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Biomedical subjects

T Kashima

Publications and source records attributed to T Kashima.

At least 109 records · Page 6Linked to original sources
PubMed1979

Echocardiographic findings in patients with aortitis syndrome.

Echocardiography was performed in 18 patients with the aortitis syndrome and in 20 age-matched normal volunteers. The aortic root dimension, the aortic dimension at the level of the sinotubular ridge, the aortic arch dimension, the left ventricular internal dimension, the left atrial dimension, the interventricular septal thickness, and the left ventricular posterior wall thickness were measured. All measurements, except for the left atrial dimension, were significantly greater in patients with aortitis syndrome than in the control subjects. We concluded (1) that the patients with the aortitis syndrome may have an enlarged or narrowed aorta, a dilated left ventricle and left atrium, and a thickened interventricular septum and left ventricular posterior wall; (2) that the incidence and the degree of these abnormalities depend on the presence of complications such as aortic regurgitation and arterial hypertension; and (3) that M-mode as well a cross-sectional echocardiography plays an important role in the assessment of the aorta and heart in the aortitis syndrome.

Adolescent↗
PubMed1978

Sympathetically induced atrial tachycardia. Successful treatment by left stellate ganglion block.

An unusual type of atrial tachycardia was observed in a 52-year-old woman. The tachycardia occurred only when the patient kept the left upper limb in the lateral and horizontal position. Propranolol, atropine sulfate, carotid sinus massage and ocular compression were not effective in terminating or preventing the arrhythmia. Left stellate ganglion block has stopped the tachycardia for at least two years. The atrial tachycardia in this patient was thought to be caused by mechanical stimulation of the left stellate ganglion resulting in pacemaker shifting, as has been demonstrated in the canine heart.

Action Potentials↗
PubMed1977

Comparison of cyclic adenosine monophosphate response of lymphocytes in normal and asthmatic subjects to norepinephrine and salbutamol.

Reduced response of beta adrenergic receptors, especially beta-2 receptors, has been suggested as a contributing factor in the etiology of asthma. Cyclic adenosine monophosphate (AMP) production in lymphocytes after exposure to 10(-3) M salbutamol, predominantly a beta-2 receptor stimulant, was significantly less in asthmatic subjects than in normal subjects, while there was no significant difference in cyclic AMP response to 10(-3) M norepinephrine, predominantly a beta-1 receptor stimulant. Both drugs evoked the maximum response at 10(-3) M. The cyclic AMP response to salbutamol of 5 asthmatic subjects being treated with steroids was diminished significantly compared with that of 7 patients not treated with steroids; however, the response to norepinephrine was similar in both groups. The degree of the abnormality in the beta-2 receptor response seems to be related to the severity of the asthma.

Adolescent↗
PubMed1977

Central nervous system actions of clonidine in hypertension.

Among 42 patients converted from clonidine to another antihypertensive medication, few sympathomimetic side effects were observed if the clonidine dosage had been less than 1.2 mg daily. Among a majority of 14 patients who had been taking larger doses, the previously reported syndrome of sympathetic hyperactivity was observed. It is particularly important to follow up patients who discontinue clonidine when this drug has been taken in excess of 1.2 mg daily.

Central Nervous System↗
PubMed1975

Relation of renin status to neurogenic vascular resistance in borderline hypertension.

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.

Adolescent↗
PubMed1975

Paroxysmal hypertension in aortitis syndrome.

Three patients with aortitis syndrome ehibited paroxysmal hypertension which seemed to result from baroreceptor dysfunction. All of the patients had signs of active inflammation of aortitis syndrome and stenotic carotid and subclavian arteries. During the attacks, the blood pressure rose to at least 230 mm. Hg systolic and the heart rate exceeded 100. However, with prolonged administration of steroid hormones, the attacks ceased. In two patients with dilated thoracic aortas and aortic regurgitation, the attacks of paroxysmal hypertension occurred without apparent precipitating factors and were followed by anginal pain with marked ST depression. The sympathicotonic state resulting from the disturbance of the baroreceptors was considered to be responsible for the attacks. In another patient, the attacks occurred in the course of treatment with a steroid hormone and were provoked only by voluntary micturition. This post-micturition hypertension was presumed to be an expression of abnormal overshooting following a fall in blood pressure after voiding.

Adult↗
PubMed1975

Altered cardiac responsiveness and regulation in the normal cardiac output type of borderline hypertension.

Of 145 patients with borderline hypertension, 30% had increased resting cardiac index (QI), whereas the remainder had normal values. The specific aim of this study was to investigate cardiac regulation in patients who had normal resting QI. Eighty-five control subjects were used for comparison. At rest, patients with normal QI showed evidence of decreased parasympathetic inhibition; the QI after injection of atropine increased less than in control subjects. After complete cardiac autonomic blockade with propranolol and atropine, QI and stroke volume were significantly lower in patients than in control subjects. The mechanism of this low QI was further analyzed. Central blood volume, which strongly correlates with stroke volume, was used as an estimate of the cardiac venous filling. After blockade, stroke volume was decreased in patients, but central blood volume was normal. Patients also showed a decreased heart rate and QI response to infusion of isoproterenol. It is therefore postulated that two components may be responsible for the low QI in the "denervated" heart: patients exhibit a decreased responsiveness to sympathetic stimulation, and they may also be less responsive to venous filling. Behind the facade of cardiac normality in these borderline hypertensive patients with normal cardiac output, there is evidence of altered autonomic control of the heart (decreased vagal inhibition) and of changed cardiac response to sympathetic stimulation and possibly to venous filling.

Adult↗