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Biomedical subjects

H Ijichi

Publications and source records attributed to H Ijichi.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1987

[Transmitral flow patterns during acute coronary artery occlusion: experimental and clinical evaluations by pulsed Doppler echocardiography].

To evaluate left ventricular diastolic properties during acute myocardial ischemia, transmitral flow patterns were analyzed by two-dimensional pulsed Doppler echocardiography. In a preliminary study of transient coronary artery occlusion in anesthetized open-chest dogs, the following results were obtained: decreased peak velocity of rapid filling, prolonged rapid filling period, and compensatory increase in the peak velocity of atrial filling. These changes occurred nearly concomitantly with decreased cardiac output, elevated left atrial and left ventricular end-diastolic pressures, and decreased left ventricular systolic pressures. With reperfusion of the coronary artery, these parameters rapidly returned to the base line values. In acute and transient myocardial ischemia induced by intracoronary balloon inflation during therapeutic percutaneous transluminal coronary angioplasty (PTCA) in man, similar changes in these parameters were observed, and the changes were more marked in PTCA for the left anterior descending artery as compared with that of the right coronary artery. In conclusion, noninvasive two-dimensional pulsed Doppler echocardiography is of practical use in evaluating deterioration of the diastolic function of the left ventricle during acute and transient myocardial ischemia.

Angioplasty, Balloon↗
PubMed1987

[Clinical utility of spatial color mapping vectorcardiography in diagnosing myocardial infarction: comparison with 201Tl scintigraphy].

The feasibility of spatial color mapping vectorcardiography in diagnosing the site and extent of the old myocardial infarct was evaluated in comparison with 201T1 scintigraphy. Vectorcardiographic data made by Frank's technique were entered in the personal computer and the QRS complexes were plotted over 112 points crossing the latitude of each 20 (from 20N to 80S) degrees and longitude of each 20 degrees from 20W to 20E on the spherical body. Eight colors were assigned according to the direction of the QRS vector. To construct a territorial map, the apical, then, the septal, anterior, lateral, inferior and posterior portions were determined from the normal 201Tl scintigrams. Myocardial images obtained in the anterior, left anterior oblique and lateral projections were analyzed by the circumferential profile curve. Diagnostic specificity for infarction was greater than 60%, and especially high (90%) in the anterior, apical and lateral regions, but relatively low (50%) in the septal, inferior and posterior regions. Accuracies exceeded 64%. The infarcted areas assessed by spatial color vectorcardiography agreed with those assessed by 201T1 myocardial scintigraphy. Thus, spatial color vectorcardiography was simple and useful for diagnosing the site and extent of myocardial infarction.

Adult↗
PubMed1987

[Right ventricular systolic and diastolic functions assessed by 81mKr scintigraphy and relation to ventricular septal ischemia].

Right ventricular (RV) systolic and diastolic functions were assessed in patients with previous anteroseptal myocardial infarction to ascertain the influence of interventricular septal ischemia on RV function. Gated right ventriculography with continuous infusion of krypton-81 m was performed in 12 normal subjects and 28 patients with infarction but without significant stenosis of the right coronary artery. Furthermore, RV contractile reserve by postextrasystolic potentiation was evaluated by gated radionuclide ventriculography with 99mTc-HSA. The patients with anteroseptal infarction were divided into two groups by the presence or absence of three hours' redistribution in the septal region on exercise thallium-201 myocardial scintigraphy. Two indices of systolic function (ejection fraction and the peak ejection rate) and three indices of diastolic function (1/3 diastolic filling rate, the peak filling rate and time to the peak filling rate) were derived from the right ventricular time-activity curve and its derivative curve. There was no difference in systolic function among normal subjects and patients with or without redistribution. However, diastolic function was impaired only in the patients without redistribution. The RV contractile reserve in the patients without redistribution was less than in those with it. Thus, RV systolic function was maintained in the patients with anteroseptal infarction, but contractile reserve deteriorated only in severe septal ischemia. Similarly, diastolic function was maintained in mild septal ischemia, but impaired in severe septal ischemia. We concluded that RV systolic and diastolic functions are closely related to interventricular septal ischemia.

Diastole↗
PubMed1987

[Evaluation of right ventricular function in severe left ventricular failure: comparison of old myocardial infarction with dilated cardiomyopathy].

To evaluate right ventricular (RV) function in severe left ventricular (LV) failure, we measured RV and LV ejection fractions (EF) in 18 patients with old myocardial infarction (OMI) and in 18 with dilated cardiomyopathy (DCM) using cardiac blood pool scintigraphy. In patients with OMI, RVEF was significantly greater in stage II LV failure than in stage III (functional class of the New York Heart Association, 47 +/- 8% and 28 +/- 12%, respectively: p less than 0.01), and this correlated well with exercise tolerance by bicycle ergometer and mean pulmonary artery pressure (r = 0.83 and r = -0.71, respectively). In patients with DCM, however, there was no correlation between RVEF and these indexes. After the oral administration of denopamine (beta 1 effector), both RVEF and LVEF increased in patients with OMI (35 +/- 13% to 45 +/- 12%, and 27 +/- 9% to 30 +/- 10%: p less than 0.01), but they did not change significantly in patients with DCM. These results indicate that RVEF in patients with OMI correlates well with subjective symptoms, exercise tolerance and RV afterload, but these correlations were not apparent in patients with DCM. We concluded that RV function in cases of severe LV failure has a different meaning between OMI and DCM.

Adult↗
PubMed1986

Modulation of prostacyclin generation in cultured human vascular endothelial cells and the effects of human alpha-natriuretic polypeptide.

Vascular endothelial cells have been known to possess not only a barrier function but also other biologically important functions maintaining vascular homeostasis. Among these, the generation of prostacyclin is one of the most conspicuous functions, and the modulation of its synthesis and liberation has been of interest with reference to the interaction with several vasoactive substances, including human atrial alpha-natriuretic polypeptide. This paper investigates the regulatory mechanism of prostacyclin generation using cultured human vascular endothelial cells as far as Ca2+ flux, (Na+ + K+)-ATPase activity, and Na+-Ca2+ exchange systems are concerned. Through these experimental studies the following results were obtained. Prostacyclin generation was triggered by an increase of Ca2+ influx, and an increase in intracellular Na+ also enhanced it, and this was accompanied by a decreased Ca2+ efflux arising from suppression of Na+-Ca2+ exchange systems. (Na+ + K+)-ATPase activity as well as prostacyclin generation was also enhanced by the increase of intracellular Na+. These results indicate a possible link between the mechanism which generates prostacyclin in the human vascular endothelial cells and the mobilization of electrolytes; however, in this aspect human atrial alpha-natriuretic polypeptide had no effect on the endothelial cells.

Atrial Natriuretic Factor↗
PubMed1986

Inhibitory roles of the hypothalamic atrial natriuretic polypeptide on the vasopressin release in the sodium-loaded rats.

Implication of the brain atrial natriuretic polypeptide on the vasopressin release was investigated using rats fed with a high-sodium containing diet. Sodium loading increased not only the blood pressure but also the urinary output of vasopressin significantly. The plasma vasopressin concentration increased about 10 times after the intracerebroventricular injections of angiotensin II. Thereby, magnitude of the response was significantly smaller in the rat fed with a high sodium diet than in rats with the regular-diet. The hypothalamic content of both vasopressin and atrial natriuretic polypeptide was significantly larger in the high-salt group than the regular-salt. The intraventricular injections of atrial natriuretic polypeptide abolished the vasopressin release induced by the intraventricular injections of angiotensin II. These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment.

Angiotensin II↗