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T Yada

Publications and source records attributed to T Yada.

At least 109 records · Page 6Linked to original sources
PubMed1995

Direct in vivo observation of subendocardial arteriolar response during reactive hyperemia.

To study the vasodilatory capacity of subendocardial (ENDO) arterioles, we evaluated the reactive hyperemic responses of ENDO as well as subepicardial (EPI) arterioles in 40 dogs by our needle-probe intravital microscope. We also examined the individual and combined effects of an ATP-sensitive K+ channel blocker (glibenclamide, 200 micrograms/kg), an inhibitor of nitric oxide synthase (NG-monomethyl-L-arginine [L-NMMA], 2 mumol/min, 20 minutes), and an adenosine-receptor antagonist (8-phenyltheophylline [8PT], 0.75 mumol/min, 15 minutes). The percent increase in end-diastolic diameter of ENDO arterioles was larger (P < .01) than that of EPI arterioles during reactive hyperemia, especially for the arterioles larger than 120 microns (P < .01). The diastolic-to-systolic vascular pulsation amplitude at the peak flow was greater in ENDO than EPI arterioles (25% versus 6%, P < .05). Compared with control conditions, the presence of both glibenclamide and L-NMMA suppressed the vasodilation responses of ENDO arterioles (P < .01 for both) and EPI arterioles (P < .05 for both). The effect of L-NMMA was greater in ENDO arterioles (P < .01), but that of glibenclamide was not different between ENDO and EPI arterioles. 8PT influenced the hyperemic response, although statistical significance was found only in the flow response. The effect of combined infusion of L-NMMA and glibenclamide with or without 8PT was greater than that of individual infusions in both ENDO and EPI arterioles. Conclusions are as follows: (1) The vasodilatory response of ENDO arterioles was even larger than that of EPI arterioles. Thus, the smaller flow reserve of ENDO arterioles may be caused by other factors, including the greater effects of myocardial compression and nitric oxide on the ENDO arterioles. (2) The vascular responses of ENDO and EPI arterioles were modulated by both endothelium-independent and -dependent vasodilative factors, and the effect of each factor including adenosine was associated with the effects of others.

Adenosine↗
PubMed1994

Cytosolic Ca2+ increase and cell damage in L6 rat myoblasts by HMG-CoA reductase inhibitors.

Acute rhabdomyolysis is caused by HMG-CoA reductase (HCR) inhibitors clinically and experimentally. To study the mechanism of muscle cell damage, we investigated the change in the cytosolic free Ca2+ concentration ([Ca2+]i) in L6 rat myoblasts stimulated with three kinds of HCR inhibitors: simvastatin, simvastatin-acid form and pravastatin. Simvastatin and simvastatin-acid form induced an increase in [Ca2+]i through two different pathways, namely, the Ca2+ release from intracellular stores and the Ca2+ influx from extracellular solution. They also caused cell puncture either in the presence or absence of extracellular Ca2+. Pravastatin induced little or no change in [Ca2+]i and no cell damage resulted. Simvastatin was 10-fold more potent than simvastatin-acid form. These results suggest that the mechanism of cell damage may relate to the [Ca2+]i elevation by these drugs and may be dependent on the lipophilicity of the inhibitors.

Animals↗
PubMed1994

Pituitary adenylate cyclase activating polypeptide is an extraordinarily potent intra-pancreatic regulator of insulin secretion from islet beta-cells.

