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Biomedical subjects

S Ishikawa

Publications and source records attributed to S Ishikawa.

At least 19 recordsLinked to original sources
PubMed1992

Bilateral innervation of the musculus levator palpebrae superioris by single motoneurons in the monkey.

The location of motoneurons innervating the musculus levator palpebrae superioris (LPS) was studied in the monkey (Macaca irus) by using Fast blue (FB) and propidium iodide (PI) as retrograde neuronal tracers. In each monkey, FB was injected into the LPS of one eye and PI into the LPS of the other eye. Neuronal cell bodies labeled with FB and/or PI were seen intermixed bilaterally through the entire rostrocaudal extent of the central caudal nucleus. While single-labeled (70%) cell bodies predominated, many double-labeled (30%) cell bodies were also encountered. Each of the double-labeled neurons was concluded to supply the LPS on both sides by way of axon collaterals.

Animals↗
PubMed1992

Stimulation of anchorage-independent cell growth by endothelin in NRK 49F cells.

Endothelin (ET) is a vasoconstrictor peptide originally isolated from vascular endothelial cells. Recent studies have revealed that ET has many biological functions including growth factor-like activity. The present study aims to clarify whether ET-1 possesses the ability to stimulate anchorage-independent cellular growth, an indicator of factors with transforming activity. We found that NRK 49F cells possess a large number of high-affinity ET-1 receptors; labeled 125I-ET-1 binding was displaced by unlabeled ET-2 in a similar dose response, but in the case of ET-3, 100-fold more was required. Specific 125I-ET-3 binding was undetectable in NRK 49F cells, indicating that ET receptors in NRK 49F cells are ET-1/ET-2 selective. NRK 49F is a cell line which is most commonly used to assay for anchorage-independent cellular growth. Therefore, we explored whether ETs promote anchorage-independent cellular growth in this cell line. ET-1 and ET-2 stimulated NRK colony formation dose dependently in the presence of 1 nM epidermal growth factor (EGF). In contrast, ET-3 did not have colony-stimulating ability. In the presence of EGF, the maximal effect of ET-1 was approximately 90% of that of transforming growth factor-beta. Moreover, in the presence of maximal stimulating concentrations of EGF and transforming growth factor-beta, ET-1 additionally induced colony formation. These results indicate that ET-1 and -2 possess transforming growth factor-like activity for NRK 49F cells. Since ET-1 and -2 increased intracellular calcium levels, this ion may participate in signal transduction pathways by which ET-1 and -2 promote colony formation.

Animals↗
PubMed1992

Protein binding of four antiepileptic drugs in maternal and umbilical cord serum.

The total and protein free levels of 4 antiepileptic drugs (AEDs) in serum from 35 maternity patients who had been treated with AED monotherapy throughout pregnancy were studied. Results were compared with those in the umbilical cord serum at the time of delivery, and the placental transfer of AEDs was evaluated from the viewpoint of the protein binding capacity of the drug. The materials consisted of 35 samples of maternal and umbilical cord serum in total and included 13 patients on phenobarbital (PB), 7 on phenytoin (PHT), 7 on carbamazepine (CBZ) and 8 on valproic acid (VPA). The mean fetal/maternal total concentration ratios were 0.86, 0.91, 0.73 and 1.59 for PB, PHT, CBZ and VPA, respectively, only the VPA ratio being above 1. On the other hand, the mean fetal/maternal free fraction ratios were 1.13, 1.10, 1.42 and 0.50 for PB, PHT, CBZ and VPA, respectively, only the VPA ratio being less than 1. Correlation of the 2 ratios showed a reciprocal proportion with a correlation coefficient of -0.90 (P < 0.005). It was considered that the fetal/maternal total concentration ratio of 4 AEDs was regulated by the fetal/maternal free fraction ratio of the corresponding AEDs and that the difference in fetal/maternal free fraction ratio depended on the type of drug being administered.

Anticonvulsants↗
PubMed1992

Intraarterial infusion chemotherapy with [Sar1,Ile8]angiotensin II for bladder cancer.

Thirty-three patients with primary bladder cancer (nine stage T1 with multifocal tumors and 24 stage T2-4) were treated with intraarterial infusion chemotherapy including cisplatin, doxorubicin, and [Sar1,Ile8]Angiotensin II(AT II). Of the 32 evaluable patients, 12 had pathologically proven complete response (CR), 19 showed partial response (PR), and one showed no change (NC); the overall response rate (CR + PR) was 97%. The blood pressure increased in response to the administration of [Sar1,Ile8]AT II in all the patients; the mean increase in the systolic blood pressure was 36 mmHg. Most of the side effects were mild to moderate in severity, transient in nature, and included nausea/vomiting (100%), alopecia (84%), leukopenia (66%), headache (9%), nephrotoxicity (6%), diarrhea (3%), skin pigmentation (3%), and neurotoxicity (3%). One patient who dropped out of the study developed hemiplegia as a result of cerebral infarction. The findings indicate that it is necessary to exercise caution in selecting the patients to be subjected to this therapy. We conclude that intraarterial infusion chemotherapy combined with a vasoconstrictor has a significant effect not only against multifocal superficial bladder cancer but also against invasive bladder cancer.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1992

Different biventricular remodelling of myosin and collagen in pulmonary hypertension.

1. To clarify the metabolism of contractile and non-contractile proteins of the ventricles during the development of right ventricular hypertrophy (RVH) and accompanying congestive heart failure (CHF) in response to a pressure overload, monocrotaline was injected subcutaneously into Sprague-Dawley (SD) rats. Myosin isoenzymes (MIE) were analysed by pyrophosphate gel electrophoresis under non-dissociating conditions. Acid-soluble collagens were analysed by an improved, noninterrupted sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE). Tissue collagen content was also measured after the estimation of hydroxyproline concentration in tissues. 2. Monocrotaline induced RVH, but not left ventricular hypertrophy, at 2 weeks after the injection of monocrotaline, with severe RVH with CHF present at 4 weeks. In the right ventricles (RV) treated with monocrotaline, MIE shifted significantly from V1 to V3 at 2 weeks. The shift of MIE was more pronounced at 4 weeks. The proportion of type III collagen increased significantly compared with controls at 2 weeks. At 4 weeks, the proportion of types III and V collagens increased significantly compared with controls. 3. In left ventricles (LV) treated with monocrotaline, a similar but less remarkable shift of MIE was observed without remodelling of collagen types at 2 and 4 weeks. The concentration of collagen in either the RV or LV treated with monocrotaline showed no significant changes at 2 and 4 weeks compared with controls. 4. These results demonstrate a remodelling of the contractile and non-contractile proteins during the development of RVH and accompanying CHF, and provide evidence for changes in protein metabolism of the counterpart of RV (i.e. the LV). These results may provide important insights into the pathophysiology of adaptive or non-adaptive cardiac hypertrophy in response to a pressure overload.

Animals↗
PubMed1992

Long-term effectiveness of antiepileptic drug treatment and seizure recurrence in patients with epilepsy.

We studied the rate of seizure recurrence in 334 patients with epilepsy who had received antiepileptic drug (AED) therapy for at least eight years. During the three-year "observation period" (April 1985-March 1988), 163 or 48.8% of the 334 patients were considered to be seizure-free. Seizures were absent in 53 or 81.5% of 65 patients with idiopathic generalized epilepsy, 48 or 40% of 120 with temporal lobe epilepsy, 39 or 39.4% of 99 with partial epilepsy other than those involving the temporal lobe, 2 or 8.3% of 24 with symptomatic generalized epilepsy and 21 or 80.8% of 26 with other epilepsies. Of the 163 patients, 15 or 9.2% suffered seizure(s) during the three-year "follow-up period" (April 1988-March 1991). There was no difference among the different types of epilepsy with respect to seizure recurrence rates. Compared with the 15 patients whose seizures recurred, more of the 148 patients with nonrecurring seizures received AED monotherapy (p < 0.05). However, no significant differences were seen between the two groups for other background factors.

Adult↗
PubMed1992

Cellular mechanisms of vasopressin and endothelin to mobilize [Mg2+]i in vascular smooth muscle cells.

The present study was undertaken to examine the effects of arginine vasopressin (AVP) and endothelin-1 (ET-1) on cytosolic free Mg2+ ([Mg2+]i) in cultured rat vascular smooth muscle cells (VSMC). [Mg2+]i was measured using the fluorescence indicator dye mag-fura-2. AVP and ET-1 at a concentration of 1 x 10(-9) M or higher induced the mobilization of [Mg2+]i and cytosolic free Ca2+ ([Ca2+]i) in a dose-dependent manner in rat VSMC. Atrial natriuretic peptide and sodium nitroprusside producing cellular guanosine 3',5'-cyclic monophosphate did not affect [Mg2+]i and [Ca2+]i. A diterpene activator of adenylate cyclase, forskolin, also did not alter [Mg2+]i and [Ca2+]i. The removal of extracellular Mg2+ enhanced the AVP-mobilized [Ca2+]i and did not change the AVP-mobilized [Mg2+]i. The Ca(2+)-free and nominally Mg2+/Ca(2+)-free states decreased the AVP-mobilized [Mg2+]i and [Ca2+]i. The Na(+)-free state enhanced the sustained, but not peak, level of the AVP-mobilized [Mg2+]i. These results indicate that AVP and ET-1 mobilize [Mg2+]i mediated through their intracellular second messenger [Ca2+]i and independent of extracellular Mg2+. Also, an increase in [Mg2+]i is indicated to stimulate the Na(+)-Mg2+ exchange to increase cellular Mg2+ efflux.

Animals↗
PubMed1992

pH dependence of the action of arginine vasopressin in renal collecting tubule.

We determined whether extracellular pH (pHe) and intracellular pH (pHi) modulate the cellular actions of arginine vasopressin (AVP) in rat renal papillary collecting tubule cells in culture. AVP significantly increased cellular adenosine 3',5'-cyclic monophosphate (cAMP) production and cellular free calcium concentration ([Ca2+]i). pHe ranging from 6.8 to 8.0 distributed the pHi between 6.94 and 7.27. The acidified pHe reduced the AVP- and forskolin-induced cAMP production, the AVP-mobilized [Ca2+]i, and [3H]AVP receptor binding, and the alkalinized pHe enhanced the AVP- and forskolin-produced cAMP. Intracellular acidification occurred under three different conditions as follows: using carbonyl cyanide-m-chlorophenylhydrazone (CCCP), acetate buffer, and bicarbonate buffer with a reduced concentration of bicarbonate. Intracellular acidification significantly diminished both the AVP- and forskolin-induced increases in cAMP production and the AVP-mobilized [Ca2+]i but did not alter [3H]AVP receptor binding. Intracellular alkalinization by NH4Cl or chloride-free bicarbonate buffer, in contrast, augmented them. These results indicate that alterations in pHi modulate the cellular action of AVP to produce cAMP and mobilize [Ca2+]i in renal papillary collecting tubule cells. Also, reduced receptor binding of AVP is involved in the mechanism of the effects of low pHe.

Ammonium Chloride↗
PubMed1992

Effects of endothelin-1 and conversion of big endothelin-1 in the isolated perfused rabbit lung.

We examined the effects of endothelin-1 (ET-1) on pulmonary hemodynamic and transvascular fluid filtration and the conversion of big endothelin-1 (big ET-1), a precursor of ET-1, in isolated perfused rabbit lungs at constant vascular and airway pressures. Furthermore we examined whether ET-1 contributes to cyclooxygenase metabolism. The perfusate flow decreased significantly after bolus administration of 1 or 0.1 nmol of ET-1. Lung weight did not increase throughout the experimental period. Big ET-1- (1 nmol) induced decrease in the flow was slow in developing, although the maximum response was comparable to that induced by the same dose of ET-1. The concentration of bit ET-1 in the perfusate progressively decreased, while that of ET-1 increased in a time-dependent manner. Phosphoramidon, an inhibitor of metalloproteinase, suppressed the pressor effect of big ET-1 (P less than 0.01) and the increase in the concentration of ET-1 in the perfusate (P less than 0.05). The present findings provide the first evidence suggesting that the potent vasocontractile effect of big ET-1 in pulmonary circulation can be attributed to the production of ET-1 by the conversion from big ET-1 in the vascular bed. ET-1-induced perfusate flow changes were not affected by indomethacin, and the concentration of 6-ketoprostaglandin F1 alpha, a metabolite of prostacyclin, did not increase after ET-1 administration.

Animals↗
PubMed1992

pH dependence of inhibition of arginine vasopressin-induced adenosine 3',5'-monophosphate production by cellular sodium depletion in rat renal inner medullary collecting duct cells in culture.

The present study was undertaken to determine whether the change in cellular Na+ concentration ( [Na+]i) or cellular pH (pHi) is essential for the modulation by Na+/H+ antiporter of the cellular action of arginine vasopressin (AVP) in renal inner medullary collecting duct cells in culture. Extracellular Na+ depletion promptly decreased [Na+]i from 15.8 to 5.4 mM (P less than 0.01), which was closely related to the decrease in pHi (7.19 to 6.97; P less than 0.01). In the presence of 0.5 mM 3-isobutyl-1-methylxanthine, AVP increased cellular cAMP production in a dose-dependent manner. This was significantly blunted in the Na(+)-depleted cells (1 nM AVP; 481.9 vs. 341.0 fmol/micrograms protein; P less than 0.01). When cells were incubated with the Na(+)-depleted medium containing 25 mM NaHCO3, [Na+]i decreased promptly, but the pHi remained unchanged. Under this condition, the AVP-induced increase in cellular cAMP production was not altered (1 nM AVP; 390.9 vs. 334.8 fmol/micrograms protein). Also, after the Na(+)-depleted cells were incubated in 20 mM NH4Cl, which promptly normalized pHi despite the decreased [Na+]i, the response of cAMP production to AVP was restored. Amiloride (1 x 10(-5)-1 x 10(-3) M), which blocks the Na+/H+ exchange, decreased pHi and AVP- and forskolin-induced cAMP production in a dose-dependent manner. These results indicate that the decrease in [Na+]i promptly inhibits AVP-induced cAMP production mediated through the reduction in pHi in renal inner medullary collecting duct cells.

Amiloride↗
PubMed1992

Increases in cellular sodium concentration by arginine vasopressin and endothelin in cultured rat glomerular mesangial cells.

The present study was undertaken to determine whether arginine vasopressin (AVP), angiotensin-II, and endothelin (ET) increase the cellular sodium concentration ([Na+]i) in cultured rat glomerular mesangial cells. [Na+]i was measured using the fluorescence indicator dye sodium-binding benzofuran isophthalate. These three vasoconstrictor hormones increased cellular free calcium ([Ca2+]i) and [Na+]i in a dose-dependent manner ([Na+]i: basal, 11.5; 10(-7) M AVP, 20.5; 10(-7) M angiotensin-II, 13.8; and 10(-7) M ET, 21.2 mM). The mobilization of [Ca2+]i was faster than that of [Na+]i. The AVP-induced increase in [Na+]i was completely blunted by the potent V1 antagonist d(CH2)5Tyr(Me)AVP. Vasoconstrictor hormones produced a biphasic cellular pH (pHi) change, characterized by a transient acidification, followed by a sustained alkalinization. The Ca(2+)-free condition markedly reduced AVP- and ET-induced increases in [Ca2+]i and [Na+]i and biphasic changes in pHi. In the Na(+)-free state, the hormonally mobilized [Ca2+]i was significantly enhanced. Basal [Na+]i decreased to below 3 mM, and there was little increase in [Na+]i after the addition of vasoconstrictor hormones, suggesting that the source of [Na+]i is extracellular space. Only early acidification was obtained in the absence of a sustained alkalinization. The [Na+]i mobilization was closely related to the biphasic change in pHi. These results indicate that AVP, ET, and angiotensin-II increase [Na+]i in glomerular mesangial cells, and that the early mobilization of [Na+]i depends on Na+/Ca2+ exchange, and the sustained phase depends on Na+/H+ exchange. The hormonally mobilized [Ca2+]i is essential for the activation of Na+/H+ exchange, and an increase in [Na+]i is suggested to play an important role in cellular alkalinization.

Angiotensin II↗
PubMed1992

Biochemical and structural remodeling of collagen in the right ventricular hypertrophy induced by monocrotaline.

We investigated biochemical and structural changes in collagen in ventricles in right ventricular hypertrophy (RVH) induced by monocrotaline injection in Sprague-Dawley rats. Rats injected with monocrotaline showed significant RVH after 2 weeks compared with the vehicle-treated rats (controls). After 4 weeks, the monocrotaline-treated rats showed severe RVH with heart failure. After 2 weeks, the proportion of type III collagen in the right ventricles (RV) of the monocrotaline-treated rats increased significantly compared with controls, with a concomitant decrease in type I collagen. After 4 weeks, there was a significant increase in the proportion of type III and type V collagens in the RV. In the left ventricles (LV), the proportion of collagen types was similar in the monocrotaline-treated and control rats at 2 and 4 weeks. There was no significant difference in collagen concentration (% collagen in dry defatted tissue) between the monocrotaline-treated rats and controls at either 2 or 4 weeks in the LV and RV. Scanning electron microscopy revealed that the collagen fibrillar sheaths around the myocytes in the endomysium of the RV had thickened and formed a dense network in the monocrotaline-treated rats. In the perimysium, tendon-like collagen fibers increased and became thicker than those in the RV of controls. Giant coiled perimysial fibers were also observed in the monocrotaline-treated RV. These structural changes were more pronounced after 4 weeks of monocrotaline-treatment: Loss of myocytes was evident and was accompanied by replacement fibrosis, where dense collagen fibers aggregated parallel to the long axes of the myocytes. Our results show that biochemical and structural remodeling of collagen occurred in the RV but not in the LV during the development of RVH and heart failure, providing important clues to the pathogenesis and pathophysiology of RVH and cardiac failure in response to pressure overload.

Animals↗
PubMed1992

Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats.

Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.

Animals↗
PubMed1992

An autopsy case of intravascular lymphomatosis (neoplastic angioendotheliomatosis) accompanied by high fever, hypertension and without focal sign.

A 75-year-old woman suffered from intermittent high-grade fever and hypertension without any focal sign. Serum lactic dehydrogenase (LDH) was markedly elevated. The fever was resistant to antibiotics and temporarily sensitive to prednisolone. She had heart failure and died. Postmortem examination revealed intravascular proliferation of B lymphocytes, indicative of the diagnosis of intravascular lymphomatosis. The clinical diagnosis is usually very difficult because of the absence of pathognomonic clinical manifestations.

Aged↗
PubMed1992

[A clinico-pathological study of inverted papilloma of the urinary bladder. Analysis of histogenesis].

A clinico-pathological study was conducted on 9 cases with inverted papilloma of the urinary bladder. 1. Clinical study: The incidence of inverted papillomas, when compared with transitional cell carcinoma of the urinary bladder, was much higher in men than in women in our study and in the literature dealing with this subject as well. Eight of 9 inverted papillomas were localized in the bladder neck. Cystoscopic examination revealed that all tumors were pedunculated and 8 of the 9 tumors had non-papillary surfaces. These clinical findings suggest that inverted papillomas localized in the bladder neck are very similar to posterior urethral polyps with prostatic type epithelium. Transurethral resection (TUR) was performed in all cases. Recurrence was not observed. 2. Pathological study: Inverted papillomas were classified into two types according to their histological patterns, determined by Hematoxylin-Eosin (H-E) staining. One pattern was glandular and the another was trabecular. Of the 9 cases, 2 were glandular, 5 were trabecular and the remaining 2 were a mixed type. Immunohistochemical staining with anti-prostate specific antigen antibody revealed 3 of the 9 tumors were stained positively, and these tumors were classified a glandular type. Inverted papilloma were classified into two patterns according to their histological patterns, determined by immunohistochemical staining with anti-keratin antibody, namely a bladder tumor pattern and a urethral tumor pattern. Inverted papillomas with a urethral tumor pattern were of the glandular type and included anti-PSA antibody positive staining tumors. These findings suggest that a portion of inverted papillomas may have arisen from neoplastic transformation of prostatic tissue.

Aged↗
PubMed1992

[Studies on the fragments of FDP in 4 patients with DIC].

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in four patients with disseminated intravascular coagulation (DIC), that were caused by various diseases. In the patients suffering from acute lymphoblastic leukemia (case 1) and acute suppurative cholangitis (case 3), DD and DY/X fragments resulting from fibrinolysis accounted for the most part of the FDP fragments. In case 3, D fragments resulting from fibrinogenolysis were also observed to much less extent. In a DIC associated with acute myeloblastic leukemia (case 2), both fibrinolysis and fibrinogenolysis were increased and resulted in high levels of D, Y and DY/X fragments, concomitant with moderate levels of DD and high molecular weight (HMW) fragments in the patient's sera. The increased fibrinogenolysis in this case was attributed to accelerated activation of plasmin. In a DIC patient of case 4, who underwent an operation due to hepatocellular carcinoma, marked increase in DY/X and HMW fragments and slight increase in DD fragment were observed on the day of operation. Hyperfibrinolysis documented in case 4 was explained by both increased production of thrombin and moderately accelerated activation of plasmin. Both qualitative and quantitative changes in the fragments of FDP during the courses of treatment in two cases of DIC were also noted. In summary, each underlying disease expresses characteristic pattern of FDP fragments in DIC.

Adolescent↗
PubMed1992

[Gianturco expandable metallic stents in the treatment of superior vena cava syndrome caused by lung cancer].

Treatment of superior vena cava syndrome (SVCS) caused by advanced lung cancer is still controversial. We inserted Gianturco expandable metallic stents (GEMS) in 5 patients with SVCS due to the extension of lung cancer. GEMSs were introduced intravenously through the catheter after intraluminal balloon dilation of the stenotic sites. SVCS was successfully and easily relieved by this method without any significant complication. GEMS placement seems to be a useful alternative to bypass grafting procedure for the treatment of SVCS.

Adult↗