Biomedical subjects

T Kitazawa

Publications and source records attributed to T Kitazawa.

At least 109 records · Page 6Linked to original sources

PubMed1988

Presence of a substance P-like peptide in an acid extract of the intestinal bulb of the carp (Cyprinus carpio).

1. The effect of an acid extract of the carp intestinal bulb (ECI) on guinea-pig ileum longitudinal smooth muscle (GPLM) and carp intestinal bulb longitudinal smooth muscle (CIBLM) was examined. 2. ECI caused a concentration-dependent contraction of GPLM and CIBLM. This ECI-induced response was reduced by atropine to 30-40% of the control, indicating that part of the contracting activity of ECI is attributable to acetylcholine. The atropine-resistant contracting activity of ECI was not mediated by histamine, 5-hydroxytryptamine, ATP, ADP, angiotensin II, neurotensin, vasoactive intestinal peptide or an opioid peptide. 3. The active material mediating the atropine-resistant contracting activity is probably a peptide, because the contraction in response to ECI was abolished on incubation with pepsin or alpha-chymotrypsin. 4. [D-Pro2, D-Trp7,9]-substance P, [D-Pro4, D-Trp7,9]-substance P (4-11) decreased the atropine-resistant contracting activity of ECI as did desensitization induced by substance P. 5. On a Sephadex G 25 column, the active material was eluted as one peak. The active fractions were pooled and then applied to another Sephadex G25 column to compare the Ve/Vo value for the active material with those for peptides of known molecular weights. The molecular weight of the active material was estimated to be 1200-1700 (1410 +/- 70, n = 6). 6. The results indicate the presence of a substance P-like peptide in the carp intestinal bulb.

Acetylcholine↗

PubMed1988

Caffeine contracture in guinea-pig ventricular muscle and the effect of extracellular sodium ions.

1. The mechanisms underlying the virtual absence of caffeine contracture in guinea-pig heart in a Na+-rich external solution were reinvestigated in small (50-120 microns thick) bundles of intact and skinned papillary muscle fibres. 2. In Na+-free solution, the peak tension of 30 mM-caffeine contracture corresponded to the maximum tension of the skinned fibres, and was independent of changes in [Ca2+]o and [K+]o. In the presence of external Na+, the peak tension, which was at most several per cent of the maximum, was affected by [Ca2+]o, [Na+]o and [K+]o, and enhanced by Mn2+ and Ni2+. 3. In the absence of Ca2+, replacement of Na+ with K+ allowed caffeine to evoke a large contracture, showing that there was sufficient calcium stored in the cells under Na+-rich conditions. After treatment with 30 mM-caffeine in the Na+-rich, Ca2+-free solution, and upon replacement of all Na+ with Li+, caffeine was still able to produce a large contracture, which was dependent upon Ca2+ pre-loading of the cells before the first caffeine treatment and upon the subsequent duration in the Na+-free solution. 4. Replacement of Li+ with Na+ during the contracture led to rapid relaxation which was delayed by an increase in [Ca2+]o, depolarization by K+, and addition of La3+ and Mn2+. After Na+-induced complete relaxation in the absence of Ca2+, upon removal of the drugs and Na+, subsequent application of caffeine to the cells evoked a large contracture without Ca2+ reloading. 5. In the skinned fibres, 30 mM-caffeine increased the Ca2+ sensitivity of the contractile system and depressed the maximum tension. An increase in Na+ from 8.4 to 58.4 mM altered neither Ca2+ sensitivity nor the rate of tension development in the absence or presence of caffeine. 6. Increase in Na+ affected neither the rate nor the amount of Ca2+ uptake by the sarcoplasmic reticulum (SR) in the absence or presence of caffeine. Increasing Na+ slightly inhibited the caffeine-induced Ca2+ release from the SR, but more than 10 mM-caffeine produced SR Ca2+ depletion. 7. In the presence of a strong Ca2+ buffer, the steady level of Ca2+ uptake by the SR with 1 mM-caffeine was equal to the amount of Ca2+ remaining in the SR just after the application of caffeine, indicating that Ca2+ release was not inactivated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Mortality, major cause of moribundity, and spontaneous tumors in CD-1 mice.

