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Biomedical subjects

C I Lin

Publications and source records attributed to C I Lin.

At least 37 records · Page 2Linked to original sources
PubMed1996

Effects of phenylephrine on intracellular Na+ and H+ activities in guinea-pig cardiac ventricular papillary muscles.

Effects of phenylephrine (PE) on the contractility, intracellular Na+ activity (aNai), intracellular H+ activity (pHi), and membrane potential in guinea-pig cardiac ventricular papillary muscles were studied. In beating fibers, PE significantly increased the twitch offsion, pHi and the action potential duration but decreased aNai. These effects could be inhibited by phentolamine, but not by propranolol. In quiescent fibers, PE also increased the resting tension and pHi, and decreased aNai. Pretreatment with phentolamine completely abolished the effect of PE. Methylisobutyl amiloride (MIA), a potent inhibitor of Na(+)-H+ exchanger, significantly decreased membrane potential, aNai, and pHi without changing the resting tension. PE in the presence of MIA increased the resting tension and further decreased aNai without significant changes in membrane potential and pHi. Ouabain significantly decreased membrane potential and pHi, and increased the resting tension and aNai. In the ouabain-treated fiber, PE further increased the resting tension without decreasing aNai or increasing pHi. From these results, it appears that PE activates the Na(+)-K+ pump and Na(+)-H+ exchange through alpha-adrenoceptors. Activation of the Na(+)-K+ pump contributes, at least in part, to the enhanced Na(+)-H+ exchange. The increase in contractile force associated with a decrease in aNai is suggested to result from the intracellular alkalization and increased sensitivity of contractile protein to Ca2+.

Animals↗
PubMed1996

Simultaneous effects of carbachol on intracellular Na+ activity, action potential, and twitch tension in guinea-pig cardiac ventricular papillary muscles.

Effects of carbachol (CCh) on the twitch tension, intracellular Na+ activity (aNai), and action potential were simultaneously measured in guinea-pig cardiac ventricular papillary muscles. In fibers driven at 60 beats/min, 100 microM CCh significantly increased the twitch tension and aNai, and decreased the action potential duration at 30 and 90% repolarization (APD30 and APD90) without changing the maximum rate of the rise of the upstroke (Vmax). Staurosporine (1 microM) alone gradually decreased the twitch tension and aNai without changing the action potential. In the presence of staurosporine, the administration of CCh restored aNai and caused the same changes in twitch tension and APD shortening with no effect on Vmax. Pretreatment with 1 microM atropine completely eliminated the effects of 100 microM CCh. Cesium (20 mM) depolarized the cell membrane and significantly increased the twitch tension and APD90 with decreases in the Vmax and aNai. CCh (100 microM) in the presence of 20 mM Cs+ biphasically decreased and increased the twitch tension and significantly decreased the Vmax and aNai with an increase in the APD90. The results suggest that the muscarinic receptor-mediated increase of aNai is protein kinase C-independent. The aNai increase is associated with the positive inotropic effect and the abbreviation of the action potential duration. In addition to the increase in aNai, the increase of the myofibrillar calcium sensitivity involved is responsible for the positive inotropic effect which is still evident after the sodium influx is inhibited by Cs+.

Action Potentials↗
PubMed1995

Electromechanical effects of caffeine in failing human ventricular myocardium.

We studied, using standard microelectrode technique, the effects of caffeine alone and in conjunction with epinephrine in ventricular myocardial fibers obtained from the failing hearts of 12 recipients of heart transplant. Results revealed that caffeine (1-3 mM) prolonged slightly the duration of fast response action potential near final repolarization and the twitch curve but slightly increased, or even decreased, the twitch force. Epinephrine (3 microM) induced a submaximal positive inotropic effect in myocardial fibers obtained from the failing hearts. Caffeine at 1 mM significantly potentiated the force of contraction and accelerated the rate of twitch relaxation increased by epinephrine. Increasing concentration of caffeine to 3 mM in the presence of epinephrine did not enhance further the twitch force but rather induced the delayed after-depolarization in two of eight experiments. In a preparation from one patient with dilated cardiomyopathy, the combination of caffeine and epinephrine induced repetitive triggered rhythms. The present findings suggest that, in human ventricular myocardium obtained from certain patients transplanted for congestive heart failure, caffeine could induce positive inotropy and triggered automaticity through a potentiation of the actions of catecholamines.

