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T Kitazawa

Publications and source records attributed to T Kitazawa.

At least 91 records · Page 5Linked to original sources
PubMed1990

Desensitization and muscarinic re-sensitization of force and myosin light chain phosphorylation to cytoplasmic Ca2+ in smooth muscle.

In alpha-toxin-permeabilized guinea-pig ileum smooth muscle, a step increase in Ca2+ caused a rapid rise in force and myosin light chain (LC20) phosphorylation, followed by their spontaneous decline to a low steady level even though Ca2+ remained constant. Carbachol resensitized the muscles to Ca2+, causing an increase in both the steady state force and LC20 phosphorylation at constant Ca2+. In beta-escin permeabilized preparations, calmodulin and okadaic acid converted the phasic responses to Ca2+ to more tonic ones. We conclude that Ca2(+)-sensitivity of force is modulated through changes in LC20 kinase/phosphatase activity ratio by Ca2+ itself (desensitization) and by agonists (sensitization).

Animals↗
PubMed1990

Hepatic vein reconstruction for preserving remnant liver function.

Hepatic malignancies often infiltrate to the major hepatic vein. Recently, we performed hepatic resection combined with hepatic vein reconstruction for preserving remnant liver function in three such patients. One patient had a saphenous vein graft. Postoperative liver function of the patients who underwent hepatic vein reconstruction was compared with those of eight patients who underwent hepatic resection of segments VII and VIII. The right hepatic vein in four of them was resected and in the remaining four was preserved by skeletalization using an ultrasonic aspirator. Although four patients with right hepatic vein resection showed severe lowering of liver function after surgery, the postoperative course of patients with preservation or reconstruction of the right hepatic vein maintained good liver function. Liver regeneration of three patients with hepatic vein reconstruction was good on computed tomography. Besides this report, to our knowledge, there is no other report of hepatic vein reconstruction for preserving the remnant liver function. Problems with hepatic resection combined with hepatic vein reconstruction are discussed. We conclude that hepatic vein reconstruction is one of the means for extending indication of the malignant tumor resection of the liver.

Adult↗
PubMed1990

Agonist-dependent modulation of Ca2+ sensitivity in rabbit pulmonary artery smooth muscle.

The effects of the stable thromboxane analogue U46619, the alpha 1-adrenergic agent phenylephrine and depolarization with high K+ on cytoplasmic Ca2+ ([Ca2+]i) and force development were determined in rabbit pulmonary artery smooth muscle. Following stimulation with each of the excitatory agents, the time course of the [Ca2+]i/force relationship described counter-clockwise hysteresis loops with the rise and fall in [Ca2+]i leading, respectively, contraction and relaxation. The rank order of the force/[Ca2+]i ratios evoked by the different methods of stimulation was: U46619 greater than phenylephrine high K+. The difference between the actions of U46619 and phenylephrine was due to the lesser Ca2(+)-releasing and greater Ca2(+)-sensitizing action of U46619. Both U46619 and phenylephrine also released intracellular Ca2+ in intact (non-permeabilized) preparations. The effects of the two agonists on force, at constant free cytoplasmic [Ca2+] maintained with EGTA, were also determined in preparations permeabilized with staphylococcal alpha-toxin, in which intracellularly stored Ca2+ was eliminated with A23187. Sensitization of the contractile response to Ca2+ by agonists was indicated by the contractile responses of permeabilized muscles to U46619 and to phenylephrine, in the presence of constant, highly buffered [Ca2+]i. These contractions were inhibited by GDP [beta S] and could also be elicited by GTP. We conclude that, in addition to changing [Ca2+]i, pharmacomechanical coupling can also modulate contraction by altering the sensitivity of the regulatory/contractile apparatus of smooth muscle to [Ca2+]i, through a G-protein-coupled mechanism.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Ca2+ entry blockers, force staircase and the onset of the positive inotropic action of cardiotonic steroids in isolated cardiac muscle.

