Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PRENYLAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed1975

Tryptamines and some other substances affecting waking and sleep in fowls.

1 Adult fowls (Gallus domesticus) with cannulae chronically implanted in the IIIrd cerebral ventricle and various other sites of the brain, received infusions or injections of tryptamines and catecholamines into the brain; effects of and interactions between these substances on behaviour, electrocortical activity and body temperature were studied. Reserpine-induced arousal, was investigated in young and adult fowls. 2 Tryptamine and alpha-methyltryptamine, given intraventricularly or into the hypothalamus of intact fowls evoked behavioural and bilateral electrocortical arousal, postural changes, elevation of body temperature and tachypnoea; behavioural and bilateral electrocortical arousal were obtained with infusions into the mesencephalon. Ipsilateral electrocortical arousal only, resulted from infusion of alpha-methyltryptamine into the hypothalamus or mesencephalon of fowl encephale isole preparations. The above effects in intact fowls were reduced or replaced by sleep following administration of noradrenaline or alpha-methylnoradrenaline into the IIIrd ventricle or hypothalamus. Pretreatment of intact fowls with an amine oxidase inhibitor surprisingly attenuated or reversed the excitant effects of intraventricular tryptamine. 3 5-Hydroxytryptamine (hydrogen maleinate, creatinine sulphate or oxalate) given intraventricularly or infused into the hypothalamus, elevated body temperature; tachypnoea and postural changes developed at some stage during the elevation of body temperature. Sleep also was induced, although with the oxalate this was succeeded by marked arousal. 4 Behavioural and electrocortical sleep induced by 5-hydroxytryptamine infused into the hypothalamus were replaced by arousal on infusing tryptamine into the hypothalamus, and vice versa. 5 Dexamphetamine infused into the hypothalamus induced drowsiness or sleep which even reversed arousal elicited by systemically administered dexamphetamine. 6 Reserpine-induced arousal was achieved in young and adult fowls pretreated with mebanazine; this arousal was attenuated or replaced by sleep following intraventricular noradrenaline or dopamine but not by 5-hydroxytryptamine nor by noradrenaline or dopamine applied to the hypothalamus. Prenylamine also induced arousal following pretreatment of chicks with mebanazine.

Animals↗
PubMed1980

Effects of vasodilator drugs, alkaline phosphatase, and cyclic AMP-dependent protein kinase on the 45calcium uptake of sarcolemmal microsomes from human umbilical arteries.

1 A microsomal fraction was prepared from human umbilical arteries by differential centrifugation. The preparation was capable of an oxalate-stimulated Ca2+ uptake at a mean rate of 0.74 nmol Ca2+ mg-1 protein min-1 which could be inhibited by a Ca2+ ionophore, A 23 187, and by Tween 80. 2 The rate of Ca2+ uptake in the fraction obtained by density gradient fractionation paralleled 5'-nucleotidase activity suggesting that vesicles of predominantly sarcolemmal origin were responsible for the microsomal Ca2+ uptake. 3 Cyclic adenosine 3',5'-monophosphate-dependent protein kinase enhanced membrane phosphorylation but did not affect Ca2+ uptake. Preincubation with alkaline phosphatase reduced membrane phosphorylation to a greater extent than Ca2+ uptake. These data are not in favour of a close correlation between Ca2+ uptake and phosphorylation. 4 None of 15 vasodilator drugs (bencyclane, carbocromen, diazoxide, dilazep, hydralazine, indapamide, isosorbide dinitrate, methyl-isobutyl-xanthine, minoxidil, naftidrofuryl, nitroglycerine, prenylamine, sodium nitroprusside, tetracaine, and verapamil) had any effect on Ca2+ uptake at 10(-5) M. This suggests that vasodilator drugs do not act by a direct influence on the Ca2+ pumps of vascular smooth muscle cells.

Alkaline Phosphatase↗
PubMed1984

An investigation into the characteristics of reperfusion-induced arrhythmias in the anaesthetized rat and their susceptibility to antiarrhythmic agents.