Action Potentials↗
PubMed1995

Electropharmacological actions of propofol on calcium current in guinea-pig ventricular myocytes.

Propofol, a widely-used intravenous anesthetic, causes bradycardia, depression in contractility and hypotension. The cellular mechanisms responsible for these cardiac toxicity remain unclear. In this study, we examined the cellular electropharmacological actions of propofol on calcium current in guinea-pig heart. Single ventricular myocytes were freshly isolated from guinea-pig using modified enzymatic method. Whole-cell voltage-clamp technique was applied with one suction pipette. Transmembrane L-type calcium current (ICa(L)) was separated from other ionic currents by voltage-control, ionic channel blockers and ion substitution methods. Our results show that propofol decreased ICa(L) in a concentration-dependent manner (KD = 54.2 microM). Slope conductance of current-voltage relation was decreased by 56 microM propofol. Propofol did not affect the steady-state activation curve, but shifted the inactivation curve to hyperpolarizing direction. Recovery from inactivation was slowed down by propofol. Marked resting block and use-dependent block were noted. In conclusion, our results indicate that propofol inhibits cardiac L-type calcium current mainly by shifting inactivation curve and retarding the recovery from inactivation.

Anesthetics, Intravenous↗
PubMed1995

Effects of endothelin 1 on calcium and sodium currents in isolated human cardiac myocytes.

We have used the whole-cell voltage-clamp technique to study the effects of endothelin 1 (ET-1, 10 nM) on L-type Ca2+ currents and voltage-dependent Na+ inward currents in human cardiac cells. Myocytes were enzymatically isolated from atrial specimens obtained during open-heart surgery and from human ventricular tissues of explanted hearts. Extracellular application of ET-1 decreased the peak amplitude of Ca2+ currents by 26 +/- 6% (n = 13) in atrial myocytes and by 19 +/- 3% (n = 8) in ventricular myocytes. In three atrial cells, treatment with 1 microM BQ123 prevented the decrease in Ca2+ currents induced by ET-1. When GTP (0.2 mM) was added to the dialyzing pipette solution, ET-1 still caused a small decline by 12 +/- 5% (n = 16), in peak Ca2+ currents, in atrial myocytes. When Ca2+ currents were increased (+210 +/- 19%) by a beta-adrenoceptor agonist (0.1 microM isoproterenol) or by the phosphodiesterase inhibitor isobutylmethylxanthine (10 microM), ET-1 reduced Ca2+ currents by 35 +/- 6% (n = 4) and 30 +/- 4% (n = 5), respectively. In human ventricular myocytes in the presence of 1 microM isoproterenol, which increased the peak Ca2+ currents by 150 +/- 30%, ET-1 also induced a drastic reduction in Ca2+ currents, by 40 +/- 11% (n = 5). The tetrodotoxin-sensitive Na+ currents measured in the presence of 5 mM [Na]o were significantly enhanced (+28 +/- 7%) by ET-1 in five atrial myocytes. The stimulatory effect of ET-1 on Na+ currents was partially reversible. The present findings in human cardiac cells show that ET-1 did not enhance the Ca2+ currents in the absence or presence of internal GTP. The positive inotropic actions induced by ET-1 in human heart may be mediated mainly by signal-transduction pathways other than the G-protein-adenylyl cyclase-cAMP system.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Comparative effects of strophanthidin in tilapia and human heart tissues.

It is well documented that the cardiotonic steroid strophanthidin increases myocardial contractile force through an inhibition of the sarcolemmal Na(+)-K+ pump in mammalian heart cells. The aim of the present study was to determine the effect of this digitalis substance on action potential and contraction in cardiac tissues obtained from a cultured freshwater fish tilapia (Oreochromis sp.) and compare with those observed in human heart tissues obtained at cardiac surgery. In tilapia atria superfused at 25 degrees C 1-2 microM strophanthidin shortened the spontaneous cycle length while increased progressively the twitch force. In tilapia ventricular tissues, strophanthidin also increased the force but shortened the APD50. When temperature of the superfusate was elevated from 25 to 37 degrees C, strophanthidin induced a smaller positive or even negative inotropic effect but increased significantly the diastolic tension through an inhibition of the relaxation process. High temperature also facilitated the occurrence of delayed afterdepolarizations, repetitive slow response action potentials and episodes of contracture. The same concentration of stroph induced rather sustained positive inotropic effects without deteriorating actions in human ventricular trabeculae driven at 37 degrees C. In human atrial trabeculae, however, 2 microM strophanthidin readily induced abnormal automatic and triggered rhythms along with the positive inotropy. The present findings provide the functional evidence for the presence of sarcolemmal Na+, K(+)-pump in fish myocardial fibers. The major differences in the electro-mechanical actions of strophanthidin in tilapia versus human heart tissues are the smaller positive inotropy and the proneness to contracture in tilapia heart at 37 degrees C.

