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Biomedical subjects

N Taira

Publications and source records attributed to N Taira.

At least 73 records · Page 4Linked to original sources
PubMed1992

K+ channel openers, cromakalim and Ki4032, inhibit agonist-induced Ca2+ release in canine coronary artery.

The effects of K+ channel openers, cromakalim and an acetoxyl derivative of KRN2391 (Ki4032), were studied on force of contraction, increases in intracellular calcium concentration ([Ca2+]i) measured by fura-2 and inositol 1,4,5-trisphosphate (IP3) production induced by the thromboxane A2 analogue, U46619, in canine coronary arteries. Upon single dose applications of U46619 at 300 nmol/l, phasic and tonic increases in [Ca2+]i and force were seen, which were almost abolished by cromakalim (10 mumol/l) and Ki4032 (100 mumol/l). In the absence of extracellular Ca2+, U46619 induced a transient increase in [Ca2+]i with a contraction. Cromakalim (0.01-10 mumol/l) and Ki4032 (0.1-100 mumol/l) concentration-dependently inhibited the increases in [Ca2+]i and contraction. The inhibitory effects of cromakalim and Ki4032 were blocked by the K+ channel blocker tetrabutylammonium (TBA) and counteracted by 20 mmol/l KCl-induced depolarization. Cromakalim and Ki4032 did not affect caffeine-induced Ca2+ release. Cromakalim reduced U46619-induced IP3 production significantly and TBA blocked this inhibitory effect. These results suggest that the hyperpolarization of the plasma membrane by K+ channel openers inhibits the production of IP3 and Ca2+ release from intracellular stores related to stimulation of the thromboxane A2 receptor.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Sudden death of calves by experimental infection with Strongyloides papillosus. I. Parasitological observations.

Recently, an unknown disease, 'sudden death', in calves has been found in Japanese beef production farms. A previous study conducted by Taira and Ura indicated that sudden death can be effected in calves by hyperinfection of Strongyloides papillosus (SPL) and that the disease is possibly caused by SPL infection. In the present work, an experimental infection of SPL in calves was conducted to confirm the field occurrence. Fifteen Holstein Friesian calves, ranging from 45.5 to 85.6 kg in body weight, were divided into six groups. Calves of Groups A, B, C, D, E and F were infected once at the rate of 100,000, 320,000, 1,000,000, 3,200,000, 10,000,000 and 32,000,000 SPL larvae per 100 kg of body weight, respectively. Five calves were assigned to Group B, while two calves were assigned to the other groups. After showing no premonitory signs, sudden death of ten calves took place. The survival time of these calves was 27.4 and 16.8 days (Group B), 14.8 and 14.8 days (Group C), 13.3 and 14.2 days (Group D), 11.0 and 11.1 days (Group E) and 11.6 and 10.8 days (Group F). Three calves of Group B did not exhibit sudden death. The results of this study demonstrate that strongyloidiasis was the cause of sudden death.

Animals↗
PubMed1992

Sudden death of calves by experimental infection with Strongyloides papillosus. II. Clinical observations and analysis of critical moments of the disease recorded on videotape.

Four calves experimentally infected with different doses of Strongyloides papillosus were examined for changes of body temperature and other clinical parameters. Also, the critical moments of death, which were recorded on videotape, were analyzed in detail. The first clinical signs included initial accelerated respiration. In general, body temperature was almost normal; however, one calf showed a slight increase after 2 or 3 days of infection, and two calves a gradual increase 7 days after infection. Vocal noises and general spasms were observed 5-14 times during the course of death. Initial vocal noises were heard between 0:50 and 1:30 (minute:second) after the appearance of the initial clinical signs. The final spasm, preceding death, occurred between 3:05 and 3:40 after the appearance of the initial clinical signs.

Animals↗
PubMed1992

Spasmolytic action of nicorandil in canine conductive coronary arteries in vivo is not modified by glibenclamide.