Mortality, major causes of moribundity, and spontaneous tumors in CD-1 mice were studied in 891 males and 890 females, which were used as controls in 11 different 2-year chronic and oncogenicity studies during the past 5 years. Average mortality of males and females at 83 weeks of age was 32.6% and 28.6%, respectively, and at 109 weeks of age was 66.4% and 63.3%, respectively. Mortality was significantly lowered in males and females born after 1980 in accordance with an abruptly decreased occurrence of systemic amyloidosis in these animals. The major cause of death or moribundity included systemic arteritis, systemic amyloidosis, auricular thrombosis, glomerulosclerosis, lymphoma, and pulmonary adenocarcinoma in both sexes. Dysuria and hepatocellular carcinoma in males and mammary adenocarcinoma in females were also critical lesions. The major tumors occurring at more than 3% incidence were systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver and adenoma/adenocarcinoma of the Harderian gland for males, and systemic lymphoma, adenoma/adenocarcinoma of the lung, adenoma/carcinoma of the liver, leiomyoma/leiomyosarcoma of the uterus, adenoma/adenocarcinoma of the pituitary (anterior), adenoma/adenocarcinoma of the mammary gland and adenoma/adenocarcinoma of the Harderian gland for females. Intralaboratory heterogeneities in the incidence were recorded as follows: systemic lymphoma in 1 of 11 control groups (1/11) and adenoma/adenocarcinoma in 1/11 for males, and systemic lymphoma in 3/11, adenoma/adenocarcinoma of the lung in 2/11, adenoma/adenocarcinoma of the liver in 1/11, and adenoma/adenocarcinoma in 1/11 for females.

Amyloidosis↗

PubMed1988

Antagonist like action of synthetic alpha 2-adrenoceptor agonists on contractile response to catecholamines in smooth muscle strips isolated from rainbow trout stomach (Salmo gairdneri).

1. The effects of some synthetic alpha 2-adrenoceptor agonists on the mechanical activity and on contractile responses to catecholamines were examined in smooth muscle strips isolated from rainbow trout stomach. 2. Contractile responses to noradrenaline and adrenaline in the rainbow trout stomach strips were due to alpha 2-adrenoceptor activation. 3. Clonidine, p-aminoclonidine, naphazoline and guanabenz caused no mechanical response but concentration-dependently inhibited the contractile responses to noradrenaline and adrenaline without affecting the responses to acetylcholine, carbachol, 5-hydroxytryptamine and methionine-enkephalin. The order of potency was naphazoline greater than p-aminoclonidine greater than clonidine greater than guanabenz. 4. It is suggested that in the smooth muscle preparation of the trout stomach, some synthetic compounds (clonidine, p-aminoclonidine, naphazoline and guanabenz), which act on mammalian preparations as alpha 2-adrenoceptor agonists, show an antinoradrenaline (-adrenaline) effect; those compounds can be classified as alpha 2-adrenoceptor antagonists.

Adrenergic alpha-Agonists↗

PubMed1988

[Clinical and experimental studies on ligation of the draining vein in the remnant liver during hepatectomy].

In recent 8 years we experienced 6 cases of No. 7 and 8 segmentectomies in 140 hepatectomies. In 4 of them resection of the right hepatic vein (RHV) was unavoidable and two were released from RHV resection by using ultrasonic aspiration method. In the former cases non-cirrhotic patients had transient elevation of transaminases after surgery, while cirrhotic patients demonstrated severe liver dysfunction. The latter cases were uneventful after surgery. In the experimental study, the two groups of rats were made by Group-I (Gr-I) with only 40% hepatectomy and Group-II (Gr-II) in which the hepatic veins draining a remnant lobe were ligated after 40% hepatectomy. The remaining liver lobes with intact veins in Gr-I and Gr-II showed normal hepatic regeneration. However, the parenchyma without draining veins in Gr-II revealed severe congestion and necrosis and transaminases in Gr-II elevated significantly higher than Gr-I soon after operation. Thereafter, DNA synthesis of the hepatocytes with 3H-thymidine had a peak value before collateral vessel formation. Consequently, however, the hepatic volume of the vein-ligated region decreased considerably. Thus, clinical and experimental results suggest that the vein-ligated region can not be expected to share the liver function after hepatic lobectomy and hepatic failure may occur in the cirrhotic patients.

