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Biomedical subjects

T Kamitani

Publications and source records attributed to T Kamitani.

At least 109 records · Page 6Linked to original sources
PubMed1989

Systemic administration of IL-2 induces lymphokine-activated killer (LAK) cells capable of killing macrophages in various tissues.

Murine lymphokine-activated killer (LAK) cells induced by systemic high-dose recombinant human interleukin 2 (IL-2) administration lysed fresh syngeneic peritoneal macrophages (M phi). LAK cells lysed resident peritoneal M phi and M phi activated in vivo with thioglycollate (TG), Corynebacterium parvum (C. parvum), or Bacillus Calmette-Guérin (BCG). The induction of anti-M phi cytolytic activity was seen in the spleen, liver, lung, lymph nodes and peritoneal cavity, but was not observed in the thymus. Fluorescence analysis revealed that the majority of infiltrated cells in the peritoneal cavity of IL-2-administered mice were Thy-1+, asialo GM1+, L3T4-, Ly2-. Surface marker analysis on peritoneal exudate cells (PEC) from IL-2-administered mice with depletion techniques using antibody (Ab) and complement (C) indicated that Thy-1+, asialo GM1+, L3T4-, Ly 2- cells were responsible for anti-M phi lysis. These studies indicate that the in vivo administration of IL-2 induces LAK cells capable of killing M phi in various tissues.

Animals↗
PubMed1985

Effect of leukotrienes, 12-HETE, histamine, bradykinin, and 5-hydroxytryptamine on in vivo rabbit cerebral arteriolar diameter.

To determine the possible role that leukotrienes (LTs) may play in the regulation of cerebral blood flow, the responses of cerebral arterioles to LTs and 12-hydroxyeicosatetraenoic acid (12-HETE) were studied in vivo in rabbits equipped with a cranial window for direct observation of the microcirculation. Topical application of LTC4, LTD4, or 12-HETE (1.6 X 10(-9)-3.1 X 10(-6) M) neither constricted nor dilated the pial arteries. LTB4 produced only a 5% vasoconstriction at 3.0 X 10(-6) M. However, bradykinin induced dose-dependent arteriolar vasodilation and histamine and 5-hydroxytryptamine induced dose-dependent arteriolar vasoconstriction. Although some LTs have potent vasoconstrictor activity in peripheral tissues and 5-lipoxygenase products have been hypothesized to be mediators of vasospasm after subarachnoid hemorrhage, LTB4, LTC4, LTD4, and 12-HETE apparently are unable to induce significant constriction of the cerebral arterioles in the anesthetized rabbit.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1985

Evidence for a possible role of the brain kallikrein-kinin system in the modulation of the cerebral circulation.

Experiments by others have shown that exogenous bradykinin dilates cerebral arterioles and that the brain contains kininogen and kallikrein, the latter being the enzyme which converts kininogen to bradykinin. The objective of these experiments was to determine if bradykinin produced from endogenous brain kininogen can affect the cerebral microcirculation. Rabbit pial arteriolar diameter was measured with a microscope using the closed cranial window technique. Topical application of bradykinin (10(-8)-10(-5) M) induced a dose-dependent vasodilation (8-46%) which was completely inhibited by the cyclooxygenase enzyme inhibitors indomethacin and meclofenamic acid. Topical application of 1 U of tissue kallikrein per milliliter of artificial cerebrospinal fluid induced 43% dilation, which could be prevented by local treatment with indomethacin or the proteinase inhibitor aprotinin. The action of aprotinin and indomethacin was specific, since aprotinin did not affect the dilation produced by bradykinin, and indomethacin did not affect dilation produced by adenosine. A second application of kallikrein had no effect on cerebral diameter, yet the arterioles still responded normally to exogenous bradykinin, indicating that the first application of kallikrein depleted brain kininogen. We suggest that activation of brain kallikrein and subsequent formation of kinin from brain kininogen may be important in modulation of cerebral blood flow or generation of cerebral edema.

Animals↗
PubMed1985

The hypotensive effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline (FR35447).