Reperfusion-induced arrhythmias were elicited in the pentobarbitone-anaesthetized rat by occlusion of the left main coronary artery and subsequent release. These arrhythmias were rapid in onset, occurring within 20 s after release of the ligature, and were of short duration (1-2 min). Their severity was dependent upon the duration of the preceding occlusion. A 5 or 15 min occlusion period produced the most severe arrhythmias on release, the incidence of ventricular fibrillation being 56 and 50% respectively. Evidence that reperfusion had occurred was provided by fluorescein dye distribution and intramyocardial temperature studies. The severity of reperfusion arrhythmias and mortality was unaffected by bilateral vagotomy, beta-adrenoceptor blockade by atenolol (2 mg kg-1 i.v.) or a combination of the two. The incidence of reperfusion-induced ventricular fibrillation was significantly reduced by Org 6001 (which blocks the fast inward sodium current), melperone (which acutely prolongs the cardiac action potential duration) and bepridil (which blocks both fast and slow inward currents). It was unaffected by nitroglycerine and the calcium antagonists verapamil, prenylamine and nifedipine. We have shown that reperfusion-induced cardiac arrhythmias can be consistently elicited in the anaesthetized rat and that they are particularly susceptible to drugs that can block the fast inward sodium current.

Anesthesia↗
PubMed1989

The pharmacological properties of the peptide, endothelin.

1. The effect of endothelin (ET-1) has been studied on isolated vascular and non-vascular preparations, using both functional and competition radioligand binding techniques. The effects of endothelin on blood pressure were studied in both anaesthetised, chemically denervated normotensive and spontaneously hypertensive rats (SHR). 2. Endothelin elicited contractile responses in the rat thoracic aorta, perfused mesenteric bed, rabbit mesenteric artery and portal vein. The maximal responses in the rat aorta were enhanced by removal of the endothelium, and were reduced in the presence of either a cyclo-oxygenase inhibitor (indomethacin) or a thromboxane receptor antagonist (SQ 29,548). In terms of potency, the most sensitive preparation was the rat endothelium-denuded aorta and rat perfused mesenteric bed (-log EC50 values = 8.2 +/- 0.07 and 8.2 +/- 0.12, mean +/- s.e.mean, n = 4, respectively). In the perfused mesenteric bed of the rat the maximum response to endothelin (219 +/- 12 mmHg, n = 4) was greater than that to either phenylephrine (maximal response = 67 +/- 9 mmHg; n = 4) or KCl (maximal response = 110 +/- 6 mmHg, n = 4). 3. Endothelin elicited contractile responses of the guinea-pig isolated ileum, oesophageal muscularis mucosae and uterus. Responses were also observed in the rat fundic strip and paced left atria. The guinea-pig urinary bladder, trachea, rat vas deferens and anococcygeus exhibited little or no response to endothelin at the concentrations studied (1 x 10(-12)-3.2 x 10(-8) M). Of the above preparations, the ileum and oesophageal muscularis mucosae were the most sensitive to endothelin (-log EC50 = 8.5 +/- 0.11 and 8.4 +/- 0.06, n = 6, respectively), exhibiting potencies similar to those observed in the endothelium-denuded aorta of the rat. 4. In competition-radioligand binding studies, endothelin did not displace either [3H]-PN 210-100 or [125I]-(-)-omega-conotoxin GVIA from binding sites in membranes from rat cerebral cortex and, skeletal muscle or from guinea-pig cerebral cortex and hippocampus, respectively. This indicates a lack of direct interaction of endothelin at the dihydropyridine binding site and the N-type calcium channel, respectively. However, in functional studies, contractile responses to endothelin (1 x 10(-8) M) in the endothelium-denuded aorta of the rat were potently reversed by nifedipine, verapamil, and prenylamine (-log IC50 values = 8.0 +/- 0.13, 7.2 +/- 0.09 and 6.6 +/- 0.08, n = 4-8, respectively). In addition, the responses to endothelin were virtually abolished in the presence of Krebs physiological salt solution containing no calcium but with 1 x 10-M EDTA added. Preequilibration with either (-)-w-conotoxin (1 x 10-6M) or tetrodotoxin (1 x 10-6M) did not affect responses to endothelin. 5. In chemically denervated rats, endothelin (1pmolkg-'-10nmolkg- , i.v.) exhibited pressor responses, which were unaffected by a 3 h pretreatment with indomethacin. In the SHR, the effects on blood pressure were not significantly different from those observed in normotensive animals at any of the doses studied. A transient (duration < 30 s) depressor response was also observed in all groups studied at a dose of 0.1-1 nmol kg-1 i.v. 6. In conclusion, endothelin is a potent contractile agonist in both vascular and non-vascular muscle. It appears to elicit responses partly via the entry of extracellular calcium (by a mechanism distinct from that of other calcium facilitators) and partly by release of endoperoxides.