Animals↗

PubMed1988

[Recurrent meningioma with malignant changes and extracranial multiple metastases].

A case of recurrent meningioma with malignant change and extracranial multiple metastases is reported. A 51-year-old female was operated on and left parasagittal meningioma was extirpated by Simpson grade II. Histological diagnosis was fibroblastic and transitional meningioma with slight atypism. Six years later, however, the tumor (transitional meningioma with slight mitosis) recurred in the same portion and was removed again by Simpson grade II. Further more, four years after the second operation, bilateral parasagittal meningioma (atypical meningioma; transitional type) was extirpated by Simpson grade I including superior sagittal sinus and falx. Only eight months after the last operation, a few tumors with central necrosis were demonstrated in the bilateral parasagittal area on a computerized tomography scan and she received radiation therapy. But the tumor had metastasized to the extracranial multiple organs including lungs, liver, pancreas, adrenal gland, muscles, multiple bones and lymph nodes. Post mortem diagnosis was malignant meningioma. We reviewed and discussed the characteristics of metastasizing meningioma, the effectiveness of radiation therapy on the prevention of recurrence of meningioma and the curative effect of radiation therapy for recurrent or metastasized meningioma.

Abdominal Neoplasms↗

PubMed1987

Carp (Cyprinus carpio) heart has a high sensitivity to the positive inotropic effect of strophanthidin despite negative force-frequency relationships.

1. The relationship between response of the heart to increased stimulation frequency and digitalis sensitivity was examined comparing the positive inotropic effect of strophanthidin and [3H]ouabain binding to sarcolemmal Na+, K+-activated adenosine triphosphatase (Na+, K+-ATPase) in carp heart, which showed a negative force-frequency relationship, and in guinea-pig heart, which has a positive relationship. 2. In ventricular muscle preparations isolated from carp heart, strophanthidin increased developed tension with a half-maximal effect observed at 0.31 microM, indicating a relatively high digitalis sensitivity of this preparation. 3. The positive inotropic effect was not altered by concentrations of propranolol sufficient to block beta-adrenergic receptors. 4. Specific binding of [3H]ouabain to homogenates obtained from ventricular muscle of carp heart showed a single class of binding sites with a Kd value of 26 nM. 5. Potency of strophanthidin to produce the positive inotropic effect and affinity of the binding sites for [3H]ouabain were both higher in carp heart compared to those in guinea-pig heart. 6. These results demonstrate a clear dissociation between the force-frequency relationship and the sensitivity of heart muscle to the positive inotropic effect of cardiotonic steroids. 7. The latter is primarily determined by affinity of sarcolemmal Na+, K+-ATPase for the cardiotonic steroids.

Animals↗

PubMed1987

Pharmacological properties of the atropine-resistant contraction of the carp (Cyprinus carpio) intestinal bulb induced by transmural stimulation.

1. The pharmacological properties of the atropine-resistant contraction of the carp intestinal bulb induced by transmural stimulation were investigated. 2. In the presence of atropine (1 microM), transmural stimulation caused frequency-dependent (2-50 Hz) contraction which was abolished by tetrodotoxin (780 nM). 3. The atropine-resistant contraction was not decreased by tubocurarine (5 microM), hexamethonium (100 microM), carteolol (5 microM) and phentolamine (5.4 microM). 4. In vitro pretreatment with guanethidine (10 microM for 1 hr) markedly decreased the noradrenaline and adrenaline contents of the carp intestinal bulb. The atropine-resistant contraction was not affected by pretreatment with guanethidine. 5. Diphenhydramine (1 microM), methysergide (3 microM) and naloxone (1 microM) did not decrease the atropine-resistant contraction, indicating that histamine, 5-hydroxytryptamine and opioid peptides were not involved in the atropine-resistant response. 6. These results indicate that a non-cholinergic, non-adrenergic excitatory nerve is present in the carp intestinal bulb. The neurotransmitter mediating the excitatory response could not be identified.

Animals↗

PubMed1987

Oral leukoplakia and costochondral hyperplasia induced by diethylnitrosamine in hamsters exposed to cigarette smoke with or without dietary vitamin C.

