Biomedical subjects

Y Hirooka

Publications and source records attributed to Y Hirooka.

At least 19 recordsLinked to original sources

PubMed1992

[A case of chronic thyroiditis with transient painful thyroiditis occurring after the administration of lipiodol].

We reported a female case of painful thyroiditis occurring after hysterosalpingography and investigated whether the destructive thyroiditis was iodine-induced. The patient, aged 28, had TBG deficiency and the previous episode of thyrotoxicosis caused by Graves' disease. Lipiodol (containing 4.8g of iodide in 10ml solution) was administered via vagina for hysterosalpingography. One month after the radiography, serum inorganic iodide and Tg were elevated abnormally, but she was asymptomatic. After the subsequent 3 months she developed a painful and 3rd grade-sized goiter with concomitant marked elevation of thyroid hormones and inorganic iodide and also high titer of MCHA (320(2)X). A dramatic response was obtained with steroid. Thereafter she was treated with acupuncture on the thyroid gland, resulting in a sudden reappearance of tender goiter. This traumatic thyroiditis disappeared successfully in 2 weeks with steroid treatment. The painful thyroiditis subsided in 5 months throughout the course and she remained euthyroid for the ensuing 2 years. Aspiration biopsy was performed twice and revealed lymphocytic thyroiditis. Values of serum Tg varied in good correlation with those of serum inorganic iodide or rT3 throughout the course, respectively (P < 0.01, P < 0.05). Significant correlations between FT4 and FT3, and also T4 and T3 were observed, respectively (P < 0.01, P < 0.05). Serum inorganic iodide was elevated to 316 micrograms/dl at the symptomatic stage of the thyroiditis and decreased to 170 micrograms/dl at the resolving phase 2 months after the inflammation. Iodide disappearance curve showed a diphasic slope. The BHL was calculated as 60.3 days during the symptomatic stage and 6.9 months in euthyroid state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

[Urinary iodide excretion in Japanese people and thyroid dysfunction].

In order to assess the Japanese dietary iodine intake, we examined the urinary iodine excretion of those on an ordinary Japanese diet chosen at random and observed whether the thyroid function might affect the amounts of urinary iodine excretion. The subjects consisted of cases of untreated hypothyroidism and chronic thyroiditis (CT) and euthyroid controls who were healthy people or had non-thyroidal disorders such as diabetes mellitus or hypertension. Eight cases of hypothyroidism were composed of 3 cases of secondary hypothyroidism with empty sella syndrome and 5 cases of primary hypothyroidism and 32 patients with CT have been maintained in euthyroid states with T4 medication. We selected 32 cases of sex and age-matched healthy people as controls. The mean levels of excreted urinary iodine were 465.6 micrograms/day in the healthy controls and 471.8 micrograms/day in patients with CT, respectively. Urinary iodine excretion was significantly correlated to serum inorganic iodide in both controls and CT patients, of which correlation coefficients were +0.35 and +0.5, respectively. Urinary iodine and serum inorganic iodide ratios (U/S) in hypothyroidism were significantly (p less than 0.05) depressed compared with those in CT. The present study indicated that recent Japanese dietary iodine intake was estimated to be approximately 470 micrograms/day and that the urinary iodine excretion would be influenced not only by iodine intake but also by thyroid function.

Adult↗

PubMed1992

[The functional outcome of patients with subacute thyroiditis].

Whether with the passage of time subacute thyroiditis leads to hypothyroidism remains to be determined. Therefore, we evaluated the thyroid function including TRH test of 66 patients with a previous history of subacute thyroiditis and age-matched control subjects with special reference to the measurement of inorganic iodide. The patients were divided into 3 groups according to time lapse since the occurrence. Group 1 consisted of 24 cases followed up for 4 to 24 months. Sixteen cases in group 2 had their courses from 2 to 5 years, and group 3 was composed of 26 cases over the past 5 to 30 years. We selected 169 subjects without history of subacute thyroiditis and divided them into three control groups matched for age, each corresponding to the patient groups (group 1a, 2b and 3c, respectively). 41.7% and 29.2% of cases in group 1 had high basal levels of serum TSH (greater than 3.6 microU/ml) and delta TSH (the increment of TSH after TRH, greater than 46.8 microU/ml). In group 2, levels of serum T3 and T4 returned to normal ranges. However, in group 3, significant higher elevations in TSH and delta TSH than those in group 3c were observed, and the T4, FT4, T3 and FT3 levels were lower than those of group 3c (p less than 0.01 and p less than 0.05, respectively). 42.3% of cases in group 3 showed high TSH, and there were 4 cases with clinical hypothyroidism. Among the cases studied, a significant negative correlation (p less than 0.01) between levels of TSH and T4 was observed, while a correlation between TSH and delta TSH was positive (p less than 0.001). High levels of serum inorganic iodide were observed in 6.1% of cases and a correlation between inorganic iodide and TSH was significantly positive (p less than 0.01) not only in patients with subacute thyroiditis, but also in the control subjects. Antithyroid autoantibodies were detected in 42.4% of all the cases with subacute thyroiditis and also in 45.6% of all the controls. In group 3, MCHA was detected in 64.5% of the cases, and the frequency was higher than that of group 3c as well as that of 25% in group 2 (p less than 0.01), respectively. In 15.4% of the cases in group 3, the titers of MCHA were more than 40(2), and the titers of MCHA were significantly higher in patients with a long-term period after the onset of subacute thyroiditis than those with a short-term period.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1992

