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S Komori

Publications and source records attributed to S Komori.

At least 127 records · Page 7Linked to original sources
PubMed1993

Effect of trimebutine on K+ current in rabbit ileal smooth muscle cells.

The effect of trimebutine on the K+ current in rabbit ileal smooth muscle cells was investigated using the whole-cell patch-clamp technique. Trimebutine (10 microM) inhibited an outward current consisting of a Ca(2+)-dependent K+ current (IKCa) and Ca(2+)-independent K+ current (IKv), elicited by stepping from -80 to -20 mV or more positive. Trimebutine reduced dose dependently the IKv amplitude with an IC50 of 7.6 microM and IKCa amplitude with an IC50 of 23.5 microM. The IKv inhibition was neither voltage- nor use-dependent. Trimebutine (1-100 microM) decreased the amplitude and discharge rate of spontaneous transient outward currents. Trimebutine (30 microM) produced a sustained membrane depolarization of about 10 mV accompanied by a decrease in membrane conductance. The results suggest that the excitatory effects of trimebutine on the gastrointestinal tract may be attributable to the inhibitory action on the K+ current.

Animals↗
PubMed1993

Oscillations of receptor-operated cationic current and internal calcium in single guinea-pig ileal smooth muscle cells.

In single cells isolated from guinea-pig ileal smooth muscle, held under voltage clamp at -40 mV or -50 mV by patch pipette in the whole-cell recording mode, carbachol (CCh) evoked an oscillatory inward cationic current. The frequency of current oscillations increased with increasing CCh concentration. CCh-evoked current oscillations were followed very closely by oscillations in intracellular free Ca2+ estimated from the Indo-1 signal, and were abolished by inclusion of EGTA in the pipette solution. Ryanodine and heparin, but not nifedipine, blocked the generation of current oscillations. CCh-evoked current oscillations were abolished upon withdrawal of extracellular calcium and restored upon its reintroduction. Inclusion of GTP[gamma S] in the pipette solution caused the generation of an oscillatory inward current, which was blocked by ryanodine. The present results are consistent with the hypothesis that CCh-evoked cationic current is gated by activation of a G protein and is steeply dependent on [Ca2+]i, fluctuations in the release of Ca2+ from stores during carbachol's action produce oscillations in [Ca2+]i which cause similar oscillations in the cationic current.

Animals↗
PubMed1993

Development of vagal innervation to the muscle of the avian gizzard.

The development of the vagal innervation to the gizzard has been investigated in chick embryos and young chicks. The membrane potential, first measurable on the 15th day of incubation, was -54 +/- 0.5 mV and increased with development to -67 +/- 0.4 mV. The latter value was attained 5 days after hatching and persisted thereafter. Stimulation of intramural nerves elicited a cholinergic, excitatory junction potential (EJP) for the first time, only in a small fraction of cells, on the 20th day of incubation. Within 3 days after hatching, cholinergic transmission showed the same features as in older chicks. Stimulation of the vagus nerve elicited no membrane potential responses before hatching but as early as 4 days after hatching, non-adrenergic, inhibitory junction potentials (IJPs) were evoked. In the next 10 days or so, the IJP was replaced with a cholinergic EJP as seen in mature tissues. After atropine (0.1-1 microM) treatment, both vagal and intramural nerve stimulation evoked a non-adrenergic IJP in a small fraction of cells immediately after hatching. The fraction of cells exhibiting the IJP increased with growth and reached 100% 5 days after hatching. Hexamethonium (50 or 100 microM) abolished the vagally-evoked EJPs. The vagally-evoked IJPs remained unchanged after application of hexamethonium in the early days after hatching, but later they were abolished in about half of the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Frequent deletion of the transgene in T cell receptor beta chain transgenic mice.

TCR V beta 8.1 transgenic mice were generated using a genomic TCR V beta gene construct under the control of its promoter and enhancer. Among three lines of transgenic mice, one line expressed the transgenic TCR on only approximately 70% of peripheral T cells, while the other two lines expressed it on almost all mature T cells. T cells which lacked expression of the transgenic TCR beta chain expressed endogenous TCR beta chains. The molecular basis underlying the lack of transgene expression in T cells of this line of transgenic mice was investigated. The transgenic TCR- cells were isolated by two methods. First, Thy-1+ V beta 8.1/8.2- cells were purified from peripheral T cells using cell sorting. Second, transgenic TCR- T cell clones were established. In both cases, Southern blotting indicated that V beta 8.1- T cells had deleted the transgenic TCR gene. Thus, deletion of the transgenic TCR can occur in a high proportion of T cells, which allows rearrangement and expression of endogenous TCR beta chains.