Male Syrian golden hamsters receiving 12 weekly subcutaneous injections of diethylnitrosamine (DEN) were subjected to cigarette smoke-inhalation and fed a diet or without 1% vitamin C supplement for a period of 58 weeks. Another group was a sham-smoked control and was not fed vitamin C. Tissues of the oral cavity and costal cartilage were examined by light and/or scanning electron microscopy. Oral leukoplakia and costochondral hyperplasia occurred with high frequency in all groups treated with DEN. Leukoplakic lesions were found in the palate, tongue, and pharynx; the early change was focal erosion with mild epithelial hyperplasia and inflammatory cell infiltration. Advanced lesions had marked mucosal thickening due to acanthosis, parakeratosis, hyperkeratosis, and submucosal infiltration of lymphocytes and plasma cells. Precancerous lesions were noted in tongue and pharynx. Scanning electron microscopy of tongues revealed destruction of filiform papillae. The incidence of leukoplakic lesions were higher in smoke-exposed hamsters than in controls, but the incidence in vitamin C-supplemented hamsters was low when compared with the smoke-exposed hamsters without vitamin C. Costochondral hyperplasia was initiated by thickening of the perichondrium followed by proliferation of chondrocytes. Costochondral hyperplasia appeared earlier, and the incidence was higher in the vitamin C-supplemented hamsters. It could not be determined whether costochondral hyperplasia was the primary lesion induced by DEN or secondary change.

Animals↗

PubMed1987

Spontaneous tumors in F344/DuCrj rats from 12 control groups of chronic and oncogenicity studies.

The types and incidences of spontaneous tumors in F344/DuCrj rats were examined in 960 males and 959 females served as the control groups of separate twelve 2-year chronic and oncogenicity studies carried out during a 1978-1983 period. The major tumors occurred at more than 5% incidence were leukemia (mononuclear cell), testicular interstitial cell tumor, preputial gland adenoma, pituitary anterior adenoma, thyroid C-cell adenoma, adrenal pheochromocytoma and subcutis fibroma for males, and leukemia, uterine endometrial polyp, pituitary anterior adenoma, thyroid C-cell adenoma and mammary gland adenoma/fibroadenoma in females. Analyses on age-related occurrence of tumors revealed that the incidences of most of the major tumors in males attained already to the plateau between 85 and 97 weeks of age while those in females showed a steep rise during the last interval of observation, 98 to 110 weeks of age. An intralaboratory heterogeneity in incidence was observed in the thyroid C-cell adenoma and the adrenal pheochromocytoma for males, and the anterior pituitary adenoma for females.

Adrenal Gland Neoplasms↗

PubMed1987

[Traumatic spinal subarachnoid hematoma presenting with Brown-Séquard syndrome].

We report a rare case of traumatic spinal subarachnoid hematoma with Brown-Séquard syndrome following hyperextension injury. A 43-year-old man was admitted to our hospital four days after hyperextension cervical injury complaining of nuchal pain, left hemiparesis and dysesthesia of the left arm. On the third hospital day, neurological examination revealed left C2,3 level Brown-Séquard syndrome. High cervical plain CT scan showed a high density area in the left spinal canal from C1 vertebral body level to C2-3 intervertebral level. Emergency operation was performed and a left-sided subarachnoid hematoma was removed. The left C2 and C3 nerve roots were markedly stretched and the cord was shifted to the right. Neither vascular abnormality nor tumor was found and no traumatic change was seen on the cord. The Brown-Séquard syndrome disappeared soon after surgery, but the weakness of the left arm and anesthesia at the level of left C2 dermatome remained until six months after operation. Review of the literature revealed no such a case as the one in which the patient developed a spinal subarachnoid hematoma following hyperextension injury without any preexisting disease or injury of the spine. Brown-Séquard syndrome caused by spinal subarachnoid hematoma was not found on the literature either. So we believe that this is the first report of case of such lesion. The mechanism of subarachnoid clot formation on hyperextension injury may be due to transient dislocation of the spine with tearing of the anterior longitudinal ligament or to crushing of the cord between the ligamentum flavum, which bulged forward on hyperextension, and the posterior aspect of the vertebral body.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Partial purification and characterization of masking protein for beta-type transforming growth factor from rat platelets.