Action Potentials↗
PubMed1995

Interaction of phosphodiesterase inhibitor and isoproterenol in human and guinea-pig ventricular tissues and myocytes.

We studied the interaction of phosphodiesterase inhibitor and isoproterenol in human and guinea-pig ventricular muscle fibers and guinea-pig ventricular myocytes. In ventricular trabeculae obtained from the explanted hearts of 5 patients with dilated cardiomyopathy, isoproterenol (Iso, 10(-8)-10(-6)M) increased twitch force in a concentration-dependent manner. Isobutylmethyl-xanthine (IBMX, 3 x 10(-6)M) alone did not change significantly the twitch force but potentiated the effect of Iso and reduced the concentration for half maximal effect (EC50) of Iso from 140 to 18 x 10(-9)M. As compared to the diseased human heart tissues, papillary muscles obtained from 6 healthy guinea-pigs were much more sensitive to the positive inotropic action of Iso but less reactive to the potentiative effect of IBMX on Iso. The EC50 for the inotropic action of Iso (10(-9) approximately 10(-7)M) in the absence and presence of 3 x 10(-6)M IBMX were 28 and 15 x 10(-9)M, respectively. In 16 guinea-pig ventricular myocytes isolated enzymatically, L-type Ca currents (ICa,L) were recorded in K-free superfusate with whole-cell voltage-clamp technique. The increase in ICa,L induced by the lowest concentration (10(-9)M) of Iso was not significant. Those induced by 10(-8)M and 10(-7)M Iso were about the same (+108 +/- 29% and +75 +/- 20%, respectively). IBMX potentiated the effect of Iso. It is concluded that indeed the ventricular muscles obtained from the failing hearts are poorly responsive to the beta-adrenoceptor agonist. This defect could be corrected at least partially by the PDE inhibitor IBMX. However, the concentration-dependent inotropic and arrhythmogenic effects in guinea-pig ventricular muscle were not accompanied by a parallel increase in iCaL at high concentration of Iso(10(-7)M), suggesting involvement of other mechanisms such as actions on intracellular Ca2+ regulation induced by Iso.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Molecular subtypes of env sequences around V3 region of human immunodeficiency virus type 1 in Taiwan.

Samples of peripheral blood mononuclear cells (PBMC) were collected during 1990-91 from seropositive healthy, male HIV-1 carriers visiting Taipei Venereal Disease Control Center, and a male AIDS patient admitted to a general hospital. The V3 and its flanking nucleotide (nt) sequences in their DNA were amplified by polymerase chain reaction (PCR) and compared with those of known HIV-1 prototypes. The nt sequences obtained from 21 individuals (e.g., TW92) clustered as Group A, which were highly homologous (95.6-99.5%) to that of HXB2 virus while those from 6 individuals (TW90, TW91, TW97, TW99, TW102 and TW104) were classified as Group B showing low similarities (73.2-84.2%) to those of HXB2 and moderate similarities (80.7-90.0%) to those of SC and Bangkok (BK) viruses. By comparison of their deduced amino acid sequences with those of consensus sequences for subtypes A-F as defined by Myers et al. (1993), both Groups A and B viruses (except TW102) together with those of HXB2, SC and BK viruses could be identified as members or variants of subtype B, and the TW102 virus as a member of subtype E viruses. Individuals with the Group A viruses included 4 homosexual and 17 heterosexual Taiwanese males, 2 of the latter having a history of i.v. drug abuse. Among individuals with Group B viruses, those with TW97, TW99, TW104 and TW91, who was an AIDS patient, were heterosexual Taiwanese males, whereas both TW90 and TW102 viruses were from individuals who were overseas heterosexual Chinese from Thailand, the former with a history of i.v. drug abuse and the latter without.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Changes of electromechanical activities in human cardiac tissues following endocardial damage.