The hypotensive effect of FR35447 was comparable to that of prazosin and was more potent than that of hydralazine, but its duration of action was shorter. Repeated administration of FR35447 or prazosin to hypertensive rats for 5 consecutive days induced no significant difference in the intensity or duration of the hypotensive effect. In contrast, marked tachyphylaxis to hydralazine or phentolamine was observed. FR35447 as well as prazosin induced only a transient increase in cardiac output in anesthetized dogs, whereas hydralazine induced a longlasting increase. This difference may contribute to no development of tolerance to FR35447 or prazosin. FR35447 decreased the pressor response to noradrenaline, but not that to angiotensin II or vasopressin in pithed rats, which indicates that FR35447 is an alpha-adrenoceptor antagonist. FR35447 has some selectivity for alpha 2-adrenoceptors, but the selectivity was far less than that of yohimbine. Since FR35447 induced only slight hypotension following intracerebroventricular injection in anesthetized cats, the hypotensive effect of the drug does not appear to be mediated through the central nervous system. Whereas prazosin induced a dose-dependent increase in blood glucose in rats, FR35447 showed no significant effect.

Animals↗
PubMed1984

Inhibitory effect of Cu2+ on nitroglycerin-induced vasodilation.

The mechanism of nitroglycerin-induced vasodilation was examined in isolated arteries. Nitroglycerin relaxed the large coronary artery preferentially whereas nitroprusside and the so-called non-specific vasodilators showed the same activities on both the large and small coronary arteries. Nitroglycerin-induced vasodilation but not the vasodilation induced by the other agents was antagonized markedly by pretreatment with CuSO4. Other metal ions except Fe2+ had no antagonizing effect. The Cu2+-induced antagonism was restored by treatment with sulfhydryl reagents. Nitroglycerin formed inorganic nitrite by non-enzymatic reaction with the tissue sulfhydryl groups; the reaction was also inhibited by Cu2+ . Cu2+ suppressed the membrane stabilizing effect of Ca2+. It seems that nitroglycerin reacts with the sulfhydryl groups on the inner surface of the cell membrane, which may take part in the selectivity of this drug, and subsequently the intermediate(s) formed may activate guanylate cyclase.

Animals↗
PubMed1984

Mechanism(s) of the hypotensive effect of synthetic 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine.

The mechanism of the hypotensive effect of 1-O-octadecyl-2-O-acetyl-glycero-3-phosphorylcholine (C18- AGPC ) was examined. Synthetic C18- AGPC caused dose-dependent hypotension in conscious rats. The activity was almost the same in DOCA and renal hypertensive rats. This suggests that it is not a renin inhibitor. Hypotension also appeared in pithed rats. This suggests that the effect is not due to a central mechanism. Hypotension did not result from platelet aggregation or bronchial constriction. Since C18- AGPC suppressed not only the pressor response to noradrenaline but also to angiotensin II and vasopressin, and furthermore, did not disturb the dose-response curve of noradrenaline in the isolated aorta, the possibility of the agent being an alpha-adrenergic antagonist is ruled out. In the PGF2 alpha-contracted rat aorta. C18- AGPC caused marked vasodilation, which disappeared after removal of the endothelium. Perfusion pressure decreased in the blood-perfused rat hindquarters but not in the Tyrode solution-perfused ones. C18- AGPC induced a positive inotropic effect in isolated rat atrium. The hypotensive effect of synthetic C18- AGPC seems to be mainly due to endothelium-dependent vasodilation.

Adrenergic alpha-Antagonists↗
PubMed1984

Presence of connectin-like protein in white blood cells and platelets.

Connectin is known to be an anchoring protein of actomyosin filaments in skeletal muscle. Attempts were made to extract this protein from white blood cells and platelets in order to investigate its properties. The purified connectin-like protein obtained had a rubbery appearance and was insoluble in water and immobile on SDS gel-electrophoresis. Amino acid composition and electron microscopic features of the protein were similar to those of skeletal muscles. FITC-labeled antibody to the protein showed a positive reaction to the membrane fractions of red cells, white cells and platelets. In moving cells fluorescence was observed not only in pseudopod, but also in whole cytoