[Hypertensive emergencies].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Tsuyusaki.
Explore the source record for details and available documents.
Exercise performance in essential hypertension (EH) and its relations to blood pressure (BP) response and left ventricular hypertrophy (LVH) were studied. Twenty-three patients with mild to moderate EH and 12 controls underwent symptom-limited (except BP elevation more than 250 mm Hg) ergometer exercise. Exercise performance was evaluated by the oxygen uptake (VO2/kg) at anaerobic threshold (AT) and at peak exercise (Peak). Left ventricular geometry and function, and left ventricular mass index (LVMI) were measured using echocardiography. The endpoints of 12 patients (group A) and controls were fatigue. The endpoints of 11 patients (group B) were BP elevation. Though both group A and group B had concentric hypertrophy, group B showed severe LVH compared to group A and controls. The VO2/kg at AT or at Peak was not different among the three groups. Neither BP response or LVMI correlated with exercise performance in EH. We conclude that exercise performance is not disturbed in EH; that BP response to exercise is not related to exercise performance in EH; and that concentric LVH may be a compensatory mechanism to maintain exercise capacity against exaggerated BP elevation in EH.
The treadmill test (TM), handgrip test (HG) and cold-pressor test (CP) are now frequently used clinically for multiple purposes. However, gas exchange analysis has not been a common procedure during HG. In particular, during CP, it has not been previously reported. Relationships between these 3 tests and blood pressure, heart rate (HR), respiratory gas exchange and the sympathetic nervous activity of normal subjects have not been reported, either. This study was undertaken to clarify these points. Symptom-limited TM was performed in 11 normal male subjects with a mean age of 45 +/- 8 yrs according to the Bruce protocol, with the HG using the weight-sustaining method (equal weight of 50% maximal voluntary contraction) for 3 min, and CP for 2 min. Systolic and diastolic blood pressures (Ps, Pd) were recorded; HR was measured every 30 sec, and gas exchange variables, such as oxygen uptake (VO2) and carbon dioxide production, were documented every 10 sec using an aereomonitor AE-280 (Minato Medical Science Co). In 10 of 11 subjects, concentrations of plasma noradrenaline (PNA) and plasma adrenaline (PAD) were measured at rest and at the times of peak values of the 3 tests. The peak values of Ps and HR were much higher during TM than during HG and CP (p < 0.01), while the peak values of Pd during HG and CP were higher than during TM (p < 0.01). The VO2 increased significantly for all of the 3 tests (TM: +781%, HG: +65%, CP: +20%), with the increment being the greatest during TM. Both PNA and PAD increased significantly for the 3 tests, with the increments of PNA and PAD being the greatest during TM. The percent change in PAD was more prominent during HG and CP than during TM. This tendency was not as clear for PNA as for PAD. There was no correlation of delta Ps and delta Pd between the 3 tests, but values of delta HR correlated partially. No significant correlations of peak VO2 were observed between the 3 tests. The peak PNA correlated between HG and CP (r = 0.77, p < 0.01), and the peak PAD correlated between TM and CP (r = 0.67, p < 0.05). In summary, numerous differences in hemodynamic and respiratory responses and in sympathetic nervous activation were observed in the 3 tests. When the 3 tests are undertaken, careful attention should be paid for their characteristics, discrepancies and limitations.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To examine the role of the ventricle in ANP secretion, the atrial natriuretic peptide (ANP) concentration in the plasma, left atrial tissue and left ventricular tissue were observed in a canine during the course of experimental reversible mitral regurgitation (MR). For reversible MR, a basket catheter was inserted into the left atrium via the pulmonary vein and fixed at the mitral valve. The regurgitation arose when the tip basket wire was extended and disappeared immediately when it was closed. Left atrial pressure (LAP), right atrial pressure (RAP) and pulmonary artery pressure (PAP) increased significantly during MR, and decreased to the normal level after recovery from MR. Plasma ANP concentration showed a reversible change in correlation with LAP and RAP in each canine studied. The ANP level in the atrial and ventricular tissue decreased during MR, and the low levels were maintained after recovery from MR. Both the left arterial and left ventricular tissue ANP levels showed the same changes in acute MR. Therefore, it was suggested that normal ventricles might play a role in ANP secretion in acute MR.