The spasmolytic effects of nicorandil, cromakalim, and nitroglycerin on coronary arteries were investigated by angiographic technique in anesthetized dogs. With intracoronary arterial (i.a.) U 46619, a thromboxane A2 mimetic, the diameter of coronary arteries decreased in a sustained manner by 36.1 +/- 1.6% from control levels (coronary spasm). With a successive i.a. injection of nicorandil (300 micrograms), cromakalim (30 micrograms), or nitroglycerin (3 micrograms), the diameter recovered control levels (102.9 +/- 3.9, 96.8 +/- 5.6, and 100.1 +/- 4.3%, respectively). In dogs treated intravenously (i.v.) with glibenclamide, a pharmacologic antagonist of K-channel openers, the spasmolytic effect of cromakalim was significantly reduced, whereas the activity of nicorandil or nitroglycerin remained unaffected. We also investigated a possible modification by glibenclamide of the increase in coronary blood flow (CBF) induced by i.a. nicorandil and cromakalim in anesthetized dogs. The dose-dependent blood flow responses to cromakalim and nicorandil were significantly attenuated by glibenclamide, whereas the response to nitroglycerin remained unaffected. These results suggest that the spasmolytic effect of nicorandil on canine conductive coronary vessels is not mediated by K-channel opening but by a nitroglycerin-like action and that the dilatation of resistive coronary vessels induced by nicorandil may be largely due to its action as a K-channel opener.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Effects of semotiadil (SD-3211), a benzothiazine calcium antagonist, on blood pressure and atrioventricular conductivity in anesthetized dogs.

We investigated the effects of semotiadil (SD-3211), a novel calcium antagonist, on blood pressure and the atrioventricular (AV) conduction time and functional refractory period (FRP) of the AV conduction system (AV conductivity) in anesthetized open-chest dogs. The heart was electrically stimulated at a constant rate. In dogs with an intact nerve supply to the heart, i.v.-injections of semotiadil (0.03 to 0.3 mg/kg) produced a fall of blood pressure in a dose-dependent manner. AV conduction time and FRP were prolonged by rather higher doses (0.3 mg/kg), and second-degree AV block occurred only with the highest dose (1 mg/kg). In dogs with the nerve supply to the heart interrupted, the vasodepressor effects and suppressant effects of semotiadil on AV conductivity were slightly enhanced. The suppressant effects on AV conductivity became marked as pacing rates were increased. These results suggest that semotiadil at appropriate doses produces a vasodepressor effect without affecting AV conductivity even in the heart deprived of nervous control, e.g., the heart with beta-adrenoceptors blocked. The frequency-dependent suppressant effect on FRP of semotiadil is also noteworthy in the treatment of reentrant supraventricular tachycardia that involves the AV node.

Anesthesia↗
PubMed1992

Ca2+ influx induced by the agonist U46619 is inhibited by hyperpolarization induced by the K+ channel opener cromakalim in canine coronary artery.

The fura-2 microscopic fluorimetric method was used to examine the effects of the thromboxane A2 analogue, U46619, on the force of contraction and intracellular calcium concentrations ([Ca2+]i) in canine coronary arteries. Upon cumulative application, U46619 increased [Ca2+]i and force. Depolarization by 20 mM KCl potentiated the increase in [Ca2+]i and increased the maximum force induced by U46619. In 5 mM KCl-PSS, the reduction of resting [Ca2+]i by cromakalim (3 x 10(-6) M) was greater than that by verapamil (3 x 10(-6) M). Cromakalim and verapamil inhibited the increases in [Ca2+]i and force induced by U46619 in 5 mM KCl-PSS. In 90 mM KCl-PSS in the presence of U46619, verapamil inhibited the increases in [Ca2+]i and force, whereas cromakalim did not inhibit them at all. The inhibitory effect of cromakalim was counteracted by depolarization by 20 or 25 mM KCl. Curves in the presence of U46619 which related force to [Ca2+]i were shifted to the left compared with that in the absence of U46619, suggesting that U46619 increases the Ca(2+)-sensitivity of the contractile proteins. Thus, U46619 produces Ca2+ influx through L-type Ca2+ channels, which are deactivated by hyperpolarization induced by cromakalim.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

ATP-sensitive K+ channels are gradually recruited in the vasodepressor response to adenosine in spinally-anesthetized dogs.