Role of endocardial endothelium in the electromechanical activity of human heart was studied in isolated human atrial and ventricular muscle fibers obtained at cardiac surgery. The endocardial endothelium was damaged by brief exposure to a bolus of the detergent Triton X-100 (0.25-1 vol%). Triton at concentrations of up to 1 vol% reduced twitch force by one-fifth and one-fourth in guinea-pig sinoatrial and ventricular tissues, respectively, but did not change the action potential configuration. In human atrial tissues, however, a brief exposure to 20 microliters of Triton (0.25-1 vol%) depressed the excitability of both fast and slow response action potentials and reduced markedly the twitch force. The effects of Triton were less potent in human ventricular tissues but Triton still decreased significantly the twitch force (-37 +/- 6.4%) at a concentration of 0.25 vol%. Also, the positive inotropic response to phenylephrine (10-100 microM) was shifted to the higher concentrations by Triton treatment. The present findings indicate that the diseased human atrial and ventricular tissues were more sensitive to the effects of endocardial damage induced by Triton exposure than the healthy animal cardiac tissues were. In addition, the electromechanical responses to the adrenergic agonist phenylephrine were decreased in human cardiac tissues with defective endocardial endothelium.

Animals↗
PubMed1993

The role of cyclic AMP and phosphodiesterase activity in the mechanism of action of tetramethylpyrazine on human and dog cardiac and dog coronary arterial tissues.

The aim of the present experiments was to explore the underlying cellular mechanisms responsible for the actions of tetramethylpyrazine (TMP) on atrial, ventricular and coronary arterial tissues. Transmembrane potentials of cardiac tissues were detected by means of the glass microelectrode technique and contractile tension by a force transducer. Tissue cyclic (c) AMP level was determined by protein binding assay. Results show that in human atrial and dog Purkinje fibres, high concentration of TMP (3 mM) induced a persistent positive inotropic effect only in the presence of adrenaline. Also, 3 mM TMP increased the cAMP level of the atrial muscle fibres, especially in the presence of adrenaline. Determination of the activity of cAMP-phosphodiesterase revealed that 0.3 and 3 mM TMP inhibited the phosphodiesterase activity of dog coronary artery and human atrial tissues in a concentration-dependent manner. When compared at the lower concentration (0.3 mM), the inhibitory effect of TMP was about 60% that of theophylline. The above findings indicate that the cardiovascular effects of TMP are related to the inhibition of phosphodiesterase activity and the subsequent elevation of the cAMP concentration.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

Pacemaker current, membrane resistance, and K+ in sheep cardiac Purkinje fibres.

OBJECTIVE: The pacemaker current in cardiac Purkinje fibres has been attributed to either a decrease in potassium conductance or an increase in a non-specific (Na-K) conductance. The former mechanism would be associated with an increase in membrane resistance (Rm) and the latter with a decrease in Rm. The aim of this study was to obtain evidence in support of one or other mechanism by measuring Rm during the pacemaker current (Idd) under conditions where there is a small or no extracellular potassium depletion. METHODS: Hearts were obtained from anaesthetised sheep and thin strands of ventricular Purkinje fibres were shortened to less than or equal to 1.6 mm. Purkinje fibres were voltage clamped to potentials positive and negative to the potassium equilibrium potential (EK) using a two microelectrode technique. Small current pulses were superimposed on Idd to measure Rm changes. Procedures were used that decrease either the background potassium current IKl or Idd in order to dissect changes in Rm due to K depletion from those due to Idd. RESULTS: Rm increased during Idd, whether the pacemaker current increased or decreased as a function of time. Increasing [K]o from 2.7 to 5.4 mmol.litre-1 decreased Rm and during hyperpolarising steps increased the instantaneous current but did not change Idd amplitude. In 2.7 mmol.litre-1 K, caesium (Cs, 2 mmol.litre-1) increased the holding current (Ih), had little effect on the instantaneous current, and eliminated Idd and associated Rm changes. In 5.4 and 10.8 mmol.litre-1 K, Cs increased Ih and decreased Idd amplitude and in 10.8 mmol.litre-1 K Cs decreased the instantaneous current on hyperpolarisation. If the current was reversed, Cs decreased but did not abolish it. In normal [K]o, barium (Ba, 0.05-0.5 mmol.litre-1) increased Ih and Rm, reduced the instantaneous current but did not increase Idd amplitude. In high [K]o, Ba instead increased the amplitude and rate of development of Idd. When Cs was applied in the presence of Ba, Idd was reduced or eliminated depending on [K]o. CONCLUSIONS: The changes in membrane resistance during the pacemaker current cannot be accounted for by K depletion and suggest that in the range of diastolic depolarisation the pacemaker current results predominantly from a time dependent decrease in K conductance.