1. Effects of alterations of Ca2+ fluxes on the force staircase phenomenon and on the positive inotropic action of strophanthidin or ouabain were examined in left atrial muscle preparations isolated from rabbit or rat heart. 2. The organic Ca2+ entry blockers converted the positive force staircase observed in rabbit heart to the negative staircase; however, Ni2+, Co2+ or a reduction of the extracellular Ca2+ concentration which reduces Ca2+ influx via the Na+/Ca2+ exchange mechanism as well as via the Ca2+ channels, failed to convert the force staircase. 3. All of these interventions or ryanodine, which inhibits Ca2+ release from the sarcoplasmic reticulum, delayed the onset of the positive inotropic effect of strophanthidin or ouabain without reducing the peak inotropic effect. 4. These results indicate that either Ca2+ antagonists reduce the Na+ influx in addition to reducing Ca2+ influx, or Ca2+ influx per se and not the Na+ influx is important for the staircase phenomenon, and that intracellular Ca2+ accumulation plays an important role in the early phase of the positive inotropic effect of the cardiotonic steroids.

Animals↗
PubMed1990

Effects of some autonomic drugs and neuropeptides on the mechanical activity of longitudinal and circular muscle strips isolated from the carp intestinal bulb (Cyprinus carpio).

1. The mechanical responses to some autonomic drugs and neuropeptides of longitudinal muscle (LM) and circular muscle (CM) strips isolated from the carp intestinal bulb were investigated in vitro. 2. Acetylcholine and carbamylcholine caused concentration-dependent transient contraction of both LM and CM strips. Tetrodotoxin had no effect, but atropine selectively decreased the contractile responses to acetylcholine and carbamylcholine. 3. Excitatory alpha-2 and inhibitory beta adrenoceptors were present in both LM and CM strips. 4. 5-Hydroxytryptamine (5-HT) caused concentration-dependent contraction of both LM and CM strips. Tetrodotoxin, atropine and methysergide decreased the contractile responses to 5-HT. 5. Some neuropeptides (angiotensin I, angiotensin II, bombesin, bradykinin, neurotensin, somatostatin and vasoactive intestinal polypeptide) did not cause any mechanical response (contraction or relaxation) in either smooth muscle strip. 6. Substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) caused contraction of both LM and CM strips. However, the time course of the contraction in LM was different from that in CM. The order of potency was NKA greater than SP greater than NKB in LM strips and NKA greater than SP much greater than NKB in CM strips. In LM strips, the contractile responses to tachykinins were unaffected by spantide and methysergide, but partly decreased by tetrodotoxin and atropine. On the other hand, the contractile responses of CM strips were unaffected by tetrodotoxin, atropine, methysergide and spantide. 7. Dynorphin (1-13) (DYN), leucine-enkephalin (L-Enk) and methionine-enkephalin (M-Enk) caused concentration-dependent contraction of both LM and CM strips. The order of potency was DYN greater than M-Enk greater than L-Enk. Naloxone selectively decreased the responses to opiate peptides. 8. The present results indicate that acetylcholine, carbamylcholine, catecholamines, 5-HT, tachykinins (SP, NKA and NKB) and opiate peptides (DYN, L-Enk and M-Enk) affect the mechanical activity of LM and CM strips isolated from the carp intestinal bulb through their specific receptors.

Animals↗
PubMed1990

Presence of four tachykinins in an acid extract of the carp intestinal bulb (Cyprinus carpio).

1. The pharmacological and chemical properties of substance P-like peptides isolated from an acid extract of the carp intestinal bulb were examined using guinea-pig ileum longitudinal smooth muscle. 2. On a Sephadex G25 column (3 x 96 cm), smooth muscle contracting material was eluted as two peaks (fraction-1 and fraction-2). The molecular weight of the fraction-1 was estimated to be 2300 and that of the fraction-2 to be 1530. 3. The pharmacological properties of the contracting materials in fraction-1 and fraction-2 resembled those of substance P and neurokinin A. 4. The susceptibility of the contracting activity of fraction-1 to proteolytic enzymes resembled that of physalaemin but, on the other hand, the susceptibility of that of fraction-2 resembled those of eledoisin and neurokinin A. 5. Ion-exchange chromatography on sulfopropyl-Sephadex C25 indicated the presence of one contracting material in fraction-1 and three contracting materials in fraction-2. The elution positions of four materials were different from that of substance P. 6. These results indicate that four tachykinins different from substance P are present in an acid extract of the carp intestinal bulb.

Amino Acid Sequence↗
PubMed1990

The mechanism of accelerated corneal epithelial healing by human epidermal growth factor.

The effect of biosynthetic human epidermal growth factor (hEGF) was investigated on a 10-mm diameter corneal epithelial defect model in rabbits. Topical application of over 10 micrograms/ml of hEGF five times a day significantly enhanced the epithelial healing rate, in a dose-dependent manner. The maximum healing rate was observed in eyes treated with 20 micrograms/ml of hEGF (1.59 +/- 0.26 mm2/h), whereas application of less than 5 micrograms/ml of hEGF did not increase the rate of epithelial regeneration compared statistically with control vehicles (1.03 +/- 0.24 mm2/h). S-phase analysis indicated that hEGF treatment induced a high rate of epithelial replication, particularly near the limbal region, during 12 to approximately 24 hours after wounding, followed by massive cell replication from 1 mm behind the leading edge through the limbus during 24-48 hours. The change in number and distribution of S-phase cells thereafter did not essentially differ between hEGF-treated and control groups. In concordance with the S-phase analysis, there was a statistically significant increase in the DNA content in regenerating epithelium at 48 and 72 hours in the hEGF-treated group. These findings indicate that hEGF-induced acceleration of large corneal epithelial wound healing is associated with about twofold cell replication in the regenerating epithelium during 24 to approximately 48 hours after wounding. It is concluded that cell proliferation induced by hEGF, particularly that in limbal and peripheral corneal epithelial cells, may play an important role in accelerating epithelial healing.

Administration, Topical↗
PubMed1989

Cytosolic heparin inhibits muscarinic and alpha-adrenergic Ca2+ release in smooth muscle. Physiological role of inositol 1,4,5-trisphosphate in pharmacomechanical coupling.

In order to test the physiological significance of inositol 1,4,5-trisphosphate (InsP3) in pharmacomechanical coupling, we have utilized two near-physiological systems, in which relatively high molecular weight solutes can be applied intracellularly and receptor coupling is retained: beta-escin permeabilization and reversible permeabilization. We showed that in smooth muscle permeabilized with beta-escin, one of the saponin esters, alpha 1-adrenergic (phenylephrine) and muscarinic (carbachol) agonists, as well as caffeine and InsP3, cause contractions mediated by Ca2+ release. These contractions were calmodulin-dependent and blocked by depletion of Ca2+ stored in the sarcoplasmic reticulum. Intracellular heparin (Mr = about 5000), a blocker of InsP3 binding to its receptor and a specific inhibitor of InsP3-induced Ca2+ release in smooth muscles, inhibited the responses to the agonists and to InsP3, but not those to caffeine, nor did it block the enhanced contractile response to cytoplasmic Ca2+ induced by agonists and by GTP gamma S. Neomycin blocked Ca2+ release induced by carbachol, but not by caffeine. In reversibly permeabilized ileum smooth muscle cells, loaded with Fura-2 acid and heparin, the intracellular heparin inhibited Ca2+ release and contractions induced by carbachol in Ca2+-free, high K+ solution. Heparin did not inhibit the high K+ contractions (with 1.2 mM Ca2+) and had no significant inhibitory effects on carbachol-induced responses in the presence of extracellular Ca2+. These results, obtained under near-physiological conditions, support the conclusion that InsP3 is the major physiological messenger of the Ca2+ release component of pharmacomechanical coupling, but not of the components mediated by Ca2+ influx or by potentiation of the contractile response to Ca2+.

Animals↗
PubMed1989

Receptor-coupled, permeabilized smooth muscle. Role of the phosphatidylinositol cascade, G-proteins, and modulation of the contractile response to Ca2+.

alpha-Adrenergic (phenylephrine) and muscarinic (carbachol) agonists and inositol 1,4,5-trisphosphate caused calcium release and contractions in smooth muscle strips permeabilized with Staphylococcus aureus alpha-toxin. The responses to phenylephrine and carbachol required or were potentiated by added GTP and could be inhibited by GDP beta S. GTP and phenylephrine also increased the contractile response of permeabilized portal vein smooth muscle to cytoplasmic Ca2+. We conclude that while the G-protein-coupled phosphatidylinositol cascade, through inositol 1,4,5-trisphosphate-induced calcium release, is a major mechanism of pharmacomechanical coupling, a second G-protein-mediated pathway that modulates the calcium sensitivity of the regulatory contractile proteins also exists.

Animals↗
PubMed1989

Histamine directly acts on beta-adrenoceptors as well as H1-histaminergic receptors, and causes positive inotropic effects in isolated ventricular muscles of carp heart (Cyprinus carpio).

1. The mechanism for positive and negative inotropic effects of histamine was studied in electrically stimulated ventricular strips of carp heart. 2. A high concentration of histamine (1 mM) caused a transient negative, and subsequent positive inotropic effects. The positive effect was significantly reduced by pyrilamine, diphenhydramine or dl-propranolol, but was not affected by cimetidine or d-propranolol. 3. Prior treatment with reserpine significantly decreased epinephrine and norepinephrine contents in ventricular muscles, and also almost completely abolished the positive inotropic effect caused by tyramine; however, this treatment failed to affect the positive inotropic effect of histamine. 4. The transient negative inotropic effect was reduced by neither atropine, diphenhydramine, pyrilamine nor cimetidine, and potentiated by pyrilamine. 5. These results suggest that the positive inotropic effect of histamine observed in the ventricular muscle of carp heart is mediated by a direct stimulation of both H1-receptors and beta-adrenoceptors. The negative inotropic effect is unrelated to either cholinergic or histaminergic receptor stimulation.

Animals↗
PubMed1989

The roles of alpha- and beta-adrenoceptors in the chronotropic responses to norepinephrine in carp heart (Cyprinus carpio).

1. The chronotropic effect of norepinephrine was studied in isolated spontaneously beating atrial preparations of carp (Cyprinus carpio) heart. 2. Norepinephrine, 0.1 microM, caused a positive chronotropic effect, while at 1 microM it caused either a positive or a negative chronotropic effect. The positive chronotropic effect, observed in 13 preparations, was potentiated by phentolamine and almost completely blocked by propranolol. 3. The negative chronotropic effect observed in the other 5 preparations was greater in the presence of propranolol, reduced by phentolamine and not affected by atropine. 4. These results indicate that alpha- and beta-adrenoceptors may coexist, mediating the negative and positive chronotropic effects, respectively, in isolated atrial preparations of carp heart.

Animals↗
PubMed1989

5-Hydroxytryptamine is a possible neurotransmitter of the non-cholinergic excitatory nerves in the longitudinal muscle of rainbow trout stomach (Salmo gairdneri).

1. The neurotransmitter of the non-cholinergic excitatory nerves in the rainbow trout stomach was identified on the basis of the pharmacological properties of the contractile responses to transmural stimulation (TMS) and nicotine. 2. TMS caused tetrodotoxin-sensitive contractions of rainbow trout stomach strips in a frequency-dependent manner (0.5-50 Hz). Atropine (1 microM) significantly decreased the contractile response to low-frequency stimulation (0.5-2 Hz), but did not affect that to high-frequency stimulation (3-20 Hz). 3. The atropine-resistant contractile response to TMS (20 Hz) was unaffected by hexamethonium (100 microM), phentolamine (5.4 microM), pyrilamine (1 microM), naloxone (1 microM) or substance P-induced desensitization. 4. 5-Hydroxytryptamine (5-HT, 3 nM-3 microM) caused atropine-resistant contractions in a concentration-dependent manner. In the presence of atropine, methysergide (1 microM) decreased the contractile responses to TMS and 5-HT. 5. Nicotine (3 microM-500 microM) induced atropine-resistant contractions that were completely abolished by tetrodotoxin or hexamethonium. Also methysergide inhibited the contractile responses to nicotine. 6. An acid extract of rainbow trout stomach exhibited atropine-resistant contractions that were decreased by methysergide, in both rainbow trout stomach and guinea-pig ileum longitudinal smooth muscle preparations. 7. The present results indicate that, in longitudinal muscle strips of the rainbow trout stomach, 5-HT is one of the mediators (neurotransmitters) of the non-cholinergic excitatory contractions induced by TMS and nicotine.

Adenosine Triphosphate↗
PubMed1989

Multiplicity of spontaneous lung tumors in CD-1 mice.

The multiplicity of the spontaneous lung tumor in CD-1 mice was investigated in 413 males from 6 different control groups of 2-year carcinogenicity studies with agrochemicals. Among a total of 152 lung tumor bearers, 95 (62.5%) were seen with 1 nodule, 36 (23.7%) with 2 nodules, and 14 (9.2%) with 3 nodules. Three males bore 4 nodules and each of 5, 7, 9 and 10 nodules was seen in one male, respectively. In one control group 20 out of 30 lung tumor bearers had 2 or more nodules presenting a significant heterogeneity among the control groups in terms of the multiplicity of lung tumor nodule.

Animals↗
PubMed1989

[Multiple intracerebral hemorrhages immediately after surgical excision of middle fossa arachnoid cysts and evacuation of chronic subdural hygroma. Case report].

A 49-year-old male was hospitalized with a 1-month history of persistent headache and vomiting. Computed tomography (CT) revealed left middle fossa arachnoid cysts and a chronic subdural hygroma. The cysts were excised after evacuation of the subdural hygroma. Postoperatively, the patient did not regain consciousness and CT showed multiple intracerebral hemorrhages in both the supra- and infratentorial spaces. Three months postoperatively, he was discharged with mental deficits and right hemiparesis. A review of the literature indicates that the possible pathogenic mechanism in this case was a sudden increase in cerebral blood flow due to faulty autoregulation. This devastating complication may have been avoided by simple drainage of the subdural hygroma, perhaps with the addition of cyst-peritoneal shunting.

Arachnoid↗
PubMed1988

Inositol trisphosphate, calcium and muscle contraction.

The identity of organelles storing intracellular calcium and the role of Ins(1,4,5)P3 in muscle have been explored with, respectively, electron probe X-ray microanalysis (EPMA) and laser photolysis of 'caged' compounds. The participation of G-protein(s) in the release of intracellular Ca2+ was determined in saponin-permeabilized smooth muscle. The sarcoplasmic reticulum (SR) is identified as the major source of activator Ca2+ in both smooth and striated muscle; similar (EPMA) studies suggest that the endoplasmic reticulum is the major Ca2+ storage site in non-muscle cells. In none of the cell types did mitochondria play a significant, physiological role in the regulation of cytoplasmic Ca2+. The latency of guinea pig portal vein smooth muscle contraction following photolytic release of phenylephrine, an alpha 1-agonist, is 1.5 +/- 0.26 s at 20 degrees C and 0.6 +/- 0.18 s at 30 degrees C; the latency of contraction after photolytic release of Ins(1,4,5)P3 from caged Ins(1,4,5)P3 is 0.5 +/- 0.12 s at 20 degrees C. The long latency of alpha 1-adrenergic Ca2+ release and its temperature dependence are consistent with a process mediated by G-protein-coupled activation of phosphatidylinositol 4,5 bisphosphate (PtdIns(4,5)P2) hydrolysis. GTP gamma S, a non-hydrolysable analogue of GTP, causes Ca2+ release and contraction in permeabilized smooth muscle. Ins(1,4,5)P3 has an additive effect during the late, but not the early, phase of GTP gamma S action, and GTP gamma S can cause Ca2+ release and contraction of permeabilized smooth muscles refractory to Ins(1,4,5)P3. These results suggest that activation of G protein(s) can release Ca2+ by, at least, two G-protein-regulated mechanisms: one mediated by Ins(1,4,5)P3 and the other Ins(1,4,5)P3-independent. The low Ins(1,4,5)P3 5-phosphatase activity and the slow time-course (seconds) of the contractile response to Ins(1,4,5)P3 released with laser flash photolysis from caged Ins(1,4,5)P3 in frog skeletal muscle suggest that Ins(1,4,5)P3 is unlikely to be the physiological messenger of excitation-contraction coupling of striated muscle. In contrast, in smooth muscle the high Ins(1,4,5)P3-5-phosphatase activity and the rate of force development after photolytic release of Ins(1,4,5)P3 are compatible with a physiological role of Ins(1,4,5)P3 as a messenger of pharmacomechanical coupling.

Animals↗
PubMed1988

Evidence that a substance P-like peptide mediates the non-cholinergic excitatory response of the carp intestinal bulb (Cyprinus carpio).

The participation of substance P in the noncholinergic contraction induced by transmural stimulation (TMS) of the carp intestinal bulb was examined. In the presence of atropine, substance P caused the contraction of carp intestinal bulb smooth muscle in a concentration dependent manner (1 nmol/l - 1 mumol/l). The EC50 value was 28 +/- 7 nmol/l (n = 6). Substance P-induced desensitization (1 mumol/l for 15 min), decreased the response to substance P and the atropine-resistant contraction induced by TMS (20 Hz) selectively. In contrast, in the absence of atropine, the contraction induced by TMS (20 Hz) was slightly attenuated with the substance P-induced desensitization. The acid extract obtained from the carp intestinal bulb contained a smooth muscle excitatory material whose pharmacological properties were consistent with those of substance P. The present results indicate that a substance P-like peptide is present in the carp intestinal bulb which is involved in the non-cholinergic contraction induced by TMS.

Acetylcholine↗
PubMed1988

Contractile response to substance P in isolated smooth muscle strips from the intestinal bulb of the carp (Cyprinus carpio).

1. The effect of substance P on the mechanical activity of carp intestinal bulb smooth muscle was investigated in vitro. 2. Bath-applied substance P (1 nM-1 microM) caused concentration-dependent contraction of the smooth muscle. The EC50 value was 20 +/- 3 nM (N = 13). 3. Pretreatment with tetrodotoxin (780 nM) or atropine (500 nM) partially decreased the contractile response to substance P, while methysergide (3 microM) did not decrease the response. 4. The contractile response to substance P was not decreased by [D-Pro2, D-Trp7.9]-substance P or [D-Pro4, D-Trp7.9]-substance P (4-11) pretreatment (10 microM for 5 min). 5. Exposure of the intestinal bulb to substance P (100 nM and 1 microM for 15 min) decreased the response to subsequent application of substance P, physalaemin and eledoisin in a concentration dependent manner, while the contractile response to acetylcholine or methionine-enkephalin was not affected. 6. Exposure of the intestinal bulb to physalaemin and eledoisin (100 nM for 15 min) decreased the response to subsequent application of substance P. 7. The above results indicate that substance P causes the contraction of the carp intestinal bulb smooth muscle through its direct action on the smooth muscle and its indirect action through enteric cholinergic nerves. Long-term exposure to substance P causes desensitization of the preparation to substance P, physalaemin and eledoisin at the receptor level.

Acetylcholine↗