Evaluation of the severity of mitral regurgitation by transesophageal Doppler flow echocardiography.

The severity of mitral regurgitation (MR) was assessed by transesophageal Doppler flow echocardiography (TEE) using new criteria in 87 patients. The severity of MR assessed by TEE (TEE-MR) was compared with that obtained by left ventriculography (LVG-MR). Although the severity of TEE-MR has been evaluated by MR jet area, it is often difficult because the MR jet extends beyond a single frame image in severe MR. We found that (1) when the MR area was larger than 3 cm2, the severity of MR was more than second-degree by LVG; (2) there was systolic turning flow (STF) of the MR jet within the left atrial cavity in 27 of 30 patients with third- and fourth-degree LVG-MR; and (3) there was late systolic backward flow (SBF) in the pulmonary veins in 9 of 10 patients with fourth-degree LVG-MR. A new grading of the severity of MR by TEE was proposed, which combined the findings of STF, SBF, and the MR area. These new criteria of the severity of TEE-MR excellently correlated with that by LVG (y = 0.94x + 0.08; r = 0.95, p less than 0.01). The criteria for MR by TEE were also useful for assessment of MR in patients with prosthetic mitral valve dysfunction (y = 0.96x + 0.04; r = 0.97, p less than 0.01). We conclude from this study that the severity of MR can be accurately assessed with TEE by measuring the MR area and the specific flow patterns in the left atrium and pulmonary veins.

Adolescent↗

PubMed1992

Mechanisms involved in aortic baroreceptor excitation during drug-induced aortic pressure elevation in intact rabbits.

Aortic baroreceptor activity during drug-induced elevation of arterial pressure in intact animals is determined not only by the magnitudes of arterial pressure elevation but also by other mechanisms such as the direct effects of drugs on aortic wall property and on baroreceptors per se. This study aimed to determine the relative contribution of arterial pressure elevation and other mechanisms on aortic baroreceptor activity during intravenous infusion of norepinephrine (NE), phenylephrine (PE) or angiotensin II (Ang II) in intact anesthetized rabbits, all of which were used to assess arterial baroreflex function in vivo. We simultaneously recorded aortic pressure (AP), afferent aortic nerve activity (ANA) and the aortic diameter (AD) during elevation of AP induced by intra-aortic balloon inflation or intravenous infusions of NE, PE, and Ang II. During Ang II-infusion or balloon inflation, AD progressively increased with increases in AP. The relationships among changes in AP, ANA, and AD were similar during balloon inflation and during Ang II infusion which indicated that increases in ANA during Ang II infusion were caused by increases in AD or strain of baroreceptors. In contrast, during NE or PE infusion, ANA increased with no changes or decreases in AD, respectively. The latter results suggest that in intact rabbits increases in ANA during NE or PE infusion resulted from mechanisms other than an increase in strain of baroreceptors, such as the direct excitatory effect on baroreceptors. Thus, different mechanisms were involved in aortic baroreceptor excitation in intact rabbits during elevation of AP caused by the vasopressor drugs, which are commonly used to assess arterial baroreflex function in vivo.

Angiotensin II↗

PubMed1992

Effects of acetylcholine on the release of thyrotropin-releasing hormone from the rat retina in vitro.

Effects of acetylcholine on the release of thyrotropin-releasing hormone (TRH) from the rat retina were studied in vitro. The retina was incubated in medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (medium) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was enhanced significantly in a dose-related manner with the addition of acetylcholine and inhibited with addition of atropine. The stimulatory effect of acetylcholine on TRH release from the retina was blocked with the addition of atropine. The elution profile of methanol-extract of the rat retina was identical to that of synthetic TRH. The findings suggest that the cholinergic system stimulates TRH release from the rat stomach in vitro.