Animals↗
PubMed1992

Ionic mechanisms responsible for the antiarrhythmic action of dehydroevodiamine in guinea-pig isolated cardiomyocytes.

1. Dehydroevodiamine alkaloid (DeHE), an active ingredient of a Chinese herbal medicine Wu-Chu-Yu (Evodiae frutus), has been shown to decrease aterial blood pressure in experimental animals and prolong action potential duration in cardiac cells. The aim of the present study was to explore the ionic basis of its possible antiarrhythmic effects. 2. Guinea-pig atrial and ventricular myocytes were isolated enzymatically and the ionic currents were recorded under whole-cell patch-clamp with single suction pipettes. 3. DeHE at a concentration of 0.1 microM inhibited reversibly the time-dependent outward K current (delayed rectifier, Ik) and the Na-dependent inward current (INa). 4. In low-K (1 mM) and high-Ca (9 mM) solution, DeHE also depressed the delayed afterdepolarizations (DAD) and the transient inward current (Iti) induced by 2 microM strophanthidin. On the other hand, DeHE occasionally induced early afterdepolarizations and slow response action potentials at a depolarized level. 5. At higher concentrations (1 microM and above), the L-type Ca current (ICa,L) was moderately inhibited. 6. The present findings indicate that DeHE may depress triggered arrhythmias in Ca-overloaded guinea-pig cardiac myocytes through its inhibitory actions on INa, Iti and, to a smaller extent, ICa. DeHE may also exert class III antiarrhythmic effect through a reduction of outward K currents (Ik) across the sarcolemma.

Action Potentials↗
PubMed1992

Arrhythmogenic mechanisms in human atrial and ventricular muscle fibers.

Mechanisms which may lead to cardiac arrhythmias were studied in atrial and ventricular tissues from human hearts. In human atrial fibers, diastolic depolarization (DD) was consistently present, but did not induce spontaneous discharge. Epinephrine enhanced DD, could induce delayed afterdepolarizations (DADs) and (in combination with strophanthidin) trigger repetitive activity. The presence of DD modified the recovery of premature action potentials. Human ventricular fibers did not exhibit DD and were more resistant to Ca overload. It is concluded that in atrial tissues the presence of DD may not induce automatic arrhythmias, but it may influence conduction and re-entry rhythms. Cardioactive drugs may induce DADs and repetitive activity in the atria and less easily in the ventricles. The attainment of a threshold may be facilitated when DADs are superimposed.

Action Potentials↗
PubMed1992

Electrophysiological basis for the bradycardic effects of 1-(1-pyrrolidinylmethyl)-2-naphthol in rodents.

In anesthetized rats, intravenous injection of 1-(1-pyrrolidinylmethyl)-2-naphthol (TPY-beta, 0.1-1 mg/kg) induced a transient (less than 1 min) decrease in arterial blood pressure and heart rate (acute responses) followed by a delayed and sustained (greater than 10 min) bradycardic response. The electrophysiological mechanisms responsible for the bradycardic effect of TPY-beta were studied in sinoatrial tissues isolated from guinea-pig hearts. Transmembrane action potential (AP) and twitch force of atrial tissues were recorded with the conventional microelectrode techniques. In sinoatrial pacemakers active spontaneously in 4 mM [K]o Tyrode solution, TPY-beta (3-100 microM) depressed the diastolic slope and the rate of spontaneous discharges. When the non-automatic atrial tissues were driven at a fixed rate, TPY-beta (10-100 microM) inhibited the upstroke velocity of phase-0 depolarization and prolonged AP duration. In atrial fibers depolarized in high [K]o (24 mM), TPY-beta depressed the phase-0 upstroke of slow response AP and the twitch force in a concentration-dependent manner. The present results indicate that TPY-beta induced direct negative chronotropic and inotropic effects on guinea-pig atrial pacemakers and myocardial fibers. The underlying mechanisms involve a general inhibition of transmembrane of Ca, K and Na ion fluxes.

Action Potentials↗
PubMed1991

Electromechanical effects of angiotensin in human atrial tissues.