beta-Transforming growth factor (TGF-beta) is stored in platelets and secreted as a high molecular weight latent form associated with a carrier protein of about 440 KD. This carrier protein could be separated from TGF-beta in 1 N acetic acid and could again mask the activity of TGF-beta under neutral conditions. Therefore, it was named the masking protein of TGF-beta. The masking protein was separated from TGF-beta by gel filtration on a Sephacryl S-300 column or by anion-exchanger FPLC on a Mono Q column in the presence of 6 M urea. Partially purified masking protein from rat platelets neutralized the activity of TGF-beta dose-dependently and was effective at 0.3 microgram/ml. This masking protein could also mask the activity of human TGF-beta, suggesting that it was not species specific. The masking protein was a heat- and acid-stable protein, but was inactivated by treatment with dithiothreitol. The Physiological role of the masking protein in the mechanisms of wound healing and liver regeneration is discussed.

Animals↗

PubMed1986

Effects of morphine and methionine-enkephalin on the smooth muscle tonus and the contraction induced by transmural stimulation in the carp (Cyprinus carpio) intestinal bulb.

The effects of morphine and methionine-enkephalin (met-enkephalin) on the smooth muscle tonus and the contraction induced by transmural stimulation were investigated in the isolated intestinal bulb of carp in vitro. Morphine (30 nM-3 microM) and met-enkephalin (3 nM-5 microM) caused dose-dependent non-sustained contraction. Naloxone (10 nM) inhibited the contraction induced by morphine or met-enkephalin in a competitive manner. Tetrodotoxin (400 nM) or atropine (500 nM) did not inhibit the contraction induced by morphine or met-enkephalin. Cooling of the bath fluid from 20 to 10 degrees C decreased nicotine- and transmural stimulation-induced contraction. But met-enkephalin-induced contraction was not affected. Transmural stimulation-induced contraction (3 Hz) was not affected by pretreatment with morphine, met-enkephalin or naloxone. The results demonstrated that morphine or met-enkephalin caused contraction of the smooth muscle directly through the activation of opiate receptors on the smooth muscle cells and neither morphine nor met-enkephalin regulated the cholinergic neurotransmission presynaptically.

Acetylcholine↗

PubMed1986

Are beta-adrenergic receptors in ventricular muscles of carp heart (Cyprinus carpio) mostly the beta-2 type?

The positive inotropic effect of isoproterenol was quantified in the presence of several beta-adrenergic blocking agents in ventricular strips of carp heart. Isoproterenol had a concentration-dependent positive inotropic effect. The effect was markedly inhibited by propranolol and carteolol, but was extremely insensitive to atenolol. Practolol totally failed to alter the effect. These results indicated that the positive inotropic effect of isoproterenol may be mediated by mostly beta-2 adrenergic receptors in ventricular strips of carp heart.

Adrenergic beta-Antagonists↗

PubMed1986

Beta-2 adrenergic receptors are not only for circulating catecholamines in ventricular muscles of carp heart (Cyprinus carpio).

Whether beta-2 adrenergic receptors are only for the circulating catecholamines in isolated ventricular muscles of carp heart was studied. Isoproterenol, epinephrine and norepinephrine had concentration dependent positive inotropic effects. The ED50 values for isoproterenol, epinephrine and norepinephrine were 6.23 +/- 1.9, 87.3 +/- 27.3 and 4500 +/- 580 nM, respectively. Phentolamine did not alter the inotropic effects. Tyramine increases the force of contraction and this action was completely blocked by propranolol and reserpine, but not by atenolol. Norepinephrine levels, in comparison with those of epinephrine, were similar in plasma and higher in ventricular muscles. However, the norepinephrine levels in ventricular muscles of carp heart were markedly lower than those in ventricular muscles of rat heart. These results suggest that ventricular muscles of carp heart contain adrenergic neurons, and that a catecholamine released from the nerve terminals, presumably epinephrine, may stimulate beta-2 adrenergic receptors.