Animals↗
PubMed1992

Blockade by antiarrhythmic drugs of glibenclamide-sensitive K+ channels in Xenopus oocytes.

1. The outward K+ current induced by KRN2391 (K+ channel opener) in Xenopus oocytes is blocked by glibenclamide. We have investigated the effects of various classes (I-IV) of antiarrhythmic drugs on this KRN2391-induced response. 2. All class I antiarrhythmic drugs (Na+ channel blockers) tested concentration-dependently suppressed KRN2391-induced responses with the rank order of potency (IC50 in microM), disopyramide (17.8) > aprindine (29.5) > propafenone (63.1) > ajmaline (145) > quinidine (151). Flecainide, SUN1165, lignocaine, mexiletine and procainamide were much less potent (IC50, 450- > 1000 microM) than quinidine. 3. The class II antiarrhythmic drugs (beta-blockers), timolol, (-)- and (+/-)- propranolol, and (+)- propranolol (a non-beta-blocker) inhibited KRN2391-induced K+ currents in a concentration-dependent manner with values for IC50 (microM) of 79, 131, 151 and 129, respectively, whilst butoxamine, oxprenolol, alprenolol, pindolol, nadolol, metoprolol and acebutolol were either weak (IC50, 300 microM-600 microM) or virtually inactive (IC50, > 1000 microM). 4. The class III antiarrhythmic drugs, amiodarone and (+)-sotalol scarcely affected KRN2391 responses. 5. All class IV drugs (Ca2+ antagonists) tested suppressed KRN2391-induced responses in a concentration-dependent manner with an IC50 of 6.3 microM for bepridil, 38 microM for prenylamine, 85 microM for verapamil and 135 microM for diltiazem. 6. In conclusion, antiarrhythmic drugs of classes I, II and IV potently blocked glibenclamide-sensitive K+ channels in Xenopus oocytes.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Anticonvulsant properties of calcium channel blockers in mice: N-methyl-D-,L-aspartate- and Bay K 8644-induced convulsions are potently blocked by the dihydropyridines.

Ten calcium channel blockers were evaluated in mice after intraperitoneal (i.p.) administration for prevention of seizures induced by various convulsants. The dihydropyridines (class II calcium antagonists, i.e., nisoldipine, nitrendipine, nicardipine, nifedipine, and nimodipine) selectively prevented seizures elicited by administration of pentylenetetrazol (PTZ), N-methyl-D,L-aspartate (NMDLA) and the dihydropyridine calcium channel agonist BAY K 8644. With regard to prevention of NMDLA-induced seizures and the subsequent mortality, these compounds were similar in potency to the noncompetitive NMDA receptor antagonist MK801. Unlike MK801 (IC50 = 0.014 microM), the dihydropyridines did not inhibit in vitro binding of MK801 to synaptic membrane fractions prepared from rat cerebrohippocampal tissue. The dihydropyridines did not influence seizures elicited by maximal electroshock (MES). Flunarizine (diphenyl-alkylamine, class IV) was selectively active in the MES test, considerably less potent against NMDLA-induced convulsions/mortality, exhibited weak noncompetitive NMDA antagonism in vitro (IC50 = 28 microM), and was inactive in the PTZ and BAY K 8644 testing paradigms. Diltiazem, a class III benzothiazepine, possessed relatively weak broad spectra of activity against MES, PTZ, NMDLA, and BAY K 8644 test situations. It was inactive in vitro as a noncompetitive NMDA antagonist. The class I compound verapamil (phenylalkylamine) displayed only moderate inhibition of NMDLA-evoked seizures/mortality. Prenylamine (class V) was moderately active against convulsions produced by MES and NMDLA while retaining a degree (IC50 = 16 microM) of noncompetitive NMDA antagonism. Lidoflazine (class VI) was inactive in all tests. The Ca2+ channel blockers and MK801 were inconsistent in their ability to prevent bicuculline (BIC)-elicited convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1980

Calcium antagonistic effects of terodiline in rabbit aorta and human uterus.