Effects of exogenous angiotensin I (AI) and angiotensin II (AII) on action potential and contractile force of isolated atrial trabeculae obtained at cardiac surgery were studied by means of a standard microelectrode technique. In trabeculae driven electrically at a cycle length of 1 s, AII (8.4 nM - 8.4 microM) increased the contractile force with a peak effect occurred near 0.84 microM. The inotropic effect of AII was markedly inhibited by 1 microM saralasin or 1 microM diltiazem. AI (0.65 nM - 6.5 microM) also induced positive inotropic effect in a concentration-dependent manner. This inotropic effect was decreased significantly after 3 microM captopril pretreatment. In trabeculae active spontaneously in normal Tyrode solution, AI and AII increased significantly rate of diastolic depolarization and spontaneous discharges as well as force of contraction. These chronotropic effects were inhibited by captopril and saralasin, respectively. Captopril (0.3 nM - 3 microM) or saralasin (0.001 - 1 microM) alone also induced dose-dependent negative chronotropic effects. The present findings suggest the existence of functional AII receptors in human atrial tissues. The stimulatory effects of angiotensin appear to be related to an increase in cellular calcium.

Action Potentials↗
PubMed1991

Electropharmacological effects of sandostatin in human atrial fibers.

We studied the actions of sandostatin (0.1-1000 nM), an analogue of somatostatin, on human atrial tissues obtained from hearts of 20 patients undergoing corrective cardiac surgery. In 3 preparations showing fast response action potential in normal [K]0 Tyrode solution, sandostatin induced little effect, even at the highest concentration (1 microM). In 10 preparations showing a slow rate of phase-0 depolarization when atrial fibers were depolarized (maximum diastolic potential near -40 mV) in high [K]0 (27 mM), sandostatin at concentrations as low as 1 nM decreased significantly the velocity of the upstroke, and the amplitude of slow response of the action potential as well as the force of contraction. In 6 experiments on spontaneously active atrial fibers (maximum diastolic potential = -53.8 +/- 2.7 mV), sandostatin increased the spontaneous cycle length in a fashion dependent upon concentration. The decrease in spontaneous rate of firing was associated with an inhibition of the late diastolic slope, a change also induced by somatostatin. A longer period of washout, however, (30 min or longer) was required for complete recovery from the depressant effects. Sandostatin (0.1-100 nM) also depressed triggered activity induced by cardiotonic agents. The present findings indicate that sandostatin induces a prolonged action in human atrial cells. Sandostatin may depress abnormal automatic rhythms through an inhibition of transmembrane influx of calcium.

Action Potentials↗
PubMed1991

Depressant effect of adenosine in isolated human and canine atrial fibres.

UNLABELLED: STUDY OBJECTIVE0--he aim was to explore the cellular mechanisms responsible for the depressant effects of adenosine in human atrial tissues. DESIGN: Conventional microelectrode technique was used to record transmembrane action potential of human atrial tissues obtained at cardiac surgery. Effects of adenosine (0.1-100 microM) on action potential characteristics and contractile force of human atrial fibres in the absence and presence of an adenosine receptor antagonist (DPSPX) were evaluated. Results were then compared with those obtained from the canine atrial tissues. EXPERIMENTAL MATERIAL: Atrial tissues obtained from hearts of 25 patients undergoing corrective cardiac surgery were used. Seven mongrel dogs were anaesthetised and strands of atrial muscle were removed and used for comparison. MEASUREMENTS AND MAIN RESULTS: In human atrial fibres showing fast response action potential (mean dV/dtmax around 100 V.s-1) in normal [K]o (4 mM) Tyrode solution, adenosine (1 nM-10 microM) did not induce consistent effects on the action potential characteristics. When the fibres were depolarised in high [K]o (27 mM) or in atrial fibres showing slow response action potential (dV/dtmax less than 50 V.s-1), however, 10 microM adenosine reduced the upstroke velocity and the amplitude of action potential significantly and markedly depressed the contractile force. In atrial fibres spontaneously active in normal Tyrode solution (maximum diastolic potential around -50 mV), adenosine inhibited rate of spontaneous discharge in a concentration dependent manner. Delayed afterdepolarisation and aftercontraction induced by adrenaline or/and high [Ca]o were also suppressed. The depressant effects of adenosine were blocked after pretreatment with 50 microM DPSPX, a specific antagonist for adenosine receptor. CONCLUSIONS: These findings show that adenosine may abolish abnormal automatic rhythms and triggered activity in human atria.

Acetylcholine↗