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Biomedical subjects

Y Yazaki

Publications and source records attributed to Y Yazaki.

At least 757 records · Page 42Linked to original sources
PubMed1989

Endothelin: a potent vasoconstrictor associated with coronary vasospasm.

Endothelin, administered into the coronary arteries of anesthetized dogs, produced a profound and long-lasting reduction in coronary blood flow with electrocardiographical evidence of myocardial ischemia. Coronary angiography revealed delayed filling of the distal branches and, in some cases, cessation of the blood flow distal to the epicardial portions of coronary arteries. The coronary vasoconstriction induced by endothelin subsided after intracoronary administration of nitroglycerin. Pretreatment with the Ca2+-channel antagonist, nitrendipine, suppressed endothelin-induced vasoconstriction. These findings suggest that endothelin, produced by vascular endothelial cells, may contribute to the pathogenesis of coronary vasospasm.

Animals↗
PubMed1989

The role of endothelin in the pathogenesis of vasospasm following subarachnoid haemorrhage.

The purpose of the present study was to evaluate the vasocontractile activity of endothelin, a newly isolated endothelium-derived constrictor peptide, in canine basilar arteries in vitro and in vivo. Endothelin at concentrations of 10(-12) M approximately 3 X 10(-8) M elicited dose-dependent contractions of canine basilar arteries in vitro. The maximum tension was larger than that induced by 40 mM KCl. The EC50 value was 1.9 +/- 0.6 X 10(-9) M (mean +/- SEM). The endothelin-induced contraction was reversed by 10(-8) M nicardipine or 10(-5) M approximately 10(-4) M papaverine. An intracisternal injection of 0.6 approximately 1.2 X 10(-12) mol/kg of endothelin caused biphasic contraction of the basilar artery lasting for more than 24 h. The initial phase of the contraction accompanied remarkable changes in vital signs such as an acute rise of blood pressure, bradycardia and respiratory arrest. An intracisternal injection of 2.0 X 10(-12) mol/kg of endothelin also induced acute contraction of the basilar artery. However, all of the dogs which received an intracisternal injection of 2.0 X 10(-12) mol/kg of endothelin died from sustained respiratory insufficiency. The present results demonstrate that endothelin induces strong and long-lasting contractions of cerebral arteries. Therefore, endothelin may play an important role in the pathogenesis of vasospasm.

Angiography↗
PubMed1989

Central effect of endothelin on blood pressure in conscious rats.

This study was conducted to investigate the effect of intracerebroventricular administration of endothelin (EDT), a novel potent vasoconstricting peptide, on blood pressure in conscious rats. The lateral cerebral ventricle of male Wistar rats was cannulated, and the femoral artery was also cannulated to measure the mean arterial blood pressure (MABP) and heart rate (HR). EDT dissolved in 10 microliters of artificial cerebrospinal fluid (ACSF) (8.25-66 pmol icv) provoked a dose-dependent increase in MABP. EDT also increased HR, although the effect of 66 pmol was variable. Intracerebroventricular ACSF did not provoke any effects on MABP and HR. Intracerebroventricular EDT also provoked contralateral rotational behavior. Pretreatment with 2 mg/kg iv phenoxybenzamine significantly suppressed the 16.5 pmol icv EDT-induced increase in MABP. Moreover, 16.5 pmol icv EDT markedly increased plasma epinephrine and norepinephrine concentration. These results indicate that EDT has a central pressor action, and the action might be mediated, at least in part, by catecholamine release to the periphery. EDT might play a role in the central control of blood pressure, although the physiological implications have not yet been determined.

Animals↗
PubMed1989

Quantification of myocardial infarct size after coronary reperfusion by serum cardiac myosin light chain II in conscious dogs.