The possible calcium antagonistic action of the anti-anginal drug terodiline was investigated by two experimental techniques. In isolated preparations of rabbit aorta and pregnant human uterus exposed to a calcium-free medium and then depolarized by potassium, terodiline in concentrations of 4.5--36 microM inhibited contractions produced by cumulative addition of calcium to the extracellular medium. This effect of terodiline could be reversed by high concentrations of calcium. Within the same concentration range, terodiline also reduced potassium-induced 45Ca influx in isolated aorta without affecting calcium efflux. It is suggested that terodiline, which structurally has similarities to prenylamine and fendiline, like these drugs can be classified as a calcium antagonist.

Adult↗
PubMed1990

Cyclosporin metabolism in human liver microsomes and its inhibition by other drugs.

The metabolism of cyclosporin was studied in human liver microsomes. There was no metabolism in the presence of cytochrome C or carbon monoxide or in the absence of cofactors, suggesting metabolism by cytochrome P-450 enzymes. The metabolism was inhibited by ketoconazole and erythromycin, by the steroids methylprednisolone and oestradiol, and by the calcium antagonists diltiazem, nifedipine, prenylamine and verapamil. These in vitro findings correlate well with previously published clinical reports suggesting that these drugs may inhibit the metabolism of cyclosporin in vivo. Our observations suggest that metabolic interactions between cyclosporin and other drugs in vivo may be predicted in vitro under proper experimental conditions.

Cyclosporins↗
PubMed1979

Uptake of 5-hydroxytryptamine in blood platelets and its inhibition by drugs: role of plasma membrane and granular storage.

The initial uptake of 3H-5-hydroxytryptamine (3H-5-HT) showed linearity for short time intervals in normal and reserpinized blood platelets of guinea-pigs, but was lower in reserpinized platelets. Teh Km values for the 3H-5-HT uptake were virtually identical in normal and reserpinized platelets, whereas Vmax was lower in the latter. Imipramine and chlorpromazine caused the same percentage inhibition of 3H-5-HT uptake in normal and reserpinized platelets; the reserpine-like compound Ro 4-1284 inhibited the uptake of 3H-5-HT in the normal, but not markedly in the reserpinized platelets. Haloperidol, prenylamine and Ro 4-9040 were more potent inhibitors in normal than in reserpinized platelets. It is concluded that (a) the Km of the initial uptake of 5-HT by platelets is probably determined by the mechanism at the plasma membrane, whereas Vmax may be codetermined by the intracellular storage capacity, (b) platelets are models for differentiating the site of action (plasma membrane or storage organelles) of drugs interfering with 5-HT uptake, and (c) neuroleptics- and reserpine-like compounds may either act selectively on the plasma membrane or on the intracellular storage organelles, or affect both of these subcellular sites.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1967

Monoamines and their metabolites in the avian brain.