Acetylcholine↗

PubMed1992

Effects of dopamine on the release of thyrotropin-releasing hormone from the rat retina in vitro.

The effects of dopamine on the release of thyrotropin-releasing hormone (TRH) from the rat retina in vitro were studied. The rat retina was incubated in the medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was inhibited significantly in a dose-related manner with the addition of dopamine, but not with pimozide. The inhibitory effects of dopamine on TRH release from the rat retina were blocked with an addition of pimozide to the medium. The elution profile of methanol-extracted rat retina on sephadex G-10 was identical to that of synthetic TRH. From these findings it is concluded that the dopaminergic system inhibits TRH release from the rat retina in vitro.

Analysis of Variance↗

PubMed1992

Atrial natriuretic peptide increases human capillary filtration and venous distensibility.

OBJECTIVE: The main aim of this study was to examine whether atrial natriuretic peptide (ANP) alters capillary filtration and venous distensibility. DESIGN: The study was designed to examine the local effects of i.a. infusion of ANP upon capillary filtration and venous distensibility in human forearms of eight healthy volunteers. METHODS: Using a water plethysmograph, we measured venous distensibility and capillary filtration from changes in forearm volume when transmural venous pressure was increased in a stepwise manner and held constant during i.a. infusion of saline, ANP and sodium nitroprusside (SNP). The doses of ANP and SNP were chosen to double baseline forearm blood flow obtained during saline infusion. RESULTS: ANP and SNP infusion both increased venous distensibility to the same extent compared with saline infusion. Capillary filtration was greater during ANP than during saline or SNP infusion. Small vein pressure was comparable during infusion of the two drugs. CONCLUSION: Our results suggest that ANP increases venous distensibility and capillary filtration in human forearms.

Adult↗

PubMed1992

Endothelium-dependent forearm vasodilation to acetylcholine but not to substance P is impaired in patients with heart failure.

It has been shown that endothelium-dependent vasorelaxation in response to muscarinic stimulation is attenuated in patients as well as animals with heart failure. This study aimed to determine if endothelium-dependent forearm vasodilation evoked with substance P (SP) as well as acetylcholine (ACh) was impaired in patients with heart failure. Forearm blood flow was measured using a strain-gauge plethysmograph and forearm vascular responses to intra-arterial infusions of ACh, SP, or sodium nitroprusside (SNP) at graded doses were examined. The drugs caused the dose-dependent increases in forearm blood flow (FBF) and the decreases in forearm vascular resistance (FVR) in patients with heart failure as well as normal subjects. However, the percent decreases in FVR by ACh were less in patients with heart failure than in normal subjects (p < 0.01). In contrast, the percent decreases in FVR by SP or SNP did not differ between the two groups. These results suggest that endothelium-dependent vasodilation of forearm resistance vessels via muscarinic receptors is specifically impaired, whereas via SP receptors, is preserved in patients with heart failure.

Acetylcholine↗

PubMed1992

Arterial baroreflex dynamics in normotensive and spontaneously hypertensive rats.

To investigate dynamic or frequency-dependent characteristics of arterial baroreflex control of efferent sympathetic nerve activity in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), we assessed the transfer function from aortic pressure (AP) to renal sympathetic nerve activity (RSNA) using a "white-noise technique." In pentobarbital sodium-anesthetized rats, we recorded RSNA as the output, while AP was randomly perturbed to impose input pressure changes with broad frequencies. We calculated the transfer function from AP to RSNA over the frequency range of 0.01-5 Hz through the spectral analysis of the input and output. The results indicated that the gain, phase shift, and coherence of the transfer function for SHR and for WKY were similar and statistically indistinguishable. The gain was relatively constant below 0.05 Hz but increased steadily by fivefold as frequency increased in the frequency range of 0.05-0.8 Hz. The phase was out of phase where coherence was high. The coherence was high (greater than 0.5) in the frequency range of 0.04-0.8 and 1.00-1.03 Hz but was low in other frequencies. These results suggest that dynamic or frequency-dependent characteristics of arterial baroreflex control of RSNA were not altered in SHR as compared with WKY.

Animals↗

PubMed1992

Effects of OPC-21268, an orally effective vasopressin V1 receptor antagonist in humans.