Insulin secretion from pancreatic islets is controlled by peptides as well as by nutrients. We report here a novel, extraordinarily potent peptidergic regulation of insulin secretion. A 27-residue form of pituitary adenylate cyclase activating polypeptide (PACAP27) as low as 10(-14) to 10(-13) M stimulated insulin release from rat islets in a glucose-dependent manner. PACAP27 also increased cytosolic free Ca2+ concentration ([Ca2+]i) in islet beta-cells. Nitrendipine, a blocker of the L-type Ca2+ channel, abolished both [Ca2+]i and insulin responses. Vasoactive intestinal peptide, a peptide exhibiting 68% amino acid homology with PACAP, also increased [Ca2+]i in beta-cells but only at concentrations in the nanomolar range, indicating that PACAP27 is 4 logs more potent. A 38-residue form of the peptide (PACAP38) stimulated insulin release and increased beta-cell [Ca2+]i in a manner similar to that of PACAP27. PACAP-like immunoreactivity was demonstrated in pancreatic nerve fibers, islets, and capillaries. The results indicate that PACAP is a physiologically occurring peptide in pancreas and that PACAP, in a glucose-dependent manner, activates beta-cells presumably via a high affinity PACAP-selective receptor, raises [Ca2+]i by increasing the activity of L-type Ca2+ channels, and consequently stimulates insulin release. PACAP appears to be by far the most potent insulinotropic peptide known.

Animals↗
PubMed1994

Changes in plasma levels of the two prolactins and growth hormone during adaptation to different salinities in the euryhaline tilapia, Oreochromis mossambicus.

Studies were undertaken to determine whether the adaptation of the tilapia, Oreochromis mossambicus, to different salinities was accompanied by changes in plasma levels of growth hormone (GH) and its two prolactins (tPRL177 and tPRL188). Transfer from fresh water to 70% seawater (22 ppt) produced significant increases in plasma GH levels in males, but not in females. Both tPRLs decreased by the first sampling interval (6 hr) after transfer to seawater in both sexes. A second group of tilapia were adapted gradually to seawater (32 ppt) and were maintained in seawater for an additional 2 weeks. The fish were then transferred from seawater to fresh water. The transfer to fresh water induced a significant decline in plasma GH levels in both males and females. Both tPRLs increased within 6 hr after transfer to fresh water in both sexes. Then, plasma tPRL177 levels decreased gradually. By contrast, tPRL188 continued to increase and attained its highest levels 3 days after transfer to fresh water. These findings show that blood levels of the two tPRLs change rapidly during freshwater and seawater adaptation. The fact that tPRL177 and tPRL188 levels followed distinctly dissimilar patterns as freshwater acclimation proceeded suggests that the secretion and/or metabolic clearance of the two PRLs may be differentially regulated. The changes in GH which occurred when tilapia were moved between fresh water and seawater are compatible with the idea proposed by others for salmonids that GH may have an important role for seawater adaptation.

Adaptation, Physiological↗
PubMed1994

Effects of nitroglycerin on diameter and pulsation amplitude of subendocardial arterioles in beating porcine heart.

We examined the effect of nitroglycerin (NTG) on the diameter and diastolic-to-systolic pulsation amplitude of large (ID > 100 microns) and small (ID < 100 microns) subendocardial arterioles with their segmental responses. In 10 open-chest, anesthetized pigs, subendocardial arterioles of beating hearts (n = 18) were videorecorded using a needle-probe videomicroscope. Subendocardial arteriolar diameter was determined before and 1-2 min after NTG administration (25 micrograms/kg i.v.). In an additional experiment using three pigs, we monitored the transient response of subendocardial small arterioles (n = 5) from the time before NTG administration until 3 min after NTG. NTG dilated large subendocardial arterioles by 13 +/- 4% (means +/- SD, n = 10, P < 0.001) at about 1.5 min after NTG, but not small subendocardial arterioles (2 +/- 2%, n = 8, not significant). However, the small arterioles responded transiently to NTG in an earlier phase, especially to a higher dose. The percent diameter change of large subendocardial arterioles between diastole and systole at 1.5 min after NTG administration was 32 +/- 4%, which was larger than that under control conditions (19 +/- 8%, P < 0.05). The pulsation amplitude of small subendocardial arterioles at this time was almost unchanged by NTG (16 +/- 8 vs. 17 +/- 6%, NS) but increased transiently in an earlier phase. In conclusion, NTG dilated large subendocardial arterioles on the plateau phase of its impulse (intravenously) response (approximately 1.5 min after NTG).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Diameters of subendocardial arterioles and venules during prolonged diastole in canine left ventricles.