To clarify the hemodynamics of anemia, 28 patients with iron deficiency anemia were investigated in respect to their parameters of left ventricular (LV) systolic and diastolic function. The subjects were categorized in three groups: 1) patients (pts) with severe anemia, whose hemoglobin (Hb) concentration was less than 7 g/dl (N = 7); 2) pts with moderate anemia, whose Hb concentration was between 7 and 10 g/dl (N = 13): and 3) pts with mild anemia whose Hb concentration was between 10 and 12 g/dl (N = 8). Changes in hemodynamic parameters were observed before and after treatment in 14 subjects. These results were compared with those of normal subjects (N = 11). In the anemic patients, LV stroke volume (SV), and heart rate both increased. An increase in SV was accompanied by an increase in LV preload (LV diastolic diameter = LVDd by M-mode echocardiography) and an increase in the Doppler parameters of early diastolic filling (peak velocity in the rapid filling phase, acceleration rate, and deceleration rate). SV correlated roughly with LVDd (r = 0.44, p less than 0.05). In addition, the indices of LV contractility as measured by the pulsed Doppler method (ET/PEP) and by M-mode echocardiography (mVcf) also increased. These factors which contributed to hyperkinetic circulation were restored as the anemia improved. It was concluded that an increase in SV is an important determinant of high cardiac output in chronic anemia, because it parallels the severity of anemia. The change in SV is preload-dependent, and is suspected of being LV contractility-dependent.
A girl, 12 years of age, developed Graves' disease compounded with rheumatic fever and idiopathic thrombocytopenic purpura. Thrombocytopenia improved under short-term treatment with steroids and her mitral valvular insufficiency, due to the rheumatic fever, disappeared 4 years later. Initially, she had been treated with propylthiouracil (PTU) for 28 months. She suffered a relapse 9 months after stopping PTU and so she was given further PTU therapy. However, hypothyroidism developed 11 months after the initiation of therapy and continued, though further PTU treatment was discontinued. She now receives 1-thyroxine and maintains a euthyroid state. At the onset of the patient's hyperthyroidism, the TSH-binding inhibitor immunoglobulin (TBII) and the thyroid stimulating antibodies (TSAb) were found to be positive. During the remission period, only the thyroid stimulation blocking immunoglobulin (TSBI) was weakly positive. At relapse, only TBII was mildly positive. When hypothyroidism developed, both TBII and TSBI were positive, and TSAb was negative in all testings of her diluted IgGs. The patient's TBII and thyroid dysfunction were unaffected by high-dose intravenous gammaglobulin therapy or by treatment with prednisolone 0.5 mg/kg/day for 2 weeks. In conclusion, the emergence of TSBI during or after anti-thyroid drug therapy might possibly lead to hypothyroidism in patients with Graves' disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To observe the effects of anatomical distribution of left ventricular hypertrophy (LVH) and the differences in blood pressure on cardiac function, borderline hypertensives (group A) and mild or moderate sustained hypertensives (group B) were studied at rest and during dynamic exercise and their results were compared with those of normal controls (group C). LVH was estimated by M-mode echocardiography, and cardiac function was assessed by radionuclide (RI) first pass and multigate methods. In each subjects, 0.5 watt/kg and 1.0 watt/kg loads of ergometer exercise were administered for 16 min in the supine position. The main results were as follows: 1. In borderline hypertension, there was significant hypertrophy of the interventricular septum, and the left ventricular mass index was greater than that in normal controls. 2. The cardiac index in borderline hypertension did not differ from that of normal controls, but that of sustained hypertension was significantly reduced. 3. Significant positive correlations were observed between blood pressure and the left ventricular mass index at rest and during exercise. 4. No difference in left ventricular ejection fraction (LVEF) at rest was observed among the three groups, but that in sustained hypertension during exercise was markedly less than that of the other groups. LVEF at 1.0 watt/kg load and delta LVEF correlated inversely with the left ventricular mass index. 5. Left ventricular end-systolic volume determined by an RI count method decreased significantly during exercise in normals and borderline hypertension, while that in sustained hypertension was not reduced during exercise. Accordingly, cardiac function in the latter group was judged to be impaired. 6. In borderline hypertension, regional LVEF in the septal portion was slightly reduced at rest and during exercise. This reduction might have been caused by an imbalance of hypertrophy between the septal and free wall portions. In sustained hypertension, regional septal LVEF was maintained at rest, but was markedly less during exercise as compared with the other groups. Regional LVEF in the free wall portion was similar in degree to that of LVEF at rest and during exercise in the three groups. 7. Though the peak filling rate (PFR) in borderline hypertension did not differ from that in controls, that of sustained hypertension was significantly reduced at rest and during exercise. Significant positive correlations were obtained between PFR and LVEF at rest and during exercise. In summary, elevated blood pressure at rest and during exercise was thought to be the most important causative factor of LVH in hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.