The effects of early coronary artery reperfusion on the relation between the extent of myocardial infarction and serum levels of cardiac myosin light chain II or plasma creatine kinase levels were evaluated in the conscious dog. Hydraulic occluders were placed on the left anterior descending arteries of 38 dogs. Seven to 10 days later, myocardial infarction was produced. Coronary reperfusion was performed 3 hours (group A1, n = 13) and 6 hours (group A2, n = 12) after the occlusion. In the other 13 dogs, coronary occlusion was sustained throughout the course of the experiment (group B). Seven days after the occlusion, the heart was cut from the apex to the base into 4-mm slices, and infarct size was determined macroscopically. Rapid appearance and early peaking of creatine kinase were observed in group A. Cumulative release of creatine kinase significantly correlated with infarct size in group A (infarct size ranged from 0.1 to 20.1 g, r = 0.90) and group B (from 0.6 to 26.8 g, r = 0.91). However, since creatine kinase release in group A was greater in comparison with that from infarcts of the same size in group B, the slope of the regression line for group A was significantly steeper (p less than 0.05). Cardiac myosin light chain II appeared as early as creatine kinase did and continued to be elevated for 7 days. A very close relation was observed between infarct size and total cardiac myosin light chain II release (r = 0.87 for group A, and r = 0.88 for group B) or peak level of light chain II (r = 0.85 for group A, and r = 0.81 for group B). In addition, the slopes of the regression lines for infarct size and both peak and total release of light chain II did not differ between group A and group B. On histological examination, viable myocardium was frequently observed in the epicardium of the ischemic area in group A1; therefore, infarct size was greater in group B than in group A1 (p less than 0.05). Also, myocardial creatine kinase content in the epicardium of the center of the ischemic area in group A1 was greater than that in group B. Cardiac myosin light chain II release in group A1 was less than that in group B, whereas no difference was found in plasma creatine kinase release among groups A1, A2, and B.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Molecular cloning and characterization of a Ca2+ + Mg2+-dependent adenosine triphosphatase from rat cardiac sarcoplasmic reticulum. Regulation of its expression by pressure overload and developmental stage.

To investigate the regulation of expression of cardiac Ca2+ + Mg2+-dependent ATPase (Ca2+-ATPase) in sarcoplasmic reticulum (SR), we isolated cDNA (pHA6) encoding a Ca2+-ATPase of rat cardiac SR. The clone consisted of 2,311 mRNA-derived nucleotides, which covered half the coding region and the entire 3'-untranslated regions. The nucleotides and deduced amino acid sequences of pHA6 showed striking homology, 89 and 98%, respectively, to those of rabbit Ca2+-ATPase of the slow-twitch form. Northern blot analyses revealed that the mRNA levels of Ca2+-ATPase were decreased by pressure overload and became 32% of sham in 1 mo. During the developmental stage the mRNA levels were very low in the fetal period and steeply increased around birth. These changes in mRNA levels were correlated with the corresponding protein levels. These results suggest that the expression of cardiac Ca2+-ATPase in SR is regulated by pressure overload and the developmental stage, at least in part, at the pretranslational level.

Aging↗
PubMed1989

Infarct sizing after reperfusion by two-dimensional echocardiography and serum cardiac myosin light chain II in conscious dogs: dissociation between early left ventricular wall motion and ultimate infarct size.

The time course of recovery of left ventricular wall motion after coronary reperfusion and how that relates to anatomical infarct size, wall motion abnormality, and the amount of cardiac myosin light chain II release were evaluated in conscious dogs. One week after the implantation of hydraulic occluders on the left circumflex arteries, myocardial infarction was induced. Coronary reperfusion was performed 3 h after the occlusion in 9 dogs (R) and occlusion was sustained in 9 dogs (C). All dogs underwent serial 2-dimensional echocardiograms and determination of serum cardiac myosin light chain II. The infarct size was identified at 14 days. Systolic wall thickening at the center of the ischemic area (SWT) at 3 h was -7.7 +/- 2.8% (C), -9.9 +/- 3.0% (R). Systolic thinning was observed even at 14 days in C. Significant recovery of contraction was observed in R, but the improvement continued for as long as 2 days. SWT at 14 days was -1.5 +/- 2.8% (C) and 7.0 +/- 4.6% (R) (p less than 0.05). All of SWT or the extent of systolic thinning (EST) 3-hour and 14-day were correlated well with infarct size in C. In group R, 14-day SWT and 14-day EST correlated with infarct size but 3-hour SWT and 3-hour EST did not. Total release of serum cardiac myosin light chain II levels correlated well with infarct size (r = 0.88), 14-day SWT (r = -0.90) and 14-day EST (r = 0.89) in all dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Clinical application of immunoassays for cardiac myosin light chains].

