconitine in the medicine wine.

Aconitine↗
PubMed1987

Gating current experiments on frog nodes of Ranvier treated with Centruroides sculpturatus toxins or aconitine.

(1) Gating currents were recorded from frog nodes of Ranvier treated either with toxins III or IV from the venom of the scorpion Centruroides sculpturatus or with the alkaloid toxin aconitine. (2) Toxins III or IV from Centruroides sculpturatus (which drastically reduce the sodium permeability PNa and slightly shift its voltage dependence in the depolarizing direction) caused a small depolarizing shift of the relation between charge (Qon) and membrane potential (E) without affecting the maximum charge Qon max. (3) On nodes treated with toxins III or IV from Centruroides sculpturatus, a depolarizing conditioning pulse (which transiently shifts the descending branch of the INa(E) curve by up to 60 mV in the hyperpolarizing direction) shifted the midpoint potential (Emid) of the Qon(E) curve by -17 mV and slightly increased the slope of the curve; it also decreased Qon max markedly but had little effect on Qon measured with small depolarizing pulses. By contrast, massive treatment with aconitine (which irreversibly shifts sodium activation in the hyperpolarizing direction) irreversibly shifted the midpoint potential of the Qon(E) curve from -28.5 to -69 mV and significantly increased Qon and Qoff measured with small depolarizing pulses; concomitantly, the voltage dependence of the on time constant of the charge movement [tau on(E)] was shifted by -44 mV. (4) The sodium current INa was exponential both in nodes treated with toxins III or IV of Centruroides sculpturatus and subjected to a depolarizing conditioning pulse and in aconitine-treated nodes; in the latter, INa started after a delay of 30-40 microseconds. The time constant of the sodium current. tau on Na, was larger than the time constant of the charge movement, tau on Q; the ratio tau on Q/tau on Na was 0.61 and 0.73 in the experiments with Centruroides sculpturatus toxins and aconitine, respectively. (5) The off time constant of the sodium current (tau off Na) was slightly increased in nodes treated with Centruroides sculpturatus toxins and subjected to a depolarizing conditioning pulse, whereas it was markedly increased in aconitine-treated nodes. With the former treatment, the off time constant of the charge movement (tau off Q) was unaffected but with aconitine treatment it was considerably increased although it remained smaller than tau off Na. Consequently, the ratio tau off Q/tau off Na (which is greater than or equal to 1 in untreated nodes) became smaller than one, reaching values as low as 0.58 and 0.44 in the experiments with Centruroides sculpturatus toxins and aconitine, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Aconitine↗