1. In the avian brain, a high concentration of dopamine was found in a sharply contoured region of the nucleus basalis which may or may not have included the nucleus entopeduncularis, and therefore lay within the palaeostriatum of the nomenclature of Crosby and Huber. This was thus the only region which may be considered biochemically homologous to the mammalian corpus striatum. For purposes of macroscopic identification only, the region is described here as the ;anterior part of the nucleus basalis'. The concentration of dopamine was 3 mug/g in the pigeon, about the same in the duck and chicken, and 7.5 mug/g in the finch. In the pigeon this region also contained some noradrenaline; the quantity of 5-hydroxytryptamine (1.4 mug/g) and 5-hydroxyindolylacetic acid (0.6 mug/g) was larger than in any other part of the brain.2. In the brain of the pigeon and the chicken, the highest concentrations of noradrenaline (1.5 and 1.4 mug/g) were found in the hypothalamus.3. The concentration of adrenaline was higher in the avian than in the mammalian brain. In the hypothalamus, it ranged from 0.4 mug/g in the pigeon to 1 mug/g in the chicken.4. Fluorescence microscopy, using the formaldehyde condensation method, showed, in the anterior part of the nucleus basalis, a large area of diffuse green-yellow fluorescence, similar in appearance to the fluorescence of the striatum of the rat. In addition this part of the brain contained a small region of fluorescent fibres and varicosities. It is suggested that the diffuse fluorescence was produced by dopamine. It was absent from brains of reserpine-treated pigeons.5. In the pigeon, reserpine, tetrabenazine and prenylamine produced a decrease in the concentration of brain monoamines, an effect which was comparable to that seen in mammals. Yet, none of these drugs raised the concentration of homovanillic acid, but they increased that of 5-hydroxyindolylacetic acid; these drugs raise the concentration of both acids in mammalian brain.6. In the pigeon beta-tetrahydronaphthylamine decreased the concentration of all monoamines and their metabolites, an action quite different from that produced in the mammalian brain.7. The main effect of morphine and of M 99 (6,14-endoetheno-7-(2-hydroxy-2-pentyl)-tetrahydro-oripavine hydrochloride) was a lowering of the noradrenaline concentration.8. As in mammals, chlorpromazine affected only the dopamine metabolism.9. In the guinea-pig and the pigeon, the administration of alpha-methyl-DOPA led to a substitution of much of the cerebral noradrenaline by alpha-methyl-noradrenaline, sometimes in excess of the lost noradrenaline. However, although the loss of dopamine was severe in both pigeon and guinea-pig, only little alpha-methyl-dopamine accumulated in the pigeon brain, so that it did not consitute a replacement for the lost dopamine; in the guinea-pig, alpha-methyl-dopamine was found in quantities similar to, or exceeding those, of the lost dopamine.

Amines↗
PubMed2005

Comparative evaluation of HERG currents and QT intervals following challenge with suspected torsadogenic and nontorsadogenic drugs.

The purpose of the present study was to comparatively evaluate human HERG currents and QT intervals following challenge with suspected torsadogenic and nontorsadogenic drugs. Various concentrations of 14 different drugs were initially evaluated in terms of their relative potency to block I(HERG) in stably transfected human embryonic kidney cells. Four general categories of drugs were identified: high-potency blockers (IC50 < 0.1 microM) included lidoflazine, terfenadine, and haloperidol; moderate-potency blockers (0.1 microM < IC50 < 1 microM) included sertindole, thioridazine, and prenylamine; low-potency blockers (IC50 > 1 microM) included propafenone, loratadine, pyrilamine, lovastatin, and chlorpheniramine; and ineffective blockers (IC50 > 300 microM) included cimetidine, pentamidine, and arsenic trioxide. All measurements were performed using similar conditions and tested acute drug effects only (<30 min of drug exposure per measurement). Since two of the drugs that were ineffective I(HERG) blockers, arsenic trioxide and pentamidine, have been associated with cardiac repolarization delays (QT interval lengthening) and torsades de pointes ventricular arrhythmias in patients, we chose to evaluate them further using the isolated perfused rabbit heart model. Neither arsenic trioxide nor pentamidine had any significant effect on QT intervals in this model, even at relatively high (micromolar) concentrations. Similar results were obtained for loratadine in this model. When the hearts were challenged with a known torsadogenic drug such as cisapride, significant QT lengthening was rapidly induced. These results demonstrate that arsenic trioxide and pentamidine are essentially devoid of direct acute effects on cardiac repolarization or inhibition of I(HERG).

Animals↗
PubMed1988

Neuroregulatory and neuropathological actions of the ether-phospholipid platelet-activating factor.