We developed four types of immunoassays for cardiac myosin light chains (LC), which are two radioimmunoassays (RIA) for canine and human LC, and an immunoradiometric assay (IRMA) and an enzyme-linked immunosorbent assay (ELISA) for human LC. The first two assays make use of polyclonal antibodies and the last two use monoclonal antibodies. By using these immunoassays, we studied the release of cardiac LC into the serum following acute myocardial infarction (AMI). In experimental AMI in dogs, cardiac LC appeared in the serum within 4-12 hours, reached the maximum at 2-5 days and returned to normal at 7-10 days. This long time-course was suggested due to the continuous liberation of LC from the infarcted myocardium on the basis of a quick disappearance rate of LC from the circulation. The peak LC values were found to correlate well with the histological infarct size. Similar results were also obtained regarding the time-course of circulating LC in clinical patients with AMI. Thus LC measurement seems useful for diagnosis of AMI as well as for estimating the extent of myocardial damage. We also developed an IRMA and an ELISA for human LC by using anti-human LC monoclonal antibodies for a more rapid LC assay and for a consistent supply of antibodies. These assays showed sufficiently high sensitivities to measure 1-100 ng/ml of serum LC. Especially, serum LC can be assayed within 2.5 hours by our ELISA. Such progress in immunoassays for cardiac LC has made the measurement of LC an important laboratory test for the diagnosis of AMI.

Animals↗
PubMed1989

[A case of spontaneous pneumomediastinum in a trombonist].

A case of spontaneous mediastinal emphysema in a 21-year-old female trombonist was reported. During light work, she experienced pain in her neck which later radiated into her chest. She had neither causal disease nor episode of straining at the onset of her work. On admission, physical examination revealed subcutaneous emphysema over the upper part of the chest and neck, and mediastinal crunch on auscultation (Hamman's sign). Roentgenograms revealed the presence of a considerable amount of air in the mediastinum and this extended upward through the mediastinum into the soft tissue of the neck bilaterally. The chest and neck CT yielded clearer information concerning the location and degree of mediastinal emphysema. She was treated with bed rest and recovered completely within five days. Spontaneous mediastinal emphysema without causal disease or apparent precipitating episode is infrequently recognized. In our case, though the trombonist had no apparent straining episode, the causative factor can be assumed to be the tenderness of the alveoli originating from frequent over-inflations of the lungs and high intra-alveolar pressures of about 150 cmH2O during trombone performance, which may result in alveolar rupture under normal intralveolar pressures.

Adult↗
PubMed1988

Endothelin stimulates c-fos and c-myc expression and proliferation of vascular smooth muscle cells.

Recently, a potent vasoconstrictor peptide, endothelin (EDT), was isolated from vascular endothelial cells. We examined its effect on rat vascular smooth muscle cells (VSMCs). EDT induced the elevation of intracellular calcium, which was dependent on extracellular calcium and inhibited by a calcium-channel antagonist in a competitive manner. EDT caused a rapid and transient increase in the c-fos and c-myc mRNA levels and stimulated the DNA synthesis of VSMCs in a dose-dependent manner. This effect of EDT on the proliferation of VSMCs might be related to the development of atherosclerosis.

Animals↗
PubMed1988

Molecular cloning and characterization of human atrial and ventricular myosin alkali light chain cDNA clones.

We have isolated essentially full-length cDNA clones for atrial (ALC1) and ventricular (VLC1) myosin alkali light chains from a human fetal heart cDNA library. Comparison of overall nucleotide sequences of ALC1 and VLC1 cDNA clones has revealed that, while these two inserts show significant DNA sequence homology (78.4%) with respect to their coding regions, the 5'- and 3'-untranslated regions are highly divergent. Our statistical analysis suggests that human ALC1 and VLC1 diverged approximately 300 million years ago, during the time of separation of birds and mammals. RNA blot analysis shows that ALC1 mRNA is expressed in fetal ventricular and fetal skeletal muscles as well as fetal and adult atrial muscles and VLC1 mRNA is expressed in adult slow skeletal muscle as well as fetal and adult ventricular muscles. Southern blot analysis indicates that each protein is encoded by a single gene. Finally, we show that VLC1 mRNA is induced in pressure-overloaded human atrium.

