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Biomedical subjects

K Ogino

Publications and source records attributed to K Ogino.

At least 199 records · Page 11Linked to original sources

Approach for quantifying the overall function of the ascending central neural integration to release vasopressin in rats.

Electrical stimulation of the intermediate portion of the solitary nucleus (SOL) is known to consistently elicit a pressor response and increase in the release of vasopressin (VP) in rats, when the cervical spinal cord and vago-sympathetic trunks are cut. The aim of the present study was to provide a methodological assessment for this technique, in order to quantify the central neuroendocrine function to release VP. Experiments were conducted on rats with cervical cordotomy and vagotomy, under 60% N2O anesthesia and artificial ventilation. The animals were maintained at their normal arterial blood pressure by infusing phenylephrine, which itself exerted little influence on the arterial plasma VP concentration (pVP) during SOL stimulation. In order to prevent blood loss, cross circulation with a donor rat was utilized in the blood sampling for pVP determination. We confirmed that this technique itself did not significantly affect the pVP level. A monopolar stimulus at a frequency of 50 Hz was found to produce the pressor response most effectively. The current spread of the stimulation (0.5 ms duration; 1 s on/1 s off; up to at least 120 microA) did not induce a false-positive pressor response mediated by other structures adjacent to the SOL. We suggest that electrical stimulation of the SOL in rats with cervical cordotomy and vagotomy, for observing the pressor response and/or increase of pVP, represents a rapid approach for screening the overall function of the ascending efferent part of the reflex mechanisms to release VP.

Animals↗

Release of vasopressin by electrical stimulation of the intermediate portion of the nucleus of the tractus solitarius in rats with cervical spinal cordotomy and vagotomy.

The cervical spinal cord and vagi were severed in anesthetized and artificially ventilated rats. Monopolar electrical stimulation of the intermediate portion of the nucleus of the tractus solitarius (NTS) resulted in subtle increases in concentration of plasma vasopressin (pVP) and in arterial pressure. We suggest that electrical stimulation of the NTS in rats undergoing such surgical preparation to observe the pressor response and/or increase in pVP, represents a rapid approach for screening the neurosecretory function of the central neural integration to release vasopressin.

Animals↗

Intrarenal beta-adrenergic stimulation enhances excretion of urinary lysosomal enzyme in anesthetized dogs.

The effects of intrarenal administration of isoproterenol on excretion of urinary enzymes were examined in dogs. Urinary N-acetyl-beta-D-glucosaminidase (NAG) and glutamyl transpeptidase (gamma-GTP) originated from lysosomes and the brush border membrane of the kidney, respectively. NAG excretion was elevated for 10 min by isoproterenol (0.2 microgram/kg/min) without a drastic change in glomerular filtration rate and renal blood flow. This elevation was inhibited by pretreatment with d,l-propranolol (0.6 mg/kg bolus injection 0.3 mg/kg/30 min) but less so by d-propranolol. Urinary gamma-GTP excretion was little affected by isoproterenol. In light of these findings, the possibility that beta-receptors may be involved in the excretion of NAG has to be considered.

Animals↗

The relevance of cardio-pulmonary-vascular reflex to regulation of the brain vessels.

In 11 cordotomized (C2) rats with the vagi cut, monopolar electrical stimulation at a current intensity of 73 +/- 21 (S.E.) microA (n = 6) to the intermediate region of the solitary nucleus elicited an increase (p less than 0.05) in regional blood flow (iodoantipyrine technique) of 71% and 43% in the frontal cortex and caudate nucleus, respectively. The findings suggest that some of the cardio-pulmonary and cardio-vascular reflex mechanisms are involved in the regulation of the blood vessels of the brain.

Animals↗

Quantitative evaluation of the pattern of shunt flow in the right ventricle and pulmonary artery of dogs with experimental ventricular septal defect.