An orally effective, nonpeptide vasopressin V1 receptor antagonist, OPC-21268 was produced for possible human use. We investigated the effects of OPC-21268 on the vascular effects of intra-arterially infused arginine vasopressin in human forearm vessels. The brachial artery was cannulated for drug infusions and direct measurement of arterial pressure. Forearm blood flow was measured by a strain gauge plethysmograph, and forearm vascular resistance was calculated. Arginine vasopressin was infused intra-arterially at doses of 0.02, 0.06, 0.09, 0.2, 0.6, and 1.2 ng/kg/min. The lower doses of arginine vasopressin increased, whereas the higher doses of arginine vasopressin decreased forearm vascular resistance (p less than 0.01). Intra-arterial infusion of phenylephrine at doses of 0.2, 0.4, and 2.4 micrograms/min increased forearm vascular resistance dose-dependently (p less than 0.01). OPC-21268 (50 mg for two, 100 mg for six, and 200 mg for two subjects) given orally did not alter resting arterial pressure, forearm vascular resistance, or heart rate. OPC-21268 decreased vasoconstrictor responses to arginine vasopressin at doses of 0.02 (p less than 0.02) and 0.09 (p less than 0.05) ng/kg/min and augmented vasodilator responses to arginine vasopressin at a dose of 1.2 ng/kg/min (p less than 0.01). However, the vasoconstrictor responses to phenylephrine were not altered by OPC-21268. These results demonstrated that OPC-21268 effectively and specifically antagonized the V1 receptor-mediated vasoconstriction in human forearm resistance vessels. These results suggest that OPC-21268 may be useful therapeutically to antagonize the vasoconstriction caused by arginine vasopressin in some pathological states.

Administration, Oral↗

PubMed1992

Captopril improves impaired endothelium-dependent vasodilation in hypertensive patients.

Animal studies suggest that some angiotensin converting enzyme inhibitors augment endothelium-dependent vasorelaxation. We aimed to determine if captopril augments endothelium-dependent vasodilation in middle-aged hypertensive patients. By using strain-gauge plethysmography, forearm vasodilation evoked with intra-arterial acetylcholine (4, 8, 16, and 24 micrograms/min) or nitroprusside (0.2, 0.4, 0.8, and 1.2 micrograms/min) was examined before and after captopril administration (25 mg per os). Before captopril, forearm vasodilation with acetylcholine was less in hypertensive patients (n = 12) than in age-matched (n = 7) or young (n = 7) normotensive subjects, but forearm vasodilation with nitroprusside did not differ among the three groups. Captopril improved forearm vasodilation in hypertensive patients (n = 7) with acetylcholine but nitroprusside did not. In contrast, nifedipine (10 mg per os) did not alter forearm vasodilation with acetylcholine or nitroprusside in hypertensive patients (n = 5). The decreases in mean blood pressure caused by captopril and nifedipine in hypertensive subjects were comparable. Captopril did not alter forearm vasodilation with acetylcholine or nitroprusside in young normotensive subjects (n = 7). These results suggest that captopril in hypertensive patients may acutely improve impaired endothelium-dependent forearm vasodilation that does not result from reduction in blood pressure per se.

Acetylcholine↗

PubMed1992

Effects of L-arginine on forearm vessels and responses to acetylcholine.

This study was designed to investigate the effects of L-arginine (the substrate of endothelium-derived nitric oxide) in human forearm vessels. We examined whether intra-arterial infusion of L-arginine dilated forearm vessels and augmented vasodilatory responses to acetylcholine in young, healthy humans. The left brachial artery was cannulated for drug infusions and direct measurement of arterial pressure. Forearm blood flow was measured by a strain gauge plethysmograph. Intra-arterial infusions of L-arginine at 10, 20, 40, and 60 mg/min increased forearm blood flow from 4.7 +/- 0.6 to 4.9 +/- 0.5, 5.7 +/- 0.5, 7.2 +/- 0.8, and 8.2 +/- 0.9 ml.min-1.100 ml-1, respectively (n = 8, p less than 0.01), whereas D-arginine at the same doses did not alter forearm blood flow (n = 7). Intra-arterial infusions of acetylcholine (n = 7) (4, 8, 16, and 24 micrograms/min) and sodium nitroprusside (n = 5) (0.2, 0.4, 0.8, and 1.2 micrograms/min) increased forearm blood flow dose dependently (p less than 0.01 for both). Arterial pressure was not altered with infusions of these drugs. Responses to acetylcholine were augmented with simultaneous intra-arterial infusion of L-arginine at 10 mg/ml (p less than 0.01) but not with D-arginine. Responses to sodium nitroprusside were not altered by L-arginine. These results in human forearm resistance vessels support the notion that vasodilation induced by acetylcholine is a result of the conversion from L-arginine to endothelium-derived nitric oxide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1992

Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina.