Using a needle-probe videomicroscope with a charge-coupled device (CCD) camera, we measured the diameter of subendocardial arterioles and venules during prolonged diastole beyond the time point at which coronary blood flow reached zero. In seven open-chest heart-blocked dogs, a sheathed needle probe with a doughnut-shaped balloon was introduced from the left atrial appendage and advanced into the left ventricle through the mitral valve. The tip of the probe was placed gently on the endocardial surface. Diameters of arterioles (n = 16) and venules (n = 16) at the beginning of long diastole ranged from 40 to 126 microns and from 32 to 192 microns, respectively. After cardiac arrest, the arteriolar diameter gradually declined with aortic pressure. Arteriolar diameters at zero flow decreased by 28 +/- 9% (mean +/- SD) compared with the initial diameter (P < .01). However, none of the subendocardial arterioles collapsed at zero flow or at 12 seconds after the beginning of prolonged diastole (8 to 9 seconds after zero flow) in an additional experiment (n = 5). In contrast to arteriolar diameter, venular diameter increased during prolonged diastole. Venular diameter at zero flow increased by 14 +/- 12% compared with the initial diameter (P < .01). We conclude that during prolonged diastole, when coronary arterial inflow ceases, subendocardial arteriolar diameter decreases without any visible collapse, whereas venular diameter increases.

Animals↗
PubMed1994

A novel D-phenylalanine-derivative hypoglycemic agent A-4166 increases cytosolic free Ca2+ in rat pancreatic beta-cells by stimulating Ca2+ influx.

It has recently been shown that N-[(trans-4-isopropylcyclohexyl)-carbonyl]D-phenylalanine (A-4166), a new nonsulfonylurea oral hypoglycemic agent, reduces blood glucose levels in nondiabetic and diabetic animals in a quicker and shorter lasting manner than sulfonylureas, and that the hypoglycemic effect of A-4166 is due to the stimulation of insulin release. However, the mechanism by which A-4166 stimulates insulin release is still unknown. In the present study, we investigated the effect of A-4166 on the cytosolic free Ca2+ concentration ([Ca2+]i) in pancreatic beta-cells from normal rats by dual wavelength fura-2 microfluorometry. In the presence of 2.8 mM glucose, A-4166 produced a rapid increase in [Ca2+]i in a concentration-dependent manner over the range of 3-30 microM. The increase in [Ca2+]i was transient, oscillatory, or sustained. A-4166 did not evoke any decrease in [Ca2+]i, whereas a high concentration of glucose (16.7 mM), a metabolized secretagogue, produced an initial decrease and a subsequent increase in [Ca2+]i. In the presence of 16.7 mM glucose, low concentrations (0.03-1 microM) of A-4166 produced an increase in [Ca2+]i in some of the beta-cells tested. The [Ca2+]i response to A-4166 was completely and reversibly inhibited under Ca(2+)-free conditions as well as by nitrendipine, a blocker of the L-type Ca2+ channel. Nitrendipine also inhibited insulin release from perfused rat pancreases stimulated by A-4166. Diazoxide, an opener of the ATP-sensitive K+ channel, blocked the [Ca2+]i response to A-4166. Sulfonylureas such as tolbutamide and glibenclamide increased [Ca2+]i in a manner similar to A-4166. These results indicate that at basal glucose concentrations, A-4166 increases [Ca2+]i in rat pancreatic beta-cells by stimulating Ca2+ influx through L-type Ca2+ channels, and that this effect is markedly augmented at elevated glucose concentrations. It appears that the increase in [Ca2+]i is related to the stimulation of insulin release by A-4166. Inhibition of ATP-sensitive potassium channels, but not stimulation of beta-cell metabolism, may be involved in the increase in [Ca2+]i by A-4166.

Animals↗
PubMed1993

Pituitary of "cobalt" variant of the rainbow trout separated from the hypothalamus lacks most pars intermedial and neurohypophysial tissue.

