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H Ijichi

Publications and source records attributed to H Ijichi.

At least 19 recordsLinked to original sources
PubMed1992

[Scanning and transmission electron microscopic studies of the ultrastructure of the corneal endothelium in developing human eye].

The ultra-microstructure of the human corneal endothelium was examined by scanning and transmission electron microscopy. The samples were corneas of 26 human eyes taken from fetuses of 5-22 weeks gestation and a newborn 10 months after birth. Corneal endothelium appeared at the seventh or eighth week after gestation. Initially, they formed an irregular structure of two to three layers. From the 17th week of gestation they formed a single layer, and assumed the form of a cuboidal epithelium. Scanning and transmission electron microscopy showed numerous microvilli protruding towards the anterior chamber. Within the microvilli uniform microtubules were observed. By the 20th week, these microvilli disappeared, and subsequently, a single long narrow cilium appeared in the center of each cell. Each cilium had an axial filament complex structure. This cilium involuted as development progressed, and was barely visible by the 10th month after birth. The significance of this cilium is not clear.

Endothelium, Corneal↗
PubMed1992

[A juvenile case of mesenchymal chondrosarcoma originating from soft tissue in the orbit].

Mesenchymal chondrosarcoma is a very rare occurrence in the orbit. A 10-year-old girl presented with right exophthalmos. Computed tomography revealed a round tumor inside the muscular cone of the right orbit. There was a sign of slight calcification inside the tumor. The tumor was surgically removed by the Krönlein-Berke procedure. Histopathological examination showed undifferentiated mesenchymal cells and cartilage tissue. A recurrent tumor was found in the same location 34 months after the surgery, which was removed by frontal approach saving the globe with normal function. Histopathology of the recurrent tumor revealed a slight difference from the primary tumor, showing hemangiopericytoma pattern without cartilage components. Immunohistochemical studies of the primary and recurrent tumors showed their cells to be positive for antifactor VIII and S-100, and negative for myoglobin and monoclonal antibody to muscle actin. Electron microscopically these undifferentiated cells had large nucleus and very scanty cytoplasm, mostly containing glycogen granules. This is probably the first description of a juvenile case of mesenchymal chondrosarcoma originating from soft tissue in the orbit.

Child↗
PubMed1991

A double-blind comparative study of doxazosin and prazosin in the treatment of essential hypertension.

Two hundred sixty-six patients took part in a multicenter comparative study of doxazosin and prazosin. Both drugs produced a significant reduction (p less than 0.001) in blood pressure and no increase in heart rate. Blood pressure was considered "markedly decreased" or "decreased" in 70.8% of patients treated with doxazosin and 70.0% of patients treated with prazosin. No statistically significant between-group differences in antihypertensive efficacy were observed. Both doxazosin and prazosin were well tolerated; seven patients (5.6%) in each group had the therapy withdrawn.

Antihypertensive Agents↗
PubMed1988

Central attenuation of aortic baroreceptor reflex in prehypertensive DOCA-salt-loaded rats.

To determine whether the arterial baroreceptor reflex can act to oppose the development of hypertension, deoxycorticosterone acetate (DOCA)-salt hypertension was produced in sinoaortic-denervated and sham-operated rats. Systolic blood pressure measured by tail cuff started to increase in both sinoaortic-denervated and sham-operated rats 7 days after DOCA treatment, and the hypertension developed identically in both denervated and sham-operated rats. These findings suggest that the baroreceptor reflex cannot act against the development of hypertension. To determine whether the baroreceptor reflex is attenuated before the development of hypertension, bradycardiac and sympathoinhibitory responses to i.v. injections of norepinephrine were examined. Bradycardic and sympathoinhibitory responses were significantly smaller in DOCA-salt-treated rats in both prehypertensive (5th day after DOCA-salt treatment) and hypertensive stages (21st day after treatment). In urethane-anesthetized DOCA-loaded and control rats on the 5th day after treatment, aortic depressor nerve stimulation elicited frequency-dependent depressor and bradycardic responses accompanied by inhibition of sympathetic nerve activity in both DOCA-loaded and control rats. However, those responses were significantly smaller in DOCA-loaded rats than in control rats. These results suggest that the central component of the baroreceptor reflex mediated by the aortic depressor nerve is impaired before hypertension develops and that this impairment may contribute to the development of hypertension in DOCA-salt-treated rats.

Animals↗
PubMed1988

[Transmitral blood flow velocity patterns evaluated by pulsed Doppler echocardiography in diagnosing transient myocardial ischemia].

To evaluate the influences of transient myocardial ischemia on transmitral blood flow velocity patterns, pulsed Doppler echocardiography was performed during coronary artery occlusion in 10 anesthetized open-chest dogs, and also during esophageal pacing or the administration of dipyridamole in 79 patients with coronary artery disease (CAD), and in 19 control subjects. During occlusion of the coronary artery, an abrupt decrease in the peak velocity of the rapid filling wave (R) was noted within one min simultaneously with rapid decrease of % wall thickening in the ischemic regions. The peak velocity of atrial filling was augmented compensatorily. Although the transmitral blood flow velocity pattern did not change in the controls with esophageal pacing, changes similar to those which were obtained during experimental studies were demonstrated in CAD patients. There were no significant differences between transmitral blood flow velocity patterns of patients with multivessel disease and those with single vessel disease. Ischemic changes in transmitral blood flow velocity patterns were not demonstrated in patients with mitral regurgitation. Sublingual nitroglycerin normalized post-pacing abnormal blood flow velocity patterns. In contrast, after the intravenous administration of 0.56 mg/kg of dipyridamole, R and A were increased and the A/R ratio was unchanged both in CAD patients and the control groups. Deceleration time, or the half time, was prolonged during both provocation tests in CAD patients, and these changes were transient and were restored within several min. Furthermore, they were noted more frequently than was the development of ST depression on ECG, or chest pain. These findings indicate that the transmitral blood flow velocity patterns obtained by pulsed Doppler echocardiography are useful for detecting transient myocardial ischemia, though they have limitations in diagnosing the extent of coronary artery disease.

Animals↗
PubMed1987

[The source and significance of increased urinary dopamine excretion during sodium loading in rats].

To investigate the source and physiological significance of urinary free dopamine (f-DA) in high sodium diet (8% NaCl) loading, the effects of renal denervation and administration of carbidopa, an inhibitor of peripheral dopa decarboxylase, on urinary f-DA excretion were studied in male Wistar rats. Carbidopa was orally administered in a dose of 20mg/kg every 12h. To ascertain the extent of denervation, kidney norepinephrine was measured. Catecholamines were assayed by HPLC with electrochemical detection. Urinary f-DA and sodium excretion were significantly increased in response to the added NaCl. There were few effects of renal denervation on urinary excretion of f-DA and sodium in high sodium diet loading, whereas carbidopa caused a significant fall not only in urinary f-DA excretion but also in urinary sodium excretion. A highly significant correlation was also found between sodium excretion and f-DA excretion on the 5th day of carbidopa treatment. The data indicates that urinary f-DA in a high sodium diet is mainly derived from the renal tubular cells but not from renal nerves and that f-DA may be an important natriuretic hormone.

Administration, Oral↗
PubMed1987

Effect of inhibition of Na+-K+ ATPase on the prostacyclin generation of cultured human vascular endothelial cells.

Prostacyclin (PGI2) generation of cultured human vascular endothelial cells (VEC) was observed coincidentally with the increase of 45Ca net influx. Ca ionophore A23187 enhanced not only PGI2 generation and 45Ca net influx but also 45Ca efflux. PGI2 generation was completely abolished by the pretreatment with Ca++ immobilizer, TMB-8. A Na+-K+ ATPase inhibitor, ouabain increased 45Ca net influx, but decreased 45Ca efflux, and enhanced PGI2 generation. These observation indicate that PGI2 generation of VEC may be regulated by not only Ca++ but also Na+, and it was suggested that enhanced PGI2 generation by ouabain might be derived from the increased cytosolic Ca++concentration by the decreased Ca++ efflux, and it was considered to be originated from the suppression of Na+-Ca++ exchange systems by the increased intracellular Na+ concentration via inhibition of Na+-K+ ATPase activity by ouabain. Enhancement of PGI2 generation of VEC by the increased ouabain like substances (OLS) in hypertension is suspected to be beneficial on the maintenance of vascular homeostasis.

Calcimycin↗
PubMed1987

Devices external pulse generator: a reliable temporary pacemaker?

Two cases of malfunctioning APC (American Pacemaker Company) Devices pacemakers are reported. Two patients with sick sinus syndrome were temporarily paced using APC Devices pacemaker models EC 4542 and EV 4543 respectively, which showed transient increase (53% and 83% of the preset rate, respectively) in pacing rate. The sudden increase of the pacing rate might be the pacemaker's design to switch to fixed-rate pacing at nominally 25% higher than the selected rate in the presence of an excessive level of electrical interference. However, the increased rate was much faster than the interference rate. Great caution should be paid when APC Devices pacemaker is to be used.

Female↗
PubMed1987

Role of renal nerves and dopamine on prostaglandin E release from the kidney of rats.

The aim of the study is to investigate the role of renal nerves and dopamine (DA) on urinary excretion of prostaglandin E (PGE) released from kidney with or without salt loading in rats. After excessive intake of high Na, urinary excretions of PGE and DA enhanced as compared with those of basal Na. In rats with renal denervation, urinary excretion of PGE and norepinephrine decreased in salt loading, and urinary Na excretion increased. Urinary PGE excretion was also enhanced by treatment of bromocriptine accompanying with augmented natriuresis. Urinary PGE excretion was suppressed by treatment of carbidopa, which also suppressed the urinary excretion of DA. These results suggest that the renal adrenergic nerve and tubular DA in kidney play an important role on the release of PGE and that these mechanisms in PGE release from kidney augment in salt loading.

Animals↗
PubMed1987

Centrally induced vasopressor responses to ouabain in DOCA-salt hypertensive rats.

To investigate the effect of inhibition of cerebral Na+, K+-ATPase on cardiovascular regulation ouabain was injected into the lateral ventricle or the posterior hypothalamus in either conscious or urethane anaesthetised, deoxycorticosterone-salt hypertensive (DOCA) and sham operated (sham) rats. Ouabain injected intracerebroventricularly produced dose dependent vasopressor responses and tachycardia in the conscious rat; the magnitude of the pressor response was consistently larger in DOCA than in sham rats. In anaesthetised rats the pressor responses were accompanied by corresponding increases in abdominal sympathetic nerve activity. Thus the magnitude of the pressor responses, tachycardia, and the increases in nerve activity was again significantly greater in DOCA than in sham rats. Intrahypothalamic injections of ouabain produced pressor responses that were accompanied by consistent increases in both heart rate and abdominal sympathetic nerve activity in anaesthetised rats. In contrast to the intracerebroventricular injections the percentage increases from baseline blood pressure were significantly greater in sham than in DOCA rats at 5 min after injection. These results indicate that the centrally induced vasopressor response to ouabain, via the periventricular or bulbospinal system or both, is increased in DOCA-salt hypertensive rats whereas the pressor mechanism via the posterior hypothalamus is suppressed in DOCA rats.

Action Potentials↗
PubMed1987

Evidence for a digitalis-like substance in the hypothalamopituitary axis in rats: implications in the central cardiovascular regulation associated with an excess intake of sodium.

The origin and the physiological role of an endogenous digitalis-like substance were investigated by measuring both the digoxin-like substance by a digoxin radioimmunoassay (RIA) and the inhibitory activity on the ouabain sensitive Na+,K+-ATPase in rats. The digitalis-like substance was in high concentration in the pituitary, and in decreasing concentration in the hypothalamus, adrenal and the other organs as measured by RIA using an antibody raised from a goat. However, the adrenal showed the highest content of digitalis-like substance as measured by the antibody raised from a rabbit. The plasma level markedly decreased during a 2-week sodium-loading, and the adrenal content decreased markedly on hypophysectomy as measured with the rabbit-antibody. Therefore, the substance measured with the rabbit-antibody must be one of ACTH-dependent adrenal steroids. The inhibitory activity on the Na+,K+-ATPase was high in the pituitary gland, and was decreased in order of the adrenal, hypothalamus and other organs. The 2-week sodium-loading increased both the content in the pituitary gland and the output in the urine, and decreased the hypothalamic content. Immunohistochemical staining of the hypothalamus with the antibody revealed that the immunoreactivity is restricted to the neurons of the paraventricular nucleus, supraoptic nucleus, magnocellular accessory nuclei and extended their fibers reaching to the inner layer of the median eminence. To determine the role of the substance in the brain, the crude extract dissolved in artificial cerebrospinal fluid was injected into the lateral ventricle; vasopressor responses, tachycardia and hyperactivity of the splanchnic nerve lasting for more than 30 min were recorded, which resembled the responses to ouabain injected similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Pathophysiological role of dopamine on the development of hypertension in rats.

The aim of the study is to investigate the pathophysiological role of dopamine (DA) in the development of hypertension in DOCA-salt hypertensive rats and spontaneously hypertensive rats (SHRs). The augmentation of dopaminergic activity by chronic administration of bromocriptine, a DA agonist, suppressed the increase of blood pressure in DOCA-salt hypertensive rats. In contrast, suppression of dopaminergic activity by chronic administration of carbidopa, an inhibitor of dopa decarboxylase, accelerated the development of hypertension in SHRs, and this acceleration was also increased by salt loading. Increased urinary excretion of norepinephrine (NE) by DOCA-salt treatment was suppressed by the treatment of bromocriptine. In contrast, administration of carbidopa and salt loading in SHRs resulted in an increase in renal NE content and in urinary NE and epinephrine (E) excretion and a decrease in urinary sodium excretion. These results suggest that dopaminergic activity participate in the development of hypertension and decreased dopaminergic activity accelerates the development of hypertension in hypertensive rats mainly through the enhancement of peripheral sympathetic nerve activity.

Animals↗
PubMed1987

Involvement of dopamine in development of hypertension in spontaneously hypertensive rat: effect of carbidopa, inhibitor of peripheral dopa decarboxylase.

The demonstration of acceleration of hypertension was investigated in spontaneously hypertensive rats (SHR) treated with carbidopa, inhibitor of peripheral dopa decarboxylase. Oral administration of carbidopa to young SHR for 4 weeks accelerated significantly (P less than 0.05) development of hypertension as compared to SHR treated with vehicle. Urinary excretion of dopamine (DA) (P less than 0.01) and renal content of DA (P less than 0.02) were significantly decreased by carbidopa treatment. Urinary excretion of sodium (P less than 0.05) was significantly decreased and renal content of norepinephrine (NE) (P less than 0.01) was significantly increased by carbidopa. Urinary excretion of NE and epinephrine (E) did not change during the experimental period. Negative correlation between systolic blood pressure and urinary excretion of sodium (P less than 0.05) or dopamine (P less than 0.01) and positive correlation between systolic blood pressure and renal content of NE (P less than 0.05) were significantly observed in both groups of SHR treated with carbidopa and with vehicle for 4 weeks. These results suggest that decreased DA biosynthesis in peripheral tissues accelerates development of hypertension mediated by decrease of natriuresis and enhanced release of NE in the kidneys of SHR. DA plays an important role in regulation of blood pressure, and reduced dopaminergic mechanisms enhance blood pressure in SHR.

Animals↗
PubMed1987

Effect of decreased dopamine synthesis on the development of hypertension induced by salt loading in spontaneously hypertensive rats.