Endothelial dysfunction has been implicated as a cause of coronary vasospasm in patients with variant angina. This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. It has been shown that SP evokes endothelium-dependent vasodilation with no direct effect on vascular smooth muscle in excised human coronary arteries. SP and ACH were infused into the coronary arteries in nine patients with variant angina in whom coronary arteriograms showed normal or mild atherosclerotic lesions. The vasomotor responses of coronary arteries were assessed by quantitative arteriography. ACH at a high dose (100 micrograms/min) provoked coronary vasospasm associated with anginal attack in all patients. In contrast, SP at graded doses (13.5, 40, and 135 ng/min) caused the dose-dependent and comparable increases in the coronary diameter at the spastic and control sites. ACH at a low dose (10 micrograms/min) also caused comparable vasodilation at the spastic and control sites in patients with normal coronary arteries. Coronary vasodilating responses to SP were comparable in patients with variant angina and those with atypical chest pain. The results indicate that endothelium-dependent vasodilation evoked with SP and ACH at the low dose was present at the vasospastic site in patients with variant angina. These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction.

Acetylcholine↗

PubMed1992

Decreased skeletal muscle vasodilation in patients with congestive heart failure.

In congestive heart failure (CHF), excessive vasoconstriction is present, which is due to overactive vasoconstrictor mechanisms although vasodilator mechanisms may be impaired. In the present study, we examined vasodilation in CHF by measuring forearm blood flow with a strain gauge plethysmograph. Patients with CHF had higher forearm vascular resistance than normal control subjects. Patients with CHF had decreased forearm vasodilation in response to intra-arterial infusions of atrial natriuretic peptide (ANP) and acetylcholine, but not in response to sodium nitroprusside or nitroglycerin. Oral captopril did not alter the degree of forearm vasodilation during handgrip exercise. These results suggest that endothelium-dependent and ANP-induced forearm vasodilation is impaired in patients with CHF but the decreased vasodilation is not due to impaired vascular smooth muscle responsiveness to a vasodilator. The renin-angiotensin system does not seem to play a major role in the maintenance of vascular resistance during exercise in CHF.

Acetylcholine↗

PubMed1992

Heterotopic intestinal membrane in a retroperitoneal tumor.

Plain abdominal X-rays of a 13-year-old girl with chief complaints of back pain revealed calcification in the upper left abdomen. A calcified tumor was confirmed at the dorsal side of the pancreatic tail upon admission. A completely formed colic membrane free of all other germ layers was discovered within the tumor, leading to a diagnosis of heterotopic colonic membrane. To our knowledge, there have been no other cases of heterotopic intestinal tissue of this type, so we consider this an extremely rare case worth reporting.

Adolescent↗

PubMed1992

Hyperparathyroidism associated with parkinsonism.

A 70-year-old woman with hyperparathyroidism associated with parkinsonism is reported. Her primary initial symptom was parkinsonism, but it was levodopa-resistant. Chemical and hormonal findings revealed that she had hyperparathyroidism. The symptoms were relieved after the surgical removal of a parathyroid adenoma. Although this type of case has been reported only rarely, it suggests that hypercalcemia might be an aggravating factor in levodopa-resistant parkinsonism.

Adenoma↗

PubMed1992

New technique using intraductal ultrasonography for the diagnosis of diseases of the pancreatobiliary system.

Intraductal ultrasonography (IDUS), a new technique for visualizing arterial structures, operates at an ultrasound frequency of 30 MHz to produce high resolution, cross-sectional images in real time. The purpose of this study was to provide a basis for interpreting IDUS images in vitro. We also attempted to determine the clinical usefulness of the IDUS system in diagnosing pancreatobiliary diseases in vivo. IDUS echograms of both the bile duct (BD) and main pancreatic duct (MPD) from autopsy specimens of 15 patients demonstrated three distinct layers with a fine reticular pattern in the pancreas in vitro. In clinical cases, the MPD and BD of four patients could be scanned by inserting the IDUS catheter via the major papilla without requiring endoscopic sphincterotomy. We hope that IDUS will become routine in scanning the BD and MPD to achieve early and accurate diagnoses of pancreatobiliary diseases.

Adenoma, Bile Duct↗