Adenohypophysial cell types and neurohypophysial tissues were investigated in the cobalt variant of the rainbow trout, which possesses an irregularly-shaped pituitary. The pituitary remnant was completely detached from the hypothalamus in all but one fish, in which a remnant was associated with the hypothalamus. Prolactin (PRL) and growth hormone (GH) cells were predominant cell types in all pituitary remnants, forming PRL and GH areas, respectively. There were fewer somatolactin (SL) and melanophore-stimulating hormone cells than in normal fish. There were few corticotropin cells in cobalt and normal trout. Although aldehyde-fuchsin positive cells were also present, positively-staining fibers were not detected in any of remnants examined. Plasma SL levels were much lower in cobalt than in normal trout. Plasma levels of GH and T3 were significantly lower in cobalt than in normal fish. Plasma levels of PRL, T4 and cortisol, plasma osmolality, ions (Na+, K+, Ca2+, and Mg2+), glucose, triglyceride, free fatty acids, and amino nitrogen concentrations were similar in the two groups. Cobalt variants thus lack hypophysial pars intermedia and neurohypophysial tissues. Various abnormalities of the cobalt variant, such as the cobalt blue body color and the fat deposition in the abdominal cavity, may be related to the absence of the pars intermedia.

Animals↗
PubMed1993

Endocardial coronary microcirculation of the beating heart.

Direct and continuous observation of subendocardial (deep myocardial) microcirculation provides essential information on coronary circulation, since cardiac contraction affects subendocardial vessels most vigorously. To achieve this aim, we developed a portable needle-probe video-microscope with a charge-coupled-device (CCD) camera to visualize the subendocardial microcirculation. Images of the subendocardial microcirculation of a porcine beating heart were successfully observed in all cases. The vascular compression by cardiac contraction decreased the diameter of subendocardial arterioles and venules by about 20%.

Animals↗
PubMed1993

Decreased mid-to-late diastolic decay of diastolic coronary artery flow velocity in pressure-overloaded left ventricular hypertrophy.

This study was carried out to investigate the characteristics of coronary arterial flow in left ventricular hypertrophy secondary to systemic hypertension. The blood velocities in the left anterior descending coronary artery (LAD) were measured by a No. 3F 20 MHz Doppler catheter in 23 hypertensive patients with left ventricular hypertrophy (systolic/diastolic pressure: 181 +/- 15/100 +/- 4 mmHg) and 13 patients with atypical chest pain, but without left ventricular hypertrophy and any abnormal hemodynamic findings. All patients had normal coronary arteriograms. The LAD blood velocity waveforms in pressure overloaded left ventricular hypertrophy were characterized by both a decreased mid-to-late diastolic deceleration rate (delta V/delta T) and a normalized value of delta V/delta T by peak diastolic velocity [delta V/(delta T.Vpeak)], as well as delayed early diastolic inflow (time for diastolic rise; TDR). The values of the delta V/(delta T.Vpeak) in the patients with hypertensive left ventricular hypertrophy and in the normotensive controls were 1.26 +/- 0.61 and 3.03 +/- 1.18/s, respectively (P < 0.001). The TDR was 145 +/- 56 and 66 +/- 15 ms (P < 0.001). In patients with hypertensive left ventricular hypertrophy, the delta V/(delta T.Vpeak) correlated well with the degree of hypertrophy (r = 0.75, P < 0.01) and with the TDR (r = 0.82, P < 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity increased with the delta V/(delta T.Vpeak) (r = 0.68, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

In vivo observation of subendocardial microvessels of the beating porcine heart using a needle-probe videomicroscope with a CCD camera.