To clarify role of dopamine in the development of hypertension, the effect of a dopamine synthesis inhibitor on blood pressure and urinary output of catecholamines was investigated in spontaneously hypertensive rats (SHR) fed with high sodium diet. Rats were orally given carbidopa, an inhibitor of peripheral DOPA decarboxylase, or the vehicle for 4 weeks. Carbidopa administration accelerated significantly the development of hypertension as compared to the control SHRs with the vehicle. Carbidopa administration resulted in a significant decrease of urinary excreted sodium, urinary dopamine and renal content of dopamine. Conversely, carbidopa administration resulted in a significant increase of urinary excreted norepinephrine, urinary epinephrine and renal content of norepinephrine as compared with control SHRs. These results suggest that decreased dopamine synthesis in kidneys and probably other peripheral tissue accelerates the development of hypertension, mediated by a decrease of natriuresis and an enhancement of sympatho-adrenomedullary activity. Dopamine plays an important role in its protective action against the development of hypertension enhanced by salt loading, and decreased dopaminergic mechanisms accelerated hypertension in SHR.

Animals↗
PubMed1987

Attenuation of hypothalamo-sympathetic hyperactivity by renal denervation in experimental hypertensive rats.

To clarify the effect of renal nerves on hypothalamic cardiovascular regulation in hypertension, posterior hypothalamus was electrically stimulated in renal denervated SHR (RD-SHR) and DOCA hypertensive (RD-DOCA) rats during recording blood pressure and sympathetic nerve activity. In urethane anesthetized SHR, mean blood pressure was not different between RD- and sham-operated SHR 48 hours after denervation, but two weeks later, blood pressure was lower in RD-SHR. Pressor and sympathetic nerve responses to hypothalamic stimulation were partly attenuated 48 hours after denervation, but two weeks later, attenuation was strong. The development of hypertension was abolished during two weeks observation in RD-SHR. In DOCA hypertensive rats, the development of hypertension was significantly inhibited by renal denervation. Pressor and sympathetic nerve responses to hypothalamic stimulation were significantly diminished in RD-DOCA rats. Water intake and urine volume was identical in both groups. These results suggest that renal denervation inhibited the development of hypertension accompanied with the inhibition of hypothalamo-sympathetic nerve system, furthermore, it is indicated that hypothalamic cardiovascular regulation controlled by afferent renal nerve could contribute to the development of hypertension in SHR and DOCA hypertensive rats.

Animals↗
PubMed1987

Central effect of captopril on baroreflex.

To clarify effect of converting enzyme inhibitors (CEI) on heart rate regulation, captopril (2 mg/kg) was injected intravenously (i.v.) with or without pretreatment of atropine and also responses to intracisternal (i.c.) injections were examined. Captopril induced bradycardia with lowering blood pressure, and this bradycardia was abolished by pretreatment of atropine. Reduction of heart rate by i.c. injection of captopril was significantly larger than those of i.v. injection. Furthermore, to determine whether CEI can modify baroreflexes centrally, the aortic depressor nerve (ADN) was stimulated electrically in captopril treated rats. Vasodepressor and sympatho-inhibitory responses induced by ADN stimulation were significantly attenuated by captopril, while the bradycardiac response was not changed. These findings suggest that captopril attenuated centrally vasodepressor and sympatho-inhibitory responses of the baroreflex and activated centrally cardiac vagal efferent activity.

Animals↗
PubMed1987

Regulation of prostacyclin generation by angiotensin converting enzyme related substances in cultured human vascular endothelial cells.

The regulation of prostacyclin (PGI2) generation by angiotensin I-converting enzyme (ACE) related substances was investigated using cultured human vascular endothelial cells. Angiotensin I (AI) or bradykinin (BK) increased PGI2 generation and ACE activity, while the ACE inhibitor, captopril decreased both of them, and angiotensin II (AII) did not show any effect. The increasing rate of PGI2 generation induced by AI or BK was not affected by the pretreatment with captopril. These results suggest that the accumulation of AI or BK via the inhibition of ACE by captopril did not cause the enhancement of PGI2 generation. Rather, it was proposed that the enhanced PGI2 generation by AI or BK might be regulated by ACE activation derived from these substances, as an autoregulation mechanism.

Angiotensin I↗