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Biomedical subjects

T Eguchi

Publications and source records attributed to T Eguchi.

At least 217 records · Page 12Linked to original sources
PubMed1980

Vascular action of high dose estrogen in rats.

Effects of estradiol hemisuccinate and diethylstilbestrol diphosphate on the cardiovascular system in male rats were examined in vivo and in vitro. In conscious rats, intravenously administered estradiol or diethylstilbestrol inhibited vascular responses to norepinephrine in a dose-dependent manner. Diethylstilbestrol in high doses significantly lowered the blood pressure of conscious rats. In the isolated mesenteric arteries perfused with Krebs bicarbonate solution, estradiol or diethylstilbestrol in the perfusate similarly inhibited vascular reactivity to norepinephrine in a dose-dependent manner. As in the in vivo experiments, a decrease in the basal pressure of the mesenteric vascular bed was observed when diethylstilbestrol was added to the perfusate at high concentrations. The results of these in vivo and in vitro studies strongly suggest that estradiol and diethylstilbestrol act directly on the vascular beds and attenuate vascular response to norepinephrine. It is also suggested that diethylstilbestrol by itself causes vasodilatation and a reduction in blood pressure when present at high concentrations.

Animals↗
PubMed1980

Mechanism of renin inhibition by beta adrenergic blocking agents. Effects of dl-, d-, l-propranolol and pindolol on renin release.

In order to reveal the mechanism of renin inhibition by beta adrenergic blocking agents, the effects of dl-, d-, l-propranolol and pindolol on renin release were studied. This was done by injecting them intraperitoneally or by using an in vitro system of rat kidney slices. In the in vivo study, dl-, d-, and l-propranolol inhibited plasma renin activity and renal renin content significantly in normal rats. Furthermore, in the in vitro study, the basal levels of renin in the media and that in the kidney were significantly inhibited by these agents. Pindolol also inhibited renin release, but its effects were significantly less than those of other agents. The finding that d-propranolol which has little beta adrenergic blocking action inhibited renin release, and that the effects of pindolol which displays strong beta adrenergic blocking action but little membrane stabilizing action, were less than those of other agents, may suggest that the inhibitory effects of beta adrenergic blocking agents on renin release are dependent mainly on the membrane stabilizing action rather than the beta adrenergic blocking action.

Adrenergic beta-Antagonists↗
PubMed1980

Effects of converting enzyme inhibitor (SQ 20881) on changes in blood pressure and plasma aldosterone induced by angiotensin I or acute hemorrhage in rabbits.

The effects of angiotensin converting enzyme inhibitor (CEI) upon blood pressure and plasma aldosterone (PA) were studied in rabbits with a simultaneous infusion of angiotensin I (ANG I) or with hemorrhagic hypotension. Pretreatment with CEI (SQ 20881), 1.0 mg/Kg, inhibited the effects of infused ANG I, 30 ng/Kg/min, upon PA and blood pressure at 30 min of the infusion, but the inhibition on PA was not significant at 60 min of the infusion. The same dose of CEI was ineffective in blocking the effect of 100 ng/Kg/min of ANG I on PA and blood pressure even at 30 min of the infusion. In rabbits with hemorrhagic hypotension, injection of CEI resulted in the decrement in blood pressure, whereas no decrement in blood pressure was observed in normal control rabbits. This study suggests that CEI exerts it's effect in part by inhibiting conversion of ANG I to angiotensin II (ANG II), but this can't exclude other mechanisms.

Aldosterone↗
PubMed1980

Traumatic intracavernous aneurysm of the internal carotid artery following surgery for chronic sinusitis.

A case of traumatic intracavernous aneurysm is presented. The aneurysm at the siphon of the internal carotid artery was produced as a result of injury during an operation for chronic sinusitis. In addition to the formation of the aneurysm, the angiogram showed an irregular intimal dissection along the internal carotid artery distal to the aneurysm. To prevent disastrous bleeding from the aneurysm and further progression, a trapping operation was made in combination with a superficial temporal-middle cerebral artery anastomosis.

Carotid Artery Injuries↗
PubMed1979

Central hypertensive actions of angiotensin I, II and III in conscious rats.