We developed a portable needle-probe videomicroscope with a charge-coupled device (CCD) camera to visualize the subendocardial microcirculation. In 12 open-chest anesthetized pigs, the sheathed needle probe with a doughnut-shaped balloon and a microtube for flushing away the intervening blood was introduced into the left ventricle through an incision in the left atrial appendage via the mitral valve. Images of the subendocardial microcirculation of the beating heart magnified by 200 or 400 on a 15-in. monitor were obtained. The phasic diameter change in subendocardial arterioles during cardiac cycle was from 114 +/- 46 microns (mean +/- SD) in end diastole to 84 +/- 26 microns in end systole (p < 0.001, n = 13, ratio of change = 24%) and that in venules from 134 +/- 60 microns to 109 +/- 45 microns (p < 0.001, n = 15, ratio of change = 17%). In contrast, the diameter of subepicardial arterioles was almost unchanged (2% decrease, n = 5, p < 0.01), and the venular diameter increased by 19% (n = 8, p < 0.001) from end diastole to end systole. Partial kinking and/or pinching of vessels was observed in some segments of subendocardial arterioles and venules. The percentage of systolic decrease in the diameter from diastole in the larger (> 100 microns) subendocardial arterioles and venules was greater than smaller (50-100 microns) vessels (both p < 0.05). In conclusion, using a newly developed microscope system, we were able to observe the subendocardial vessels in diastole and systole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Glucagon-like peptide-1-(7-36)amide and a rise in cyclic adenosine 3',5'-monophosphate increase cytosolic free Ca2+ in rat pancreatic beta-cells by enhancing Ca2+ channel activity.

Glucagon-like peptide-1 (GLP-1), in the form of either GLP-1-(7-36)amide or GLP-1-(7-37), has been shown to potently stimulate insulin release in a glucose-dependent manner and is suggested to be a physiological incretin. To explore the mechanisms by which GLP-1-(7-36)amide stimulates insulin release, we investigated its action on the cytosolic free Ca2+ concentration ([Ca2+]i) in single rat pancreatic beta-cells by the dual wavelength microfluorometry with fura-2. In the presence of 8.3 mM glucose, GLP-1-(7-36)amide at a concentration as low as 3 x 10(-12) M produced a rapid transient increase in [Ca2+]i in some of the single beta-cells. GLP-1-(7-36)amide at 10(-11) M or more evoked the [Ca2+]i response in the majority of beta-cells. In the presence of 2.8 mM glucose, GLP-1-(7-36)amide was without effect. The [Ca2+]i response to GLP-1-(7-36)amide was completely and reversibly inhibited under Ca(2+)-free conditions and by 1 microM nitrendipine, a blocker of L-type Ca2+ channels. Elevation of cAMP in beta-cells by either 10 microM forskolin, an activator of adenylyl cyclase, or 5 mM (bu)2cAMP (db-cAMP) produced an increase in [Ca2+]i similar to that caused by GLP-1-(7-36)amide. The db-cAMP-induced increase in [Ca2+]i was also completely blocked by nitrendipine. In the continuous presence of GLP-1-(7-36)amide and after the transient [Ca2+]i increase it elicited, db-cAMP failed to evoke the [Ca2+]i response. It is concluded that GLP-1-(7-36)amide at physiological concentrations and a rise in cAMP increase [Ca2+]i in pancreatic beta-cells by enhancing the activity of L-type Ca2+ channels in the beta-cell plasma membrane. It is suggested that the cAMP-operative mechanism is involved in the GLP-1-(7-36)amide action to increase [Ca2+]i in beta-cells.

Animals↗
PubMed1993

Severe respiratory failure caused by recurrent pulmonary hemorrhage in Takayasu's arteritis.

We encountered a 52-year-old man with Takayasu's disease (pulseless disease) and severe respiratory failure due to recurrent pulmonary hemorrhage. Angiography revealed occlusion of multiple branches of the pulmonary artery, which were filled via collateral circulation from the coronary, intercostal, and intermammary arteries. This is a rare case that causes massive pulmonary bleeding and respiratory failure in Takayasu's arteritis.

Hemorrhage↗
PubMed1993

Glucose metabolism by rat pancreatic beta-cells produces dual change in cytosolic Ca2+.

