Biomedical subjects

H Ijichi

Publications and source records attributed to H Ijichi.

At least 109 records · Page 6Linked to original sources

PubMed1984

Centrally induced vasopressor and sympathetic nerve responses to carbachol in rats.

Blood pressure rose when carbachol was injected into the cerebral ventricles in conscious rats, but the heart rate fell. When rats were later anesthetized with urethane to allow recording of abdominal sympathetic nerve activity, carbachol injected similarly produced the following biphasic responses: initial vasodepression followed by a sustained pressor phase accompanied by corresponding changes in peripheral sympathetic nerve activity. The heart rate was transiently suppressed following the injection. Spinal section abolished the initial hypotensive phase and accompanying bradycardia and made the response purely pressor. By contrast, intravenous injections elicited purely vasodepressor responses. Thus, carbachol administered centrally caused vasopressor responses possibly via both activation of sympathetic vasomotor centers and a release of pituitary hormones. Since anesthesia attenuated the pressor responses and made them biphasic, these results indicate that central cholinergic mechanisms are inhibited during anesthesia and that a sympatho-inhibitory mechanism of cholinergic receptors exists behind the pressor responses, as disclosed during anesthesia.

Anesthesia↗

PubMed1984

The role of prostaglandins in the regulation of blood pressure with special reference to vascular reactivity.

The role of prostaglandins (PGs) in the regulation of blood pressure was analysed from the point of view of vascular reactivity to PGs and also of PG-induced modulation of pressor response. The vasodepressor effect of PGE1 was more sensitive in the patients with essential hypertension than in the normotensive subjects. In the normotensive subjects or in rats, pressor response to norepinephrine was modulated by PGE1, enhanced under treatment with indomethacin, an inhibitor of PG biosynthesis, and suppressed under an infusion of PGE1. These results indicate that pressor response to norepinephrine is modulated by exogenous and endogenous PGs. The PG-induced modulation disappeared after chemical sympathectomy, suggesting that the PG-induced modulation of pressor response is regulated by the sympathetic nervous system. In sympathetic neurotransmission, PGs could play an important role in the regulation of norepinephrine release. Renal content of norepinephrine was reduced under treatment with indomethacin, indicating an enhanced release of norepinephrine and an enhanced turnover of norepinephrine in the kidneys under treatment with indomethacin. These results suggest that a deficient state of PG may enhance the pressor response and norepinephrine release. As there is much evidence indicating that the reduction of PG synthesis in patients and animals with hypertension, vascular reactivity to PGs and PG-induced modulation of pressor response may play significant roles in the regulation of blood pressure and could be causal factors of hypertension.

Adult↗

PubMed1984

Retardation of the development of hypertension in DOCA-salt rats by renal denervation.

To determine the importance of the renal nerves in DOCA-salt hypertension, either renal denervation or a sham-operation was carried out on both DOCA-salt-treated and non-DOCA-treated rats. The systolic blood pressure of the non-DOCA rats remained within normotensive levels, in which the difference in blood pressure levels between the renal denervated and the sham-operated groups was not significant. On the other hand, the blood pressure of the rats treated with DOCA, and having intact renal nerves, began to rise by the end of the first week and rose consistently thereafter, whereas, in the renal denervated DOCA-salt rats, the blood pressure started to rise by the second week and then proceeded to increase gradually. The differences between the sham and the denervated rat groups were significant throughout the four weeks. The mean arterial pressure, directly measured from the caudal artery of conscious rats during the fourth week of this study, was 166 +/- 7 mmHg in the sham-operated and 129 +/- 4 mmHg in the renal-denervated rats (the data having an 1% significant difference). To test the effects of renal denervation on the natriuresis, pentobarbital-anesthetized rats were infused intravenously with physiological saline. The renal denervated rats which had received DOCA excreted more sodium than did the sham-operated rats. When the rats were later anesthetized with urethane to allow intracisternal injections of hypertonic saline, the mean blood pressure in renal denervated rat groups was again lower than that of the sham-denervated rat groups. However, subsequent intracisternal injections of 5% saline produced similar pressor responses as well as tachycardia in both DOCA groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1984

Tachyarrhythmia provoked by coughing and other stimuli.

A rare case of cough-induced tachyarrhythmia is described. The effectiveness of atropine sulfate, and worsening of the arrhythmia resulting from administration of digitalis, suggests that vagal reflex might be the mechanism responsible for the tachyarrhythmia.

Cough↗

PubMed1984

Comparison of LATS activity and TSH receptor antibody in Graves' disease.

TSH-receptor antibody (TRAb) activity and LATS activity of Graves' sera were compared. All of 50 LATS-positive cases were TRAb positive, although only 63% of LATS-negative cases were TRAb positive. Binding of 125I-TSH to the TSH receptors was inhibited dose-dependently by LATS-immunoglobulin. However, no correlation between TRAb activity and LATS activity was observed. TRAb was positive in 2 LATS-positive cases even when the symptoms of hyperthyroidism were controlled by treatment (antithyroid or radioisotope). The positive TRAb was not changed in 4 Graves' disease patients whose LATS activity had disappeared following antithyroid treatment. These clinical studies show that TRAb is more sensitive than LATS and suggest that LATS may be one of a heterogenous population of antibodies to the TSH receptor in Graves' disease.