Animals↗
PubMed1993

Membrane current responses to externally-applied ATP in the longitudinal muscle of the chicken rectum.

1. Membrane current responses to ATP in enzymically-dispersed single smooth muscle cells from the chicken rectum were investigated by the whole-cell voltage clamp technique. 2. In cells dialysed with a KCl-rich solution under voltage clamp at a holding potential of -40 mV, ATP (10 microM) produced an inward current followed by an outward current. When the holding potential was changed to 0 mV and -80 mV, the biphasic current response to ATP was converted to an outward current alone and an inward current alone, respectively. 3. External application of tetraethylammonium (TEA, 5 mM), intracellular dialysis with a CsCl-rich solution, or inclusion of EGTA (10 mM) in the pipette abolished the outward current response to ATP. 4. Neither depletion of Ca2+ store with caffeine (10 mM) nor block of voltage-gated Ca2+ channels with nifedipine (10 microM) affected the biphasic current response to ATP. After removal of the extracellular Ca2+ the outward current response to ATP was abolished. 5. alpha,beta-methylene ATP (100 microM) elicited a current similar to the ATP-induced current. In the presence of alpha,beta-methylene ATP (100 microM), application of ATP (100 microM) was without effect. 6. In CsCl-filled cells, ATP analogues elicited an inward current and the order of potency was ATP not equal to alpha, beta-methylene ATP > ADP >> AMP. 7. Inclusion of GTP gamma S (0.2 mM) or GDP beta S (2 mM) in the pipette did not affect the ATP-induced inward current in CsCl-filled cells. The reversal potential of the ATP-induced inward current was about 0 mV and was completely inhibited after replacement of the cations in the bath solution by Tris. The reversal potential remained almost unchanged after replacement of Na+ in the bath solution with 1 10 mM Ca2+, but shifted in the negative direction after replacement of Na+ or both Na+ and Ca2+ with glucosamine.8. The results suggest that ATP acts on P2 purinoceptors to cause activation of cation channels with selectivity for Ca2+ over Na+. Moreover, it appears that no G-protein-mediated mechanism is involved and increased Ca2+ entry through the cation channels causes activation of Ca2+-activated K+ channels.

Adenosine Triphosphate↗
PubMed1993

Effect of trimebutine on voltage-activated calcium current in rabbit ileal smooth muscle cells.

1. The effect of trimebutine on the voltage-dependent inward Ca2+ current was investigated by the whole-cell voltage-clamp technique in single smooth muscle cells from rabbit ileum. 2. Trimebutine (3-100 microM) reduced the Ca2+ current in a concentration-dependent manner. The inhibitory effect on the Ca2+ current was also dependent on the holding potential. The Ca2+ current after a low holding potential was inhibited to a greater extent than that after a high membrane potential: the IC50 values were 7 microM and 36 microM at holding potentials of -40 mV and -60 mV, respectively. The Ca2+ current elicited from a holding potential of -80 mV could not be reduced by as much as 50% of the control by trimebutine at concentrations as high as 100 microM. 3. Trimebutine (30 microM) shifted the voltage-dependent inactivation curve for the Ca2+ current by 18 mV in the negative direction. The affinity of the drug for Ca2+ channels was calculated to be 36 times higher in the inactivated state than in the closed-available state. 4. Blockade of the Ca2+ current by trimebutine, unlike verapamil, was not use-dependent. 5. The results suggest that trimebutine inhibits the voltage-dependent inward Ca2+ current through a preferential binding to Ca2+ channels in the inactivated state in the smooth muscle cell from rabbit ileum. The inhibitory effect of trimebutine on gastrointestinal motility is discussed in the light of the present findings.

Action Potentials↗
PubMed1993

Stable production of recombinant human sperm immobilizing antibody using cDNA expression vectors.