It was reported that glucose stimulation initially lowers as well as subsequently raises the cytosolic free calcium concentration ([Ca2+]i) in pancreatic islet cells from hyperglycemic ob/ob mice. In the present study, [Ca2+]i in single pancreatic beta-cells from normal rats was measured by fura-2 microfluorometry. Following elevation of the glucose concentration to 16.7 mM from either 2.8 mM (basal) or 5.6 mM, an initial decrease and subsequent increase in [Ca2+]i were demonstrated. An elevation of the glucose concentration from 2.8 to 5.6 mM induced the decrease in [Ca2+]i but not usually the increase. Removal of extracellular Ca2+ eliminated the increase in [Ca2+]i without affecting the decrease. Mannoheptulose and KCN, inhibitors of glucose metabolism and TCA cycle, eliminated both the decrease and increase in [Ca2+]i. These results demonstrate that the glucose-induced bimodal change in [Ca2+]i is a physiological response of islet beta-cells, and that the decrease and increase in [Ca2+]i are generated by mutually-independent mechanisms which are operated through glucose metabolism by islet beta-cells.

Animals↗
PubMed1992

Isolation and characterization of type IX collagen-proteoglycan from the Swarm rat chondrosarcoma.

Type IX collagen was partially purified from the Swarm rat chondrosarcoma by a series of a conventional salting-out procedures. The preparation was further separated by anion exchange chromatography into an unbound and a bound fraction in an A230 ratio of about 5:1. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the bound fraction appeared as a broad band, whose molecular mass ranged from 250 to 270 kDa. Digestion with chondroitinase ABC reduced the apparent molecular mass of the bound fraction to about 250 kDa, a value comparable to the molecular mass of the unbound fraction. Tryptic peptide maps of the protein moieties of unbound and bound forms showed that their molecular structures were basically identical. A monoclonal antibody specific for LMW, one of the pepsin-resistant fragments of the rat sarcoma type IX, reacted with both the unbound and bound fractions. Together the results indicate that the unbound and bound fractions represent a type IX collagen devoid of the chondroitin sulfate chain and its proteoglycan form with covalently bound chondroitin sulfate, respectively. The extent of glycosaminoglycan attachment to type IX collagen molecules in rat chondrosarcoma (about 16%) is quite different from the extents described in chick embryo cartilage (about 80%), chick vitreous humour (100%) and bovine cartilage (less than 5%). Further studies on the neoplastic tissue will offer additional information regarding the biological basis and biological consequences of the glycosaminoglycan attachment to type IX collagen molecules.

Animals↗
PubMed1992

Changes in growth hormone and prolactin messenger ribonucleic acid levels during seawater adaptation of amago salmon (Oncorhynchus rhodurus).

To examine the changes in secretion of growth hormone (GH) and prolactin (PRL) with reference to their osmoregulatory roles, changes in pituitary mRNA levels and plasma concentrations of these hormones were examined during seawater adaptation in silvery juveniles (smolts) and precociously mature males (dark parr) of amago salmon (Oncorhynchus rhodurus). Transfer to seawater increased plasma sodium levels in both smolts and dark parr. Smolts adjusted their plasma sodium to the level associated with seawater-adaptation (165 mEq/liter) within 3 days, whereas no adjustment was seen in dark parr; the latter failed to survive in seawater for more than 3 days. In smolts, plasma GH levels increased significantly 1 day after transfer, whereas there was no significant change in dark parr. An increase in GH mRNA levels was observed in smolts in association with increased plasma GH, whereas there was no change in dark parr. In contrast, a reduction in plasma PRL levels was consistently observed in both smolts and dark parr after transfer to seawater. However, there was no significant change in PRL mRNA levels in either smolts or dark parr. These results suggest that both gene expression and release of GH are activated by seawater transfer only in smolts with adequate seawater adaptability, whereas PRL gene expression is decreased after seawater transfer regardless of seawater adaptability.

Adaptation, Physiological↗