Autoantibodies↗

PubMed1984

Augmented central cholinergic mechanisms in spontaneously hypertensive rats. Involvement of deranged noradrenergic mechanisms in the brain.

Intracerebroventricular (ICV) injections of carbachol produced biphasic blood pressure responses consisting of initial vasodepression of short duration followed by a sustained pressor phase, which were accompanied by corresponding changes in sympathetic nerve activity in normotensive outbred-Wistar rats (NT) under urethane-anesthesia. In both normotensive Kyoto Wistar rats (WKY) and spontaneously hypertensive rats (SHR), on the other hand, carbachol elicited purely pressor responses, and accompanying sympathetic nerve activity was little affected. The magnitude of the pressor responses was larger in SHR than in WKY or NT rats. Spinal sectioning did not affect the magnitude of the pressor responses. Vasopressor responses to intravenous injections of arginine-vasopressin were not significantly different between WKY and SHR. These results indicate that carbachol injected intracerebroventricularly produces vasopressor effects mainly by releasing pituitary hormones, probably vasopressin, and that augmented pressor responses in SHR may be due to excessive release of vasopressin. When central noradrenergic neurons had been destroyed with ICV injections of 6-hydroxydopamine in both NT and WKY rats, carbachol-induced vasopressor responses were markedly augmented and resulted in responses similar to those of SHR. These findings indicate that central noradrenergic vasodepressive neurons are deficient and that the augmented vasopressor responses to carbachol resulted from deranged central noradrenergic mechanisms in SHR.

Animals↗

PubMed1984

Simultaneous changes of left ventricular and left atrial size and function in normal subjects during exercise.

We performed dual M-mode exercise echocardiography, which records left ventricular (LV) and left atrial (LA) echocardiograms simultaneously, in 10 normal subjects to investigate mechanisms of cardiac adaptation to dynamic exercise. The LV end-diastolic dimension (EDD) increased significantly as exercise increased from mild to moderate (3-5%, p less than 0.05 and 0.001). At peak exercise the EDD was slightly increased, but it returned to the baseline during recovery. The LV end-systolic dimension (ESD) showed a progressive decrease with the severity of exercise (5-13%, p less than 0.05 and 0.001). It decreased further immediately after exercise (17-20%) and then returned to the resting value. The LV stroke dimension and fractional shortening increased as exercise changed from mild to moderate and reached a plateau at peak exercise. During recovery, they showed a transient increase and then decreased. By contrast, the LA dimensions, both maximum and minimum, increased significantly as exercise changed from mild to moderate (15-16% and 16-19%, p less than 0.01 and 0.001, respectively), but they were lower at peak exercise (12 and 14%). They returned rapidly to the resting values immediately after exercise. Thus, during exercise, LV function is augmented by the Frank-Starling mechanism in combination with increased contractility, while the LA is enlarged to receive the increased venous return accompanying dynamic exercise. These exercise-induced changes in LV performance return gradually to the resting state, but LA size recovers rapidly after the cessation of exercise.

Adolescent↗

PubMed1984

Centrally-induced vasopressor responses to ouabain are augmented in spontaneously hypertensive rats.

Dihydroxyouabain (ouabain), 1.0-10 micrograms, per rat, injected intracerebroventricularly, produced dose-related vasopressor responses accompanied by corresponding increases in abdominal sympathetic nerve activity in 16 weeks old Wistar (NT) rats anesthetized with urethane. The heart rate then also increased, dose-dependently, to ouabain injected in doses up to 10 micrograms. However, 100 micrograms produced arrhythmia resulting in bradycardia. Pressor effects were appreciable within one minute after the ouabain injection, but did not become maximal until between 7-10 min later. Either the removal of sympathetic vasomotor tone by surgical section of the spinal cord or intravenous pretreatment with a vasopressin antagonist significantly reduced the vasopressor responses in the NT rat. Ouabain, 10 micrograms, injected intraventricularly in 16 weeks old Kyoto Wistar rats produced similar cardiovascular responses to those in the NT rat, but the magnitude of the blood pressure responses, along with the heart rate and sympathetic responses, was larger in SHR than in WKY. These results suggest that dihydroxyouabain acts centrally to elevate the blood pressure by increasing not only the sympathetic discharge but also, perhaps, the secretion of vasopressin. In light of previous studies showing that SHRs exhibit both sympathetic hyperactivity and hypersecretion of vasopressin, the present results suggest that their enhanced responsiveness to ouabain could result from both the sympathetic hyperactivity and an enhanced vasopressin release as a result of the centrally injected ouabain.

Animals↗

PubMed1984