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Biomedical subjects

M Imanishi

Publications and source records attributed to M Imanishi.

At least 163 records · Page 9Linked to original sources
PubMed1988

Increases in renal angiotensin II content and tubular angiotensin II receptors in prehypertensive spontaneously hypertensive rats.

To examine the role of the intrarenal renin-angiotensin system in the development of hypertension in spontaneously hypertensive rats (SHR), we measured angiotensin II contents and tubular 125I-angiotensin II binding sites in the kidney of SHR and age-matched Wistar-Kyoto rats (WKY). In prehypertensive (4-week-old) SHR, not only the kidney angiotensin II content but also the angiotensin II receptor density in brush border membranes were significantly higher than in the WKY. In contrast, angiotensin II levels in the 20-week-old SHR kidneys were significantly lower than in the WKY. Acceleration of the intrarenal renin-angiotensin system and the increased density of tubular angiotensin II receptors in young SHR may therefore play an important role in the development of high blood pressure in SHR.

Angiotensin II↗
PubMed1988

Quantitative estimation of dietary intake in patients on hemodialysis.

A simple method to calculate the amount of dietary (protein, sodium and potassium) intake in hemodialyzed patients was developed. In 8 nutritionally stable patients, the amount of dietary intake was monitored conventionally by a dietary record method. In contrast, assuming that the amount of dietary intake was equal to the amount of accumulation in the body, the former was calculated as the change in the product of serum concentrations and total body fluid volume, which was estimated based on the sex and body build of each patient. The urea accumulation was converted to the protein intake. The interdialytic dietary protein and sodium intake calculated by this method, 120 +/- 10 g and 240 +/- 40 mEq, respectively, was not significantly different from that obtained by the dietary record, while the interdialytic potassium accumulation, 60 +/- 7 mEq, was significantly smaller than the dietary intake, 110 +/- 9 mEq, obtained by the record method, though the correlation was significant. Thus, the amount of protein and sodium intake can be calculated simply without diet research or body fluid volume measurements. Although potassium intake can not be calculated exactly because of intestinal loss, this simple method gives us a rough estimate. In addition, multiple regression analysis showed that the amount of energy intake obtained by the record method may be explained by the protein and sodium intake estimated by simple calculation.

Blood Urea Nitrogen↗
PubMed1986

[Clinical characteristics of contrast medium extravasation from intracranial aneurysms during cerebral angiography: studies on personal experience and review of the literature].

Angiography is essential to diagnosis and treatment for the patients with ruptured intracranial aneurysm in early stage, but on the other hand angiography always involves a risk that extravasation (EV) occurs from the aneurysm during angiography. Once EV occurs, the patient's outcome is poor and, in general, the patient tends to be regard as hopeless of recovery. Over the past 5 years, in 154 patients with ruptured intracranial aneurysm angiography was performed, and in 7 of them EV occurred. We performed neck clipping for ruptured aneurysm in 3 of 7 patients and were able to save the life of 2 patients. We investigated factors to cause EV and to decide outcome in 7 cases and 75 cases of literature, totally 82 cases. Following results were obtained. Occurrence of EV seems to be related to the causal factors of the time interval (within 6 hours) from SAH to angiography and the severity of disturbance of consciousness prior to angiography. It is considered that the patient's outcome is related to age, pre-angiographic severity of disturbance of consciousness, and also time interval from SAH to angiography, but the extent of EV and the number of past history of SAH are not important as the factors related to the outcome. Consequently, the utmost care must be taken for cerebral angiography particularly in patients within 6 hours after the onset of SAH, and in patients with severe disturbance of consciousness. Even if EV should occur, there is a fair chance for life-saving by an emergency surgery in cases with mild disturbance of cerebral function before angiography.

Adult↗
PubMed1983

Renin-angiotensin system and prostacyclin biosynthesis in streptozotocin diabetic rats.

The relationship between the renin-angiotensin system (RAS) and prostacyclin (PGI2) biosynthesis was studied in experimental diabetic rats. The group with diabetes induced by streptozotocin (STZ, 3.3 mmol/kg i.v.) showed prolonged hypertension, and plasma renin activity decreased markedly from 8.4 +/- 0.7 to 2.4 +/- 0.3 and 1.2 +/- 0.3 ng angiotensin I/ml per h at 2 and 8 weeks after STZ treatment. Plasma PGI2, determined as 6-keto-PGF1 alpha, decreased significantly at 8 weeks, with the values for the STZ-treated and control groups being 1490 +/- 99 and 2210 +/- 90 pg/ml, respectively. Significant suppression of renin release from renal cortical slices was observed at 8 weeks in the diabetic group, although no significant change was found in the renal renin content when compared with that of the controls. The release of PGI2 from the renal medullary slices of the diabetic group was suppressed at 2 and 8 weeks, with the suppression in aorta and renal cortical slices being apparent only at 8 weeks. These results indicate that suppression of the RAS may be related to PGI2 biosynthesis in diabetes mellitus.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Zonal heterogeneity of prostaglandin and thromboxane release in the dog kidney.

The release of prostaglandin(PG) and thromboxane(TX) was examined in the six different areas of the normal dog kidney, i.e., renal arterial and venous strips(RA and RV), superficial and deep cortical slices(SC and DC) and outer and inner medullary slices(OM and IM). These tissues were incubated in Krebs-bicarbonate buffer(pH 7.4, 37 degrees C), and the released PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2(as stable metabolites of PGI2 and TXA2, respectively) were determined by radioimmunoassay. In RA, RV, SC and DC, 6-keto-PGF1 alpha was predominant, however, there were no quantitative differences between RA and RV, or SC and DC. The release of 6-keto-PGF1 alpha reached a maximum in IM, similar to findings on the release of PGE2 and PGF2 alpha. The release of TXB2 was uniform in OM and IM. The amount of PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2 released from IM was 2800, 400, 60 and 50 times higher, respectively, than the extent of the release from the cortical slices. These results suggest that PGI2 as well as PGE2 and PGF2 alpha, may be involved in renal PG, and that TXA2 is biosynthesized in the normal dog kidney.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

[Value of contrast-enhanced CT scan in prediction of development of contusional hemorrhage].

It is often experienced that even if there are no significant findings on the initial plain CT scan in the patient with cerebral contusion, the patient has thereafter a serious clinical course and requires emergency operation for so-called contusional hemorrhage. In order to predict of the development of contusional hemorrhage we performed contrast-enhanced CT scan at the time of patient's arrival within 12 hours after injury, if there was cerebral contusion on 24 hours after the contrast-enhanced CT scan. If enhancement was demonstrated on the contrast-enhanced CT scan, we predicted the development of contusional hemorrhage and if not demonstrated, we predicted no more development of contusional hemorrhage and then we studied the correlation between the prediction and the plain CT 24 hours after the contrast-enhanced CT scan. The results were as follows: 1) The prediction was correct in 13 cases out of 16 cases in which the development of contusional hemorrhage was observed. In 18 cases where no development of contusional hemorrhage was observed, the prediction was correct without exception. 2) Most of the cases in which enhancement was demonstrated were ones examined not before 3 hours after injury. 3) The extent of enhancement shown on contrast-enhanced CT scan was well consistent with that of contusional hemorrhage on the plain CT scan 24 hours after the contrast-enhanced CT scan. From these results, the contrast-enhanced CT scan in acute stage of head injury was considered to by very useful in prediction of the development of contusional hemorrhage.

Adolescent↗
PubMed1981

Effect of calcium on prostaglandin E2 release in dogs.

Prostaglandin E2 (PGE2) concentration in arterial and renal venous plasma was determined by radioimmunoassay in anesthetized dogs, and the PGE2 secretion rate was calculated. Intrarenal arterial infusion of CaCl2 (0.68 meq/min) resulted in a biphasic effect on renal blood flow (RBF) and an initial increase followed by a gradual decrease below the preinfusion level. PGE2 secretion rate increased from 7.2 +/- 4.4 to 95 +/- 28 ng/min, with a marked increase of RBF after 3 min of CaCl2 infusion. An equivalent amount of NaCl infused into the renal artery did not affect either the RBF or the PGE2 secretion rate. One-tenth the dose of CaCl2 (0.068 meq/min) infused into the renal artery did not increase either RBF or PGE2 secretin rate, and the RBF gradually decreased after infusion. The transient renal vasodilation observed during infusion of a high dose of CaCl2 ceased with the combined intrarenal infusion of verapamil (100 micrograms/min), and was also abolished by pretreatment with indomethacin (5 mg/kg i.v.). Infusion of CaCl2 (0.68 meq/min) into the femoral artery did not enhance the PGE2 secretion rate from the hindlimb, and femoral blood flow decreased immediately after the infusion. These results suggest tht the renal vessels as well as other resistance vessels are essentially constricted by calcium and that endogenous PGE2 released by calcium may modify this renal vasoconstriction.

Animals↗
PubMed1980

Effects of calcium ionophore, A23187, on prostaglandin E2 and renin release in dogs.

Effects of calcium ionophore, A23187, on prostaglandin E2 and renin release, and the interrelationship were investigated in anesthetized dogs. PGE2 concentration in arterial and renal venous plasma was measured by radioimmunoassay, and secretion rate (pg/g-min) from the kidney was calculated. The renin secretion rate (ng/g-min) was calculated simultaneously. Intrarenal infusion of A23187 at a rate of 0.5 mg/min for 2 min resulted in a significant increase in RBF. PGE2 secretion rate increased from 61 +/- 26 to 1012 +/- 566 1222 +/- 500 and 388 +/- 125 at 5, 9 and 17 min. Renin secretion rate also increased rom 1.4 +/- 0.8 to 2.3 +/- 1.3, 5.8 +/- 2.7 and 5.9 +/- 1.6 at 5, 9 and 17 min. However, systemic administration of A23187 at a rate of 0.5 mg/min for 2 min did not alter the parameter. Thus, intrarenal infusion of A23187 affects RBF, renin release and PGE2 release directly within the kidney. In indomethacin treated dogs (5 mg/kg, i.v.) intrarenal infusion of A23187 significantly decreased RBF. The renin release with A23187 was also abolished with indomethacin as well as PGE2 release. These results suggest that calcium mobilization within the kidney plays an important role in PGE2 synthesis and release, and that the renal vasodilation and renin release are secondary effects of renal PGs synthesis and release.

Animals↗
PubMed1980

Effects of prostaglandin I2 and E2 on renal hemodynamics and function and renin release.

The effects of PGI2 and PGE2, given in the same doses were compared as to renal hemodynamics and functions and renin release. The same experimental conditions were used for both compounds and experiments were carried out in pentobarbital anesthetized dogs. Adrenergic influences were excluded by renal denervation. Given intrarenally at doses at 0.1 microgram/min and 1 microgram/min, PGE2 caused significant increase in RBF, UF and UNaV, but had no effect on BP and GFR. Intrarenal infusion of PGI2 at a rate of 1 microgram/min resulted in a significant increase of RBF and in a marked fall of BP, but only little change in GFR, UF and UNaV. With a dose of 0.1 microgram/min, the parameters remained the same. Intravenous infusion of PGI2 (1 microgram/min) caused a significant fall in BP with no change in the other parameters. Both PGI2 and PGE2 had a similar effect on intrarenal hemodynamics, i.e., caused a progressively greater proportional vasodilation from superficial to deep cortex. Given intrarenally in a dose of 1 microgram/min, PGI2 and PGE2 increased renin release. But with a dose of 0.1 microgram/min and 1 microgram/min, i.v., renin secretion was not influenced. The effect of PGI2 on systemic blood pressure was more potent than that of PGE2, however, with regard to renal vasodilating action and tubular effects, PGE2 was the more potent. Present data indicate that PGI2 and PGE2 stimulate renin secretion through a direct action on the juxtaglomerular cells.

Animals↗
PubMed1980

Effects of an orally active converting enzyme inhibitor (YS-980) on renal function in dogs.

The angiotensin converting enzyme inhibitor is a valuable pharmacological tool for studying the role of intrarenal humoral factors such as the renin-angiotensin and kallikrenin-kinin systems and prostaglandins as related to the regulation of renal function and the interrelation among them. An intrarenal infusion of such an inhibitor, YS-980 (thiazolidine carboxylic acid derivative), at a rate of 0.1 mg/min resulted in a significant fall in systemic arterial blood pressure and a significant increase in renal blood flow, urine flow, urinary excretion of sodium and renin release in anesthetized dogs. These renal effects evoked by YS-980 were abolished after the inhibition of kallikrein as induced by aprotinin (900 kallikrein inhibitory units per min). In addition, YS-980 given after the administration of indomethacin (5 mg/kg i.v.) had no effect on the renal hemodynamics and renin release except for the urinary excretion of sodium. These findings suggest that both the kallikrein-kinin system and prostaglandins contribute to the renal action and the vasodepressor effect of YS-980. It would appear that the intrarenal administration of this angiotensin converting enzyme inhibitor induced marked renal effects through activation of kinin and prostaglandins and that the relative contribution of the renin-angiotensin system is negligible in anesthetized dogs.

3-Mercaptopropionic Acid↗
PubMed1979

Diuretic action of metolazone in dogs.

Metolazone, the sulfonamide diuretic was investigated to determine the sites of action. We used a radioactive microsphere, clearance and stop-flow method in anesthetized dogs. Urine flow and urinary excretion of sodium and potassium were increased at 5--60 min when metolazone was given intravenously at doses of 0.2--5.0 mg/kg, while total renal blood flow, distribution of cortical renal blood flow and GFR did not change. The urinary excretion rate of sodium to potassium (Na/K) increased from 5.69 +/- 0.82 to 8.07 +/- 0.76 in a dose of 1.0 mg/kg, i.v. Osmolar clearance and free water reabsorption increased almost proportionally, indicating that metolazone has little effect on the medullary portion of the ascending limb of Henle and may have a proximal site of action. In stop-flow experiments, a significantly raised U/PNa/U/Pcreatinine was observed at the dip situated distally to the ascending limb of Henle. These findings indicate that the diuretic action of metolazone may be due to the inhibition of sodium reabsorption in the distal nephron segments, in addition to the absence of modification of the cortical regional blood flow.

Animals↗