Platelet-activating factor (PAF) is a naturally occurring phospholipid that serves as a critical mediator in diverse biological and pathophysiological processes. In this study of the interactions of PAF with neuronal cells, it was found that PAF increased the intracellular levels of free calcium ions in cells of the clones NG108-15 and PC12. The increase was dependent on extracellular calcium and was inhibited by the antagonistic PAF analog CV-3988 and by the calcium-influx blockers prenylamine and diltiazem. A functional consequence of this interaction was revealed by measuring a PAF-elicited, Ca2+-dependent secretion of adenosine triphosphate from PC12 cells. Exposure of NG108-15 cells for 3 to 4 days to low concentrations of PAF induced neuronal differentiation; higher concentrations were neurotoxic. Thus, by influencing Ca2+ fluxes, PAF may play a physiological role in neuronal development and a pathophysiological role in the degeneration that occurs when neurons are exposed to circulatory factors as a result of trauma, stroke, or spinal cord injury.

Adrenergic Fibers↗
PubMed1988

Voltage-sensitive Ca2+ channels in rat brain neocortical noradrenergic nerve terminals. Different sensitivity to inorganic and organic Ca2+ channel antagonists.

In rat cerebral cortex slices we investigated the Ca2+ dependency of noradrenaline release and the influence of inorganic and organic Ca2+ antagonists. Slices were preincubated with 3H-noradrenaline and then superfused with noradrenaline-free medium. Release of 3H-noradrenaline was elicited by electrical pulses. The stimulation-evoked release was dependent on the external Ca2+ concentration and was inhibited by Cd2+, Co2+ and Mg2+ in a concentration-related manner. These results indicate that electrically stimulated noradrenaline release depends on the Ca2+ influx after opening of voltage-sensitive Ca2+ channels. Organic Ca2+ antagonists were used in concentrations which had no major influence on the basal release rate. Of the drugs tested (bepridil, diltiazem, flunarizine, nimodipine, isradipine, prenylamine, verapamil) only flunarizine and nimodipine showed a minor inhibition of the stimulation-evoked release, which was less than 20% at 1 mumol/l. With nimodipine 10 mumol/l, there was a 6% facilitation of release. All other drugs except flunarizine and verapamil caused a slight facilitation of the stimulation-evoked release. The results provide evidence that the organic Ca2+ channel antagonists investigated do not or only minimally interfere with the noradrenergic nerve terminal Ca2+ channels in a tissue slice preparation. The release-facilitating effects of most organic Ca2+ antagonists cannot be interpreted by the present results.

Animals↗
PubMed1983

Interaction of verapamil and other calcium channel blockers with alpha 1- and alpha 2-adrenergic receptors.

To determine the specificity of the previously demonstrated competition of verapamil with radioligand binding to alpha-adrenergic receptors, we examined the interaction of calcium channel blockers with alpha 1- and alpha 2-adrenergic receptors on several tissues. Verapamil competed for [3H] prazosin binding to alpha 1-adrenergic receptors and for [3H]yohimbine binding to alpha 2-adrenergic receptors in several tissues (human platelets, rat kidney and heart, and cultured muscle cells) with dissociation constants of 0.6-6 microM. The calcium channel blockers D600, D591, fendiline, and prenylamine--which are structural analogues of verapamil--also competed for [3H]yohimbine binding to human platelets. Two other calcium channel blockers, diltiazem and nifedipine, did not compete for [3H] yohimbine binding to human platelets or [3H]prazosin binding to membranes prepared from rat ventricles. We used [3H]nitrendipine binding to identify putative calcium channels on rat myocardial membranes. Nifedipine and verapamil blocked these [3H]nitrendipine-binding sites on ventricular membranes, but epinephrine and prazosin did not, indicating that the ventricular alpha 1 receptors and calcium channels are distinct. We found no specific [3H]nitrendipine binding to human platelets. We conclude that the interaction of verapamil with alpha-adrenergic receptors is not receptor subtype or tissue specific, that interaction with alpha-adrenergic receptors is not a property of all calcium channel blockers, and that the interaction of verapamil with alpha-adrenergic receptors and its interaction with calcium channels occur at at least two distinct sites.

Animals↗
PubMed1985

Lidocaine-induced second-degree mobitz type II heart block.