Hyporesponsiveness of GH to insulin-induced hypoglycemia has previously been reported in hyperthyroid patients. In order to clarify the GH secretion in thyrotoxic patients, sleep-related increases in the serum GH concentration were investigated. Eight thyrotoxic females ranging in age from 7 to 15 were treated with PTU. Blood samples for measurement of GH were drawn every 15 minutes during the first few hours of sleep before and during the treatment lasting about three months. The mean maximum serum GH level before the treatment was 10.0 +/- 5.5 ng/ml (mean +/- SD); this rose to 23.2 +/- 14.6 ng/ml (P less than 0.02) during the treatment. The maximum value of more than 10 ng/ml was detected in only 3 out of the 8 patients before treatment. On the other hand, serum GH levels during PTU administration rose to above 10 ng/ml in all patients except one. It was revealed that sleep-related elevations of GH occurred early in sleep and in close association with a slow-wave EEG pattern. The results show that sleep-related GH release is low in the hyperthyroid state, but becomes significantly elevated during PTU administration. However, even in the hyperthyroid state, the sleep-related secretion of GH is closely correlated with the slow-wave sleep stage as in the euthyroid condition.
Serum thyroid hormone and TSH concentrations were measured before and after the administration of TRH (10 micrograms/kg body weight) and bovine TSH (10 IU) in 14 children with chronic lymphocytic thyroiditis. The TRH test showed that the responsiveness of TSH was positively correlated with the basal TSH (P less than 0.001) and inversely with the increase in serum thyroid hormones, for delta T3 (P less than 0.05) and for delta T4 (P less than 0.001). Overall, the patients had significantly lower mean values for basal T4, but not for T3. The TSH test revealed that the delta T3 was positively correlated with delta T4 (P less than 0.05). delta T3 after TSH administration was positively correlated with it after TRH (P less than 0.05). The patients were divided into three groups on the basis of their peak TSH values after TRH administration. In Group 1 (peak value below 40 microU/ml; N = 5); T3 increased significantly after TRH and TSH administrations (P less than 0.05 and P less than 0.025, respectively). In addition, delta T4 was significant after TSH administration. In Group 2 (peak TSH above 40 and less than 100 microU/ml; N = 6); only delta T3 after TRH was significant (P less than 0.05). In Group 3 (peak TSH above 100 microU/ml; N = 3); the response of thyroid hormones was blunted. Thus, the thyroid hormone responses to endogenous TSH coincided with that to exogenous TSH, and the exaggerated TSH response to TRH indicates decreased thyroid reserve.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In order to investigate the degree of pituitary reserve of TSH secretion and the fluctuation of thyroid function in children with chronic lymphocytic thyroiditis, TSH response to TRH was examined in 42 patients, and the thyroid function was carefully followed up in two patients retrospectively and in four prospectively. Increased basal TSH levels were revealed in seven patients (16.8%), and an exaggerated response of TSH to TRH loading in 15 (35.8%). We retrospectively observed spontaneous recovery of thyroid function in two cases. In one of them, two episodes of a transient decrease in thyroid function over a period of several years were noted. Prospectively, low normal T4, elevated TSH and normal T3 were detected in two cases at the first visit. Thereafter, TSH levels decreased to the normal range and the exaggerated response of TSH to TRH became normal. In two other cases, typical transient hypothyroidism occurred during the observation period. These fluctuations lasted for only a few months, and concomitant changes in the size of the thyroid gland were observed. No signs or symptoms suggesting viral infection were noted during the study period. Nor were changes in titers of thyroid auto-antibodies detected. These results show that the secretion of TSH is exaggerated and the thyroid function is decreased in adolescents with chronic lymphocytic thyroiditis, but the thyroid function may fluctuate from euthyroid to hypothyroid within a short period. The causes of these changes, especially of the transient hypothyroidism remain to be classified.