Cineangiographic studies in patients with ventricular septal defect (VSD) have occasionally demonstrated that part of the blood across the defect is ejected immediately into the pulmonary artery (PA) passing through the outflow tract of the right ventricle (RV), but without being trapped in it. We attempted to make a quantitative evaluation of the flow of a partial shunt pathway (a direct VSD-PA pathway) that drains that part of the blood from the defect. Our method depended on a thermal dilution technique to obtain the ejection fraction of the RV and to observe a simultaneous pair of dilution curves at the roots of the aorta and PA after introduction of tracer into the left atrium. An analytical process was specially designed by incorporating a stable one-pass deconvolution technique. The method was applied to eight anesthetized dogs with acutely produced experimental VSD on the entrance of the outflow tract of the RV. The flow through the direct VSD-PA pathway was, in most cases, greater than 50 and up to 85% (mean of the eight, 57 +/- 5% SE) of the total left-to-right shunt flow. This would imply that less than 50%, and down to as little as 15%, of the total amount of shunt flow contributed to extra work of the RV in these cases. In addition, the impact on the pulmonary vasculature due to such a large amount of pulsatile flow through the direct VSD-PA pathway may accelerate the development of hypertrophy of the pulmonary vessel wall.

Animals↗

The inactive to active renin ratio in the kidneys and the plasma in diabetic nephropathy.

We examined the inactive to active renin ratio in the renin granules of the cadaver kidneys and the plasma in patients with diabetic nephropathy. The inactive renin in the break-through fraction when the plasma or the renin from the renin granules was put into a pepstatin column was determined. The inactive renin in this fraction was activated by trypsin. Concerning plasma, the inactive to active renin ratio was 90 in the patients and 9 in the normal subjects. On the other hand, this ratio was 0.29 in the patients' kidneys and 0.28 in the control kidneys. These results suggest that the increase of the inactive to active renin ratio in plasma of diabetic nephropathy does not result from the change of the renin storage in the kidneys.

Blood Proteins↗

The existence of inactive (trypsin-activated) renin in dog plasma and renin granules from the kidney.

Trypsin-activated renin (inactive renin) was detected in the break-through fraction when dog plasma or renin extracted from renin granules (stored renin) was applied to a pepstatin column, respectively. The appearance of the renin activity by trypsin treatment was not due to acid protease. Production of angiotensin I from homologous renin substrate by the trypsin-activated renin was proportional to the time of incubation. The trypsin-activated renin had an affinity for the pepstatin column. The maximum amount of trypsin-activated renin was obtained with incubation for 15 min at 37 degrees C at 1000 micrograms/ml in plasma or at 100 micrograms/ml in case of stored renin. The ratio of inactive to active renin was calculated to be 1.6 or 0.002 in plasma or stored renin, respectively, under conditions of a standard sodium diet.

Animals↗

Total venous capacity in two-kidney, one clip Goldblatt hypertensive rats.

To assess possible time-related changes in total venous capacity, mean circulatory filling pressure (MCFP) and blood volume (BV, Evans blue) were determined in conscious rats with early, intermediate and chronic phases of two-kidney, one clip Goldblatt hypertension. MCFP, and index of whole-body venous activity, was measured while the circulation was arrested by the brief inflation of a balloon inserted into the right atrium. Compared with shamoperated control rats, Goldblatt rats showed unchanged MCFP and BV in early phase, unchanged MCFP with marginally (0.05 less than p less than 0.10) decreased BV in intermediate phase, and significantly (p less than 0.05) increased MCFP with unchanged BV in chronic phase. Thus, decreased total venous capacity, which is reflected in increased MCFP relative to BV, occurred with a continuation of hypertension. MCFP/BV curves, obtained by measuring MCFP before and after rapid BV change, appeared to shift toward the pressure axis in all Goldblatt groups. There were no significant differences in total vascular compliance, which is the inverse of the slope of this curve and is an index of total venous compliance, between Goldblatt and control groups at any time-period studied. These results suggest that decreased venous capacity observed in chronic hypertensive rats may be a secondary hemodynamic state and may not be related to decreased venous compliance.

Animals↗

Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome.

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administration of triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenal scintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tubule in handling sodium and potassium which is similar to that in Liddle's syndrome.

Adrenocorticotropic Hormone↗

Provocation experiment: Pneumocystis carinii in several kinds of animals.

Provocation experiments of P. carinii in several kinds of laboratory animals were carried out in an animal house where P. carinii of rat strain had been maintained for several years. The organism propagated in cortisone treated rats, rabbits and mice without difficulty as reported by some authors in the past. The organism also propagated in the lungs of rats which had been bred with protein free diet. The present paper first indicates that guinea pig is susceptible to P. carinii. On the other hand, it becomes evident by repeated experiments, that golden hamster seems to be non-susceptible to P. carinii of rat strain even if enough dose of corticosteroid hormones is given. The presence of non-susceptible animal to a certain strain of P carinii is quite interesting from an epidemiological point of view.

Animals↗