The effects of intracerebroventricular administrations of three natural angiotensins, angiotensin I (ANG I 3.8 X 10-11-9.4 X10-10 mol/kg body weight), II (9.6 X 10-12-2.4 X 10-10 mol/kg body weight) and III (2.7 X 10-10 2.5 X 10-9 mol/kg body weight) on systemic blood pressure were investigated in conscious rats. Angiotensin II (ANG II), ANG I and angiotensin III (ANG III), increased blood pressure in a dose-related manner. The order of potency of angiotensins was ANG II greater than ANG I greater than ANG III. The intraventricular administration of a converting enzyme inhibitor (SQ 14225, 6.9 X10-8 mol/kg) abolished the central effect of ANG I, while an angiotensin II analogue ([Sar1-Ala8]ANG II, 1.1 X 10-8 mol/kg) administered intraventricularly inhibited the central pressor effects of these three angiotensins. These results suggest that ANG II is a main mediator of the renin-angiotensin system in the central nervous system.

Angiotensin I↗
PubMed1979

Responses of aldosterone-producing adenomas to ACTH and angiotensins.

To elucidate the control mechanism of aldosterone production in primary aldosteronism, in vivo and in vitro studies were done in 7 patients with aldosterone-producing adenomas. In the in vivo study, plasma aldosterone was stimulated more significantly by (Formula: see text), synthetic ACTH than by angiotensin II or furosemide. Diurnal variations of plasma aldosterone, which were studied in 4 patients, were similar to those seen in normal controls. In agreement with the results in the in vivo study, the in vitro study also revealed ACTH stimulated aldosterone and deoxycorticosterone (DOC) from the adenoma more markedly than angiotensin II or III. There was no adenoma which was more sensitivie to angiotenion II or III than to ACTH. From these results it is considered that changes in plasma aldosterone induced by the exogenous administration of angiotensin II or ACTH in patients with aldosterone-producing adenoma are mainly based on changes in aldosterone production in the adenoma. Furthermore, in patients with an aldosterone-producing adenoma in whom diurnal variations of plasma aldosterone similar to those in normal subjects are observed, responses of aldosterone to angiotensin II are supposed to be less than those to ACTH.

Adenoma↗
PubMed1979

[Posterior subtemporal transtentorial approach for a lower basilar trunk aneurysm (author's transl)].

A lower basilar trunk aneurysm is rare and it has been difficult to operate on this kind of aneurysm which is located in so-called "no man's land". We have recently operated on the aneurysm which was located between the vertebrobasilar junction and the origin of AICA. The aneurysm was approached posterior-subtemporal-transtentorially and wrapped with a muscle piece because of its broad neck. After the operation the patient developed amnestic aphasia which, however, disappeared 4 months postoperatively. The advantage of this approach is that it enables a better visualization of the lower basilar trunk, the lateroventral portion of the pons, the distal part (5 mm) of both vertebral arteries and the upper portion of the medulla oblongata than any other approaches hitherto reported. The retraction of the temporal lobe and subsequent brain damage may be minimized by using intraoperative ventricular drainage and microtechnical maneuver.

Amnesia↗
PubMed1978

Role of renin-angiotensin system in the controls of blood pressure and aldosterone in patients with cirrhosis and ascites.

In an attempt to evaluate the role of renin-angiotensin system in the contols of blood pressure and aldosterone secretion in the patients with cirrhosis and asictes, 7 patients were infused of an antagonist of angiotensin II, Sar-1 Ile-8 angiotensin II, intravenously to inhibit the action of renin-angiotensin system and to observe changes in arterial pressure and plasma aldosterone. In 1 patient with recent onset of severe ascites and high plasma renin activity, blood pressure and plasma aldosterone decreased during the infusion. In contrast, mild rise in blood pressure and various changes in plasma aldosterone were observed in the other 6 patients with normal plasma renin activity. These results suggest variable angiotensin dependency in the controls of blood pressure and plasma aldosterone in the patients with cirrhosis and ascites according to the stage of the disease, the states of sodium and water balance and/or palasma renin activity.

Adult↗