PROBLEM: Sperm immobilizing antibodies present in sterile women may be one of the principal causes of immunological infertility. We already established cell lines that secrete recombinant human IgG sperm immobilizing antibody using class-switched (from IgM to IgG) genomic immunoglobulin genes. However, these transfectants produced a small quantity of antibody and required continuous use of a medium with selective reagents. We have now constructed cell lines that stably secrete the antibody in large quantities using immunoglobulin cDNAs and cDNA expression vectors. METHOD: The immunoglobulin heavy chain cDNA was cloned from transfectants that secrete the class-switched human IgG sperm immobilizing antibody. The light chain cDNA, which had already been cloned, and the heavy chain cDNA were inserted into the modified bovine papilloma virus-based cDNA expression vectors BCMGSNeo and BCMGSHyg, respectively. These constructs were sequentially transfected into a mouse myeloma cell line by electroporation. RESULTS: The established transfectants produced recombinant antibody that retained human sperm immobilizing activity in nonselective medium for at least 30 days. Moreover, the production of the antibody was increased three times over that of the previous cell lines. CONCLUSION: We have established an unique method that improves the production of sperm immobilizing antibody stably and in large quantities.

Animals↗
PubMed1993

Contractile responses to histamine and GTP gamma S in beta-escin-treated skinned smooth muscle of guinea pig ileum.

To characterize the calcium (Ca2+)-releasing effects of histamine and GTP gamma S, the drug-induced tension developments were measured in beta-escin-treated skinned longitudinal smooth muscle of guinea pig ileum. Intracellular Ca2+ stores were loaded with Ca2+ by incubating the muscle for 10 min in a Ca(2+)-containing solution. Histamine (10-100 microM), applied after Ca(2+)-loading, produced a transient rise in tension. The effect of histamine was not preserved after treatment with 20 mM caffeine, a Ca(2+)-store releaser. The effect of histamine was potentiated by GTP; inhibited by GDP beta S, an antagonist of GTP for binding to G-proteins; or heparin, an antagonist of inositol 1,4,5-trisphosphate (IP3) for binding to its receptor; and mimicked by IP3. When GTP gamma S (20 microM) was applied and continued to be present for 15 min, a transient rise in tension followed by a small, sustained rise in tension was elicited. The effect of GTP gamma S was completely inhibited by GDP beta S. The initial, transient component of the biphasic GTP gamma S response was abolished or markedly inhibited after treatment with caffeine, heparin or the calcium ionophore A23187. The present results suggest that histamine and GTP gamma S cause a release of Ca2+ from caffeine-sensitive stores which is mediated by IP3 formed through a G-protein-coupled mechanism. The GTP gamma S-induced Ca2+ release is not considered to involve such an IP3-independent process as described in chemically-skinned arterial muscle.

Animals↗
PubMed1993

Single nucleotide substitution of the androgen receptor gene in a case with receptor-positive androgen insensitivity syndrome (complete form).

Complete androgen insensitivity syndrome is caused by X chromosome linked disorder resulting in a target organ insensitivity to androgen. Two variants have been described in this syndrome. In the first, the binding of [3H]dihydrotestosterone (17 beta-hydroxy-5 alpha-androstan-3-one) to the androgen receptor is undetectable (receptor-negative), whereas in the second variant normal levels of androgen receptor are detectable but the binding of [3H] dihydrotestosterone to the androgen receptor is significantly thermolabile under certain conditions (receptor-positive). In receptor-negative cases, genetic disorders of the androgen receptor gene have been demonstrated. On the other hand, the genetic disorder of androgen receptor in receptor-positive cases is little known. In this study, the gene structure of androgen receptor in a receptor-positive case using a polymerase chain reaction technique is studied in the fibroblasts cultured from genital skin. The results demonstrate that the substitution of nucleotide (guanine-->cytosine) in exon G of the androgen receptor causes the replacement of an amino acid in position 820 (glycine-->alanine) which occurs in the hormone-binding domain of the androgen receptor. The substitution of nucleotide may explain the thermolability of the androgen receptor in a case with receptor-positive androgen insensitivity syndrome.

Adult↗
PubMed1992

Inhibition of abnormal T cell development and autoimmunity in gld mice by transgenic T cell receptor beta chain.