Animals↗

PubMed1986

Presynaptic alpha-adrenoceptor mediated inhibition of the neurogenic cholinergic contraction in the isolated intestinal bulb of the carp (Cyprinus carpio).

The effects of norepinephrine, epinephrine and clonidine on neurogenic cholinergic contraction were examined in the presence of a beta-adrenoceptor blocking agent, carteolol (5 X 10(-6) M), in the isolated intestinal bulb of the carp. Norepinephrine, epinephrine (10(-9)-10(-6) M) and clonidine (10(-8)-10(-5) M) inhibited the contraction induced by low frequency (2 or 5 Hz) transmural stimulation (TMS) without inhibiting the contraction induced by acetylcholine (ACh, 6 X 10(-8)-4 X 10(-7) M). Methoxamine (10(-4) M) and phenylephrine (10(-4) M) showed no such inhibitory effect on the TMS-induced contraction. The inhibitory effects of catecholamines and clonidine were decreased by phentolamine (5.4 X 10(-6) M) and yohimbine (10(-7)-10(-6) M) but not by prazosin (7 X 10(-7)-10(-6) M). Nicotine (10(-6)-10(-4) M) and serotonin (3 X 10(-8)-3 X 10(-6) M) caused contraction of the intestinal bulb indirectly by releasing endogenous ACh. This contraction was inhibited by norepinephrine, epinephrine and clonidine in a concentration-dependent manner. The present results suggest that catecholamines and clonidine inhibit cholinergic transmission via the activation of a presynaptic alpha-adrenoceptor (presumably of alpha-2 type) located on the cholinergic nerve terminals innervating the smooth muscle of the intestinal bulb of the carp.

Animals↗

PubMed1986

Is there functional cholinergic innervation in the frog duodenum (Rana catesbeiana)?

To determine if functional cholinergic innervation occurs in the frog duodenum or not, the effects of exogenous acetylcholine and electrical transmural stimulation, the contractile activity of an acid extract from the frog duodenum, and the distribution of acetylcholinesterase (AChE) activity in the wall of the frog duodenum were investigated. Acetylcholine caused non-sustained contraction in a dose-dependent manner (100 nM-1 mM). The ED50 value was 17 +/- 2.4 microM. Atropine (500 nM) shifted the dose-response curve for acetylcholine parallel to the right. Transmural stimulation of the frog duodenum caused frequency-dependent (0.5-50 Hz) contraction which was not decreased by atropine (500 nM) at all. The acid extract from the frog duodenum caused contraction of a longitudinal muscle strip of guinea-pig ileum but atropine (500 nM) had no significant effect on the contraction. Only a little AChE activity was found in Auerbach's plexus of the frog duodenum compared with that of the rat ileum. These results suggest that a cholinergic nerve is present in the frog duodenum but its physiological significance is very small.

Acetylcholine↗

PubMed1986

Alpha 2-adrenoceptor-mediated contractile response to catecholamines in smooth muscle strips isolated from rainbow trout stomach (Salmo gairdneri).

The type of adrenoceptor involved in the contractile response to catecholamines in smooth muscle strips isolated from rainbow trout stomach was determined. Noradrenaline (10 nM-10 microM) and adrenaline (10 nM-3 microM) caused non-sustained contractions which were markedly decreased by phentolamine (5.4 microM) but not by carteolol (5 microM). Phenylephrine (1 microM-1 mM) was less effective in causing muscle contraction and methoxamine produced no contraction. Clonidine (100 nM-300 microM) caused no mechanical response but inhibited the contraction to noradrenaline or adrenaline but not acetylcholine or 5-hydroxytryptamine. Yohimbine (10 nM-1 microM) decreased the contraction induced by noradrenaline or adrenaline but prazosin (1 microM) did not. Tetrodotoxin (780 nM) partially reduced the contraction induced by noradrenaline or adrenaline but atropine (500 nM) did not. In the presence of atropine (1 microM), electrical transmural stimulation caused frequency-dependent, tetrodotoxin-sensitive contractions. These results suggest that the contractile response induced by noradrenaline or adrenaline is mediated by alpha 2-adrenoceptors. It is also suggested that noradrenaline and adrenaline contract the smooth muscle by direct action and by indirect action through the non-cholinergic excitatory nerve.

Animals↗