Lidocaine-induced atrioventricular (AV) conduction disturbances are an ill-defined phenomenon. Electrophysiological studies in both animal and human subjects have shown that therapeutic doses of lidocaine have no significant effect on AV nodal and His-Purkinje conduction time in the presence of intact AV conduction. Sporadic reports of accelerated AV conduction or complete heart block following lidocaine administration have been published. One case of Mobitz type II heart block has been reported in a patient with a prolonged QTc interval (0.61 sec) who was also receiving prenylamine. Electrophysiological studies designed to evaluate lidocaine's effects on AV conduction present conflicting observations. We report a case of Mobitz type II heart block following therapeutic doses of lidocaine in the absence of acute myocardial infarction or concomitant cardioactive drug administration. This case, in conjunction with other reported data, suggests the occurrence of lidocaine-induced AV block to be unpredictable. Although its occurrence may be infrequent, the severity of these reactions warrants careful selection and monitoring of patients who are to receive lidocaine.

Aged↗
PubMed1988

Effect of antiarrhythmic drugs on the ventricular fibrillation induced by low intensity train pulses.

We evaluated the effects of antiarrhythmic drugs on ventricular fibrillation threshold (VFT) by analysing the electrophysiologic parameters obtained from strength-interval curves. The VFT determined by low intensity train pulses was significantly increased from the control value under the administration of clinical dosage of procainamide, lidocaine, propranolol, bepridil and prenylamine, although not verapamil. The elevation of VFT could be explained by changes in the strength-interval curve induced by the drugs, including disappearance of dip phenomenon, supernormal period, prolongation of effective refractory period (ERP) and elevation of end diastolic threshold (EDT).

Animals↗
PubMed1986

Contractile effects of jellyfish toxin extracted from Carybdea rastonii on isolated rabbit aorta.

Effects of the toxic component of jellyfish (Carybdea rastonii) (pCrTX) on the smooth muscle tension of isolated rabbit thoracic aorta were examined. pCrTX, at concentrations higher than 10(-7) g/ml, caused slowly developing tension that reached its maximum after about 1 hr. This contraction was partially inhibited by pretreatment of the tissue with phentolamine (5 X 10(-6) M) or indomethacin (10(-5) M). The contraction induced by pCrTX was partially inhibited by nicardipine (10(-7) M) and markedly augmented by Bay k8644 (10(-6) M). In low-Na+ solution, the rate of rise of the pCrTX-induced contraction was significantly reduced. Removal of external Ca2+ inhibited the pCrTX-induced contraction by about 30%, while chlorpromazine, trifluoperazine, prenylamine and papaverine (10(-4) M) completely inhibited the contraction. pCrTX itself did not cause any contraction in saponin-skinned smooth muscle and had no effect on the Ca2+-induced contractile tension. It has been reported that pCrTX-induced contraction is attributable to the release of endogenous catecholamines and also to the increase in Ca2+ influx in smooth muscle (Azuma et al., 1986). The present results confirmed the previous suggestion and further suggested that a portion of the contraction is due to release of prostaglandin(s) and also to the direct effect on smooth muscle which is not dependent on Ca2+ influx.

Animals↗
PubMed1983

Stimulation of amylase and sialic acid releases from dog submandibular gland slices by pilocarpine or high K+ medium: a possible role of calmodulin for their releases.

The mechanism of amylase and sialic acid releases stimulated by pilocarpine or high K+ medium was investigated in the slices of dog submandibular glands. The release of both amylase and sialic acid was dose-dependently increased by pilocarpine and a considerable release was observed at pilocarpine concentrations of more than 1 microM. Similar effects were observed when K+ concentration in the medium was increased and the maximal response was observed at 75 mM K+. The release of amylase and sialic acid by pilocarpine or K+ considerably decreased by removing Ca2+ from the medium and the slices. The release of amylase in the Ca2+-deficient slices was nearly recovered by the addition of 2.5 and 5.0 mM Ca2+, whereas that of sialic acid was recovered by only 60-75%. Ca2+ inhibitors, La3+ and verapamil, and calmodulin inhibitors, trifluoperazine, prenylamine, and W-7, significantly inhibited the release of amylase and sialic acid induced by the stimulants. These results suggest that the release of amylase and sialic acid stimulated by pilocarpine or K+ is dependent on the presence of Ca2+, and that the activation of calmodulin is involved in the process of the release.

Amylases↗