Mice homozygous for the gld (generalized lymphoproliferative disease) mutation developed systemic autoimmune disease and severe lymphadenopathy due to an age-related accumulation in the peripheral lymphoid organs of polyclonal T cells bearing a unique phenotype (CD4-CD8-TCR alpha beta+B220+). These T cells overexpress T cell receptor (TcR) alpha beta chain RNA, proto-oncogenes c-myb and fyn, and proliferate poorly in response to TcR-mediated stimulation. The origin of these T cells is poorly understood. To study the influence of a functionally rearranged TcR beta chain on the T cell developmental abnormality of the gld mutation and autoimmunity, we have backcrossed TcR V beta 8.1-transgenic mice to C3H-gld/gld to homozygosity (transgenic gld mice). In transgenic gld mice, lymphadenopathy was markedly inhibited and the accumulation of CD4-CD8- T cells did not occur, although the remaining T cells overexpressed c-myb and proliferated poorly in response to TcR occupancy. These features indicate that the pattern of proto-oncogene expression and abnormal function persist in phenotypically normal T cells in transgenic gld mice, and that these characteristics can be dissociated from the accumulation of CD4-CD8- T cells. The hypergammaglobulinemia and anti-double-stranded DNA (anti-dsDNA) antibody production was partially improved in transgenic gld mice, supporting the critical role of T cells in abnormal B cell activation described in autoimmunity-prone mice. To investigate further the mechanisms underlying the inhibition of CD4-CD8- T cell accumulation in transgenic gld mice, the fetal ontogeny of T cells in transgenic mice was compared with that of non-transgenic mice. In transgenic thymus, development of TcR alpha beta+ cells was accelerated as detected by earlier expression of CD4, CD8 and TcR in fetal thymus. In contrast, the number of TcR gamma delta+ cells was reduced. We suggest that altered T cell development in transgenic mice directly or indirectly inhibits the accumulation of abnormal T cells in gld mice.

Animals↗
PubMed1992

Reye's syndrome in Olmsted County, Minnesota: did it exist before 1963?

In this study, our goals were to determine whether Reye's syndrome existed before the first published report of this entity in 1963 and to describe the long-term incidence and trend of this syndrome. Medical and pathologic records and pathologic specimens for Mayo Clinic patients, including those who were residents of Olmsted County, Minnesota, were reviewed through the facilities of the Rochester Epidemiology Project. On review, 12 cases were identified for the period 1920 through 1962; 2 of these cases were in Olmsted County residents. Of the 12 cases identified before 1963, 10 were in patients younger than 5 years of age. In addition to the aforementioned two cases, five others in Olmsted County were diagnosed between 1963 and 1989. Incidence rates were computed for the Olmsted County population. The number of cases and rates per 100,000 persons younger than 18 years of age in that population were 2 cases (0.3) for 1920 through 1962, 4 cases (0.7) for 1963 through 1980, and 1 case (0.4) for 1981 through 1989. Although cases found during the earlier periods may have included disorders that mimic Reye's syndrome, the recommended criteria from the Centers for Disease Control were applied to review of medical records and supported by pathologic findings in the liver. The data showed an age distribution tending toward young patients and no seasonality of occurrence. The incidence rates in Olmsted County, Minnesota, showed an increase for 1963 through 1980 over previous decades, followed by a decrease. The small numbers preclude any conclusion about trends in the incidence rates.

Child↗
PubMed1992

Antiarrhythmic effects of preconditioning in anaesthetised dogs and rats.

OBJECTIVE: The aim was to determine the relationship of the duration of short coronary artery occlusions and of the reperfusion period to the extent of the antiarrhythmic effect of preconditioning. METHODS: A prolonged occlusion of a coronary artery in 102 anaesthetised rats and 55 anaesthetised dogs was preceded by a variable number of preconditioning coronary artery occlusions, of varying duration and with variable reperfusion periods between them and the prolonged occlusion. RESULTS: Preconditioning in both species reduced the severity of ischaemia induced arrhythmias, epicardial ST segment changes, and alterations in the degree of inhomogeneity of conduction during a subsequent prolonged coronary artery occlusion, provided that the reperfusion time was less than 30 min (in rats) and 1 h (in dogs). This antiarrhythmic effect of preconditioning was marked; eg, in dogs following two preconditioning occlusions survival from a combined ischaemia-reperfusion insult was 40% (cf, 0% in the controls). CONCLUSIONS: Short preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. The optimum time for this preconditioning occlusion in rats is 3 min and protection is still apparent 30 min later. In dogs, the protective effect is especially clear with two short (5 min) coronary artery occlusions. The protection in this species lasts for less than 1 h.

Animals↗
PubMed1992

Response of V beta 8.1+ T cell clones to self Mls-1a: implications for the origin of autoreactive T cells.