Adult↗
PubMed1988

A novel potent vasoconstrictor peptide produced by vascular endothelial cells.

An endothelium-derived 21-residue vasoconstrictor peptide, endothelin, has been isolated, and shown to be one of the most potent vasoconstrictors known. Cloning and sequencing of preproendothelin complementary DNA shows that mature endothelin is generated through an unusual proteolytic processing, and regional homologies to a group of neurotoxins suggest that endothelin is an endogenous modulator of voltage-dependent ion channels. Expression of the endothelin gene is regulated by several vasoactive agents, indicating the existence of a novel cardiovascular control system.

Amino Acid Sequence↗
PubMed1988

Long-term outcome following programmed electrical stimulation in patients with high-grade ventricular ectopy.

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.

Death, Sudden↗
PubMed1988

Atrial natriuretic peptide distribution in fetal and failed adult human hearts.

The distributions of atrial natriuretic peptide (ANP) in human hearts during the developmental stage and in adult pathological states was examined with an antibody specific to human alpha-ANP. With immunoblotting and immunofluorescence methods, we found that a 17-kDa protein, which is a pro ANP, was expressed in human fetal ventricles, in which the numbers of myofibers containing ANP granules were more abundant in the subendocardial region than the subepicardial region. As determined by radioimmunoassay, the content of immunoreactive ANP (per milligram protein) in the developing heart was greatest in the left atrium and occurred decreasingly in the right atrium, right ventricle, and left ventricle, respectively. Because ANP content in the left ventricle declined during the progress of gestation in developing hearts and because it was very low, if ever detectable, in normal adult hearts, ventricular ANP expression appears to be developmentally regulated from the early gestational stage. However, it was reexpressed in the ventricles of patients who had suffered from severe congestive heart failure. In this situation, we found that the ventricular ANP expression was more marked in patients with dilated cardiomyopathy than in patients with severe valvular disease. Interestingly, in the ventricles of patients with dilated cardiomyopathy, ANP contents were higher in the left ventricular free wall than in the right ventricular free wall, although the left ventricular subendocardium contained more ANP than the subepicardium, showing a transmural gradient similar to that expressed in fetal ventricles. Thus, the expression of ANP in human ventricles is developmentally regulated from the early gestational stage, and even adult ventricular myofibers can synthesize ANP during severe congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Expression of cellular oncogenes in the myocardium during the developmental stage and pressure-overloaded hypertrophy of the rat heart.

Proto-oncogenes have been revealed to participate in normal cell proliferation as well as in cell transformation. Since cardiac myocytes are terminally differentiated, they cannot divide except in the fetal period. To determine the role of cellular oncogenes in the growth of the heart, the expression pattern of eight cellular oncogenes during the developmental stage and pressure-overloaded hypertrophy of the rat hearts were examined in vivo. Northern blot analysis was performed with eight oncogene probes (myc, fos, Ha-ras, src, erbA, erbB, sis, myb). Pressure overload increased the levels of cellular (c-) fos, c-myc, and c-Ha-ras. An increase of c-fos and c-myc was detected at 30 minutes and 2 hours, respectively; the levels peaked at 8 hours, and they returned to baseline by 48 hours after aortic constriction. However, the level of c-Ha-ras showed a gradual increase. During the course of development, the expression of c-myc was detectable only in the embryonic stage, whereas the expression of c-fos was not detected in the fetal period, was increased after birth, and peaked in 200-day-old adults. The expression of c-Ha-ras was almost the same throughout the development. Cellular oncogenes were expressed in the heart in response to pressure overload and in a stage-specific manner. These results suggest that cellular oncogenes may participate in the normal developmental process and hypertrophy of hearts and that the cellular hypertrophy induced by pressure overload may share a similar mechanistic pathway with cell proliferation.

Animals↗