Vasodepressor mechanisms of adenosine were investigated in spinally-anesthetized dogs. An i.v.-infusion of adenosine (0.1-10 mumol/kg/min) caused a slowly developing and sustained decrease in blood pressure (BP). This vasodepression was antagonized by glibenclamide, a blocker of ATP-sensitive K+ (KATP) channels. On the other hand, a transient decrease in BP caused by a single bolus i.v.-injection of adenosine was not antagonized by glibenclamide in our previous study. These results suggested that the opening of KATP channels is gradually recruited in the vasodepressor mechanisms for adenosine-induced sustained vasodepression.

Adenosine↗
PubMed1992

KCl-depolarization potentiates the Ca2+ sensitization by endothelin-1 in canine coronary artery.

In Ca(2+)-free solution containing endothelin-1 (ET-1), depolarization by high KCl increased the force of contraction without any changes in intracellular calcium concentration ([Ca2+]i) in canine coronary artery. The [Ca2+]i-force relationships were examined in the absence or presence of ET-1 in 5 or 90 mM KCl. The relation curve in the presence of ET-1 in 90 mM KCl-PSS was shifted to the left and upward compared with that in 5 mM KCl. These results suggest that KCl-depolarization potentiates the Ca2+ sensitization by ET-1.

Animals↗
PubMed1992

Sudden cardiac death in calves with experimental heavy infection of Strongyloides papillosus.

For obtaining the preliminary data on the pathogenesis of sudden death in calves naturally heavily infected with Strongyloides papillosus, we monitored 8 Holstein calves experimentally infected with the larvae on electrocardiographic and pneumographic changes. Six calves died suddenly on days 11 to 17 after infection. Sinus tachycardia had been recorded continuously since 1 to 6 days before death. Heart rates increased gradually until death. Since 1 or 2 days before death, various patterns of tachyarrhythmia and bradyarrhythmia had been observed among patterns of sinus tachycardia. Arrhythmias included serious ventricular premature beat, paroxysmal ventricular tachycardia, complete atrioventricular block and so on. The terminal pattern observed suddenly in all of the cases was ventricular arrhythmias consisting of serial ventricular tachycardia, flutter and fibrillation, which were followed by respiratory arrest. Abnormal pneumograms were not obtained before the terminal ventricular fibrillation. Two of 8 calves recovered from the infection, only one of which showed sinus arrest and the second degree of atrioventricular block transiently. We concluded that calves heavily infected with the larvae died due to sudden cardiac arrest.

Animals↗
PubMed1991

Cardiohemodynamic effect of FK409, a novel highly potent nitrovasodilator, in anesthetized dogs.

The cardiohemodynamic effect of (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409), a novel potent vasodilator, was studied in anesthetized open-chest dogs. FK409 (1 to 10 micrograms/kg, i.v.) decreased mean blood pressure, cardiac output and venous return (sum of the flow through the inferior and the superior vena cava). These changes accompanied decreases in left ventricular pressure, in its maximum rate of rise and in right atrial pressure. This cardiovascular profile of FK409 is very similar to those of classical nitrates.

Anesthetics↗
PubMed1991

The group at C2 of N-ethylnicotinamide determines the vasodilator potencies and mechanisms of action of nicorandil and its congeners in canine coronary arteries.

The relaxant mechanisms of action of nicorandil and its congeners (SG-86, SG-103, SG-209 and SG-212) on large coronary arteries were investigated in isolated canine circumflex arteries contracted with 25 mmol/l KCl or 10(-7) mol/l U46619, a thromboxane A2 analogue. SG-212, SG-86, SG-209 and SG-103 were obtained by replacement of the nitroxy group of nicorandil by bromine, the hydroxy, acetoxy and nicotinoyloxy groups, respectively. Nicorandil (10(-6)-10(-3) mol/l), SG-212 (3 x 10(-4)-10(-2) mol/l), SG-209 (10(-4)-10(-2) mol/l), SG-103 (3 x 10(-4)-10(-2) mol/l), and SG-86 (10(-3)-10(-2) mol/l) all produced a concentration-dependent relaxation in KCl- or U46619-contracted arteries. The order of relaxant potency was as follows: Nicorandil much greater than SG-209 greater than SG-212 = SG-103 greater than SG-86. The relaxant effect of nicorandil was not affected by glibenclamide but antagonized by methylene blue. In the presence of glibenclamide, the concentration-relaxation curves for SG-209 underwent rightward parallel shifts. The relaxant effect of SG-209, however, was not affected by methylene blue. The concentration-relaxation curves for SG-212 underwent rightward parallel shifts only to a limited extent in the presence of glibenclamide, but they were not affected by methylene blue. The relaxant effect of SG-103 was affected by neither glibenclamide or methylene blue. The relaxant effect of SG-86 was not affected by glibenclamide. The relaxant effect of nicorandil accompanied an increase in cyclic-GMP levels but that of SG-209 did not.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Differential antagonism by glibenclamide of the relaxant effects of cromakalim, pinacidil and nicorandil on canine large coronary arteries.