Clonal deletion and anergy are two major mechanisms of self-tolerance. However, the molecular mechanisms underlying clonal deletion and anergy, as well as the threshold of TCR affinity/avidity required for these processes, are not known. Expression of the V beta 8.1 TCR correlates with the reactivity of the T cells to the minor lymphocyte stimulating locus-1a (Mls-1a) and T cells expressing this TCR are deleted in the thymus of Mls-1a mice. Similarly, in TCR V beta 8.1 transgenic mice, the number of CD4+CD8-T cells is reduced in Mls-1a mice. However, small numbers of CD4+CD8-T cells remain in the periphery of adult Mls-1a transgenic mice. We have generated T cell clones from TCR V beta 8.1 transgenic mice by stimulation of lymph node T cells with C57BL/6 alloantigens. Interestingly, CD4+CD8-V beta 8.1+ clones isolated from the transgenic mice of Mls-1a background responded to the self-antigen Mls-1a, to which they did not respond in primary assay. Reactive patterns of the clones were compared with clones derived from Mls-1b mice. Proliferation and cytokine production of the clones from Mls-1a mice to the self-antigen Mls-1a were generally reduced when compared with clones from Mls-1b mice. More importantly, T cell clones from Mls-1a mice required more Mls-1a antigen for their activation, and were more susceptible to the inhibitory effects of anti-CD4 antibody on the proliferative responses to Mls-1a than those from Mls-1b mice. These results suggest that the T cell receptor on clones derived from Mls-1a mice have functional but reduced affinity/avidity for self-antigen Mls-1a.

Animals↗
PubMed1992

Membrane potential and current responses to neurotensin in the longitudinal muscle of the rectum of the fowl.

1. The effects of neurotensin (NT) on membrane potential and membrane current of the longitudinal smooth muscle of chicken rectum were investigated by intracellular recording and whole-cell voltage clamp. 2. NT (3 nM-1.2 microM), when applied via the bathing medium, produced a concentration-dependent membrane depolarization with an EC50 of 18 +/- 2 nM (n = 7) which was accompanied by an increase in the membrane conductance. The effect was biphasic: an initial, rapid depolarization reached a peak within 2-3 min and then declined to a lower but still elevated level which was sustained until washout. 3. Excitatory junction potentials (e.j.ps), which were non-adrenergic non-cholinergic (NANC) in nature, were decreased in amplitude and total duration in the presence of NT (0.6 microM). The depression of the e.j.p. was due mainly to the reduction of the membrane resistance. 4. When NT was applied locally by means of pressure ejection from a micropipette containing NT, some cells responded with a membrane depolarization and some failed to respond, whereas e.j.ps could invariably be elicited from all of them. 5. In single muscle cells enzymatically isolated from the muscle and dialyzed under voltage clamp at -50 mV with a CsCl-rich solution, NT (5 or 10 microM) produced an inward current. NT-induced inward currents were obtained with inclusion of 10 mM EGTA in the pipette solution and their reversal potential was around 0 mV. In cells dialyzed under voltage clamp at 0 mV with a KCl-rich solution, NT (5 microM) produced a brief outward current followed by abolition of spontaneous transient outward currents.6. The present results suggest that the membrane depolarization, which may arise from activation of non-selective cation channels, and release of calcium from internal stores produced by neurotensin are responsible for its contractile activity in the longitudinal smooth muscle of chicken rectum. Further, the depolarizing effect may provide support for the involvement of NT in the NANC transmission in this preparation.

Adenosine Triphosphate↗
PubMed1992

GTP-binding protein involvement in membrane currents evoked by carbachol and histamine in guinea-pig ileal muscle.

1. Single smooth muscle cells obtained by enzymic dispersion of the longitudinal muscle layer of guinea-pig ileum were used for recording membrane currents under whole-cell voltage clamp in response to carbachol (100 microM, unless otherwise stated) or histamine (100 microM) applied extracellularly. 2. At a holding potential of 0 mV, a transient outward current was evoked by carbachol and histamine. Responses to the two agonists were very similar in size and time course to the current response to caffeine (10 mM). The response to carbachol was virtually absent in the presence of histamine, and vice versa. Caffeine was without effect in the presence of either of these agonists. Inclusion of EGTA (10 or 20 mM) in the pipette abolished the responses to carbachol, histamine and caffeine. Thus, the outward current responses were considered to represent opening of Ca(2+)-activated K+ channels in response to a massive release of Ca2+ from the same stores by these three agents. 3. An inward current was evoked by carbachol and histamine, but not by caffeine at a holding potential of -40 mV, which was considered to represent opening of cationic channels. The carbachol-induced inward current was much longer in duration and larger in size than the histamine-induced inward current. 4. Inclusion of GDP beta S (2 mM) in the pipette abolished the inward and outward current responses to histamine, but inhibited only part of those to carbachol. 5. When the holding potential was held at 0 mV with inclusion of GTP gamma S (0.1-1 mM) in the pipette, spontaneous transient outward currents appeared immediately after break-through but disappeared a few minutes later. Under these conditions, caffeine (10 mM) was almost without effect, suggesting that GTP gamma S had released Ca2+ stores. When the holding potential was held at -40 mV and GTP gamma S (0.1 or 0.2 mM) was present in the pipette, an inward current developed a few minutes after break-through. During the GTP gamma S-induced inward current, application of carbachol or histamine produced no further inward current. However, when 0.01 mM-GTP gamma S was included in the pipette solution, carbachol- and histamine-induced inward currents were potentiated. 6. Pretreated with 2-5 micrograms/ml pertussis toxin (PTX) did not change noticeably the outward current responses to carbachol and histamine, but abolished or markedly reduced the inward current responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

The effect of pretreatment with moricizine on early arrhythmia resulting from myocardial ischemia in rats.

Moricizine (moracizine) is a new class I antiarrythmic drug which is undergoing a large scale clinical trial at present. A rat model was used to compare the effects of moricizine (5 mg/kg i.v.), disopyramide (DSP 5 mg/kg i.v.) and mexiletine (MXT 5 mg/kg i.v.) on early ventricular arrhythmias occurring within 30 min after ligation of the left coronary artery. After intravenous administration, all three drugs slowed the heart rate significantly (p less than 0.01), and compared to the control group only moricizine significantly increased the systolic, diastolic and mean arterial blood pressures. The total number of premature ventricular complexes were as follows; control group (n = 9); 1666 +/- 250 beats, moricizine group (n = 7); 1645 +/- 417 beats (NS), DSP group (n = 10); 325 +/- 155 beats (p less than 0.01 vs control) and MXT group (n = 10); 733 +/- 147 beats (p less than 0.01 vs control). The incidence of primary ventricular fibrillation, was significantly reduced by DSP and MXT (10% reduction and 20% reduction respectively) (p less than 0.05), while moricizine (incidence 80%) had no effect in comparison to the control group (incidence 90%). Death due to arrhythmia was completely abolished by DSP and MXT; although moricizine showed a slight tendency to increase the mortality rate, but the difference was not significant. In conclusion, moricizine has no obvious protective effect on early ventricular arrhythmias resulting from coronary artery occlusion in rats.

Animals↗
PubMed1992

Inhibitory effect of moricizine on reperfusion induced tachyarrhythmias in rats--a comparison study with disopyramide and mexiletine.

Acute ligation of proximal left coronary artery was performed on forty male Sprague-Dawley rats. Five min later, occlusion was released in order to evaluate the effectiveness of the 3 antiarrhythmic drugs in eliminating reperfusion ventricular arrhythmias. The drugs evaluated were moricizine (5 mg/kg), disopyramide (DSP) (5 mg/kg) and mexiletine (MXT) (5 mg/kg), which were administered intravenously 5 min before ligation of the coronary artery. Compared to control rats that underwent identical experimental procedures, all 3 drugs significantly lowered the mortality rate from 90% of the control group to 20, 20 and 0% for moricizine, DSP and MXT groups. The incidence of ventricular fibrillation (Vf) was also decreased significantly by these drugs. The duration of ventricular tachycardia (VT) and Vf of surviving rats in drug groups were 111.7 +/- 35.0 sec, 71.6 +/- 29.4 sec and 32.9 +/- 14.6 sec for moricizine, DSP and MXT, respectively. Many of the drug treated rats could be restored to the normal sinus rhythm and survived. All 3 drugs slowed the heart rate significantly, but as for the blood pressure only MXT showed significant suppressing effect. In conclusion, moricizine has the same significant preventive effect on reperfusion induced ventricular tachyarrhythmias as DSP and MXT.

Animals↗