The relaxant mechanisms of action of cromakalim, pinacidil and nicorandil, potassium channel openers, on large epicardial coronary arteries were investigated in isolated canine left circumflex arteries contracted by 10(-7) mol/l U46619, a thromboxane A2 analogue, or addition of 25 mmol/l KCl in comparison with nitroglycerin. Cromakalim (3 x 10(-8)-3 x 10(-5) mol/l), pinacidil (10(-6)-10(-4) mol/l), nicorandil (3 x 10(-6)-10(-3) mol/l) and nitroglycerin (3 x 10(-8)-10(-5) mol/l) all produced a concentration-dependent relaxation in both U46619- or KCl-contracted arteries. At their maximum effects pinacidil, nicorandil and nitroglycerin produced full relaxation in arteries contracted by either means. In contrast, cromakalim produced about a 73% relaxation in KCl-contracted arteries, although it caused full relaxation in U46619-contracted ones. In the presence of glibenclamide the concentration-relaxation curves for cromakalim in U46619- or KCl-contracted arteries underwent rightward parallel shifts. Schild regression had a slope of 1.00 and yielded a pA2 of 7.47 for glibenclamide in U46619-contracted arteries, and corresponding values obtained in KCl-contracted arteries were 0.86 (not significantly different from unity) and 7.28. The concentration-relaxation curves for pinacidil in U46619-contracted arteries also underwent rightward parallel shifts in the presence of glibenclamide, however, Schild regression had a slope of 0.60. The concentration-relaxation curves for pinacidil in KCl-contracted arteries underwent rightward parallel shifts only to a limited extent in the presence of glibenclamide. The concentration-relaxation curves for nicorandil and nitroglycerin in U46619- or KCl-contracted arteries were not affected by glibenclamide in concentrations which antagonized cromakalim.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Sudden death in calves associated with Strongyloides papillosus infection.

In recent years, a total of 152 calves have died suddenly on three farms in the southern part of Japan which used sawdust as litter. Calves often died within a few minutes of a violent fall without showing previous clinical signs. On necropsy of these cases, only a slight lesion was observed, although all showed heavy infection with Strongyloides papillosus (SPL). They appeared to have not only a large number of SPL eggs in the faeces, together with many adult SPL worms in the intestine, but also many migratory SPL larvae in tissues such as the lung and muscle. These outbreaks ceased following medication with thiabendazole or ivermectin. It is concluded that 'sudden death' is associated with heavy infection with SPL.

Animal Husbandry↗
PubMed1991

Dynamics of faecal egg counts in rabbits experimentally infected with Strongyloides papillosus.

An experiment using rabbits was carried out to determine basic data to maintain the calf strain of Strongyloides papillosus (SPL). Rabbits treated with four different numbers of doses of dexamethasone were exposed to 50,000 or about 100,000 infective larvae of SPL (Himeji strain, 1988). As a result, faecal egg output was valid in individual rabbits, regardless of dexamethasone administration. Eggs appeared in the faeces 9 or 10 days after exposure, and increased to as much as 20,000-573,000 eggs per gram (EPG). Thirteen of 18 rabbits died (72%) 12-29 days after infection. Five surviving rabbits discharged eggs in their faeces for more than 1 month; however, the EPG value of these cases on the last day was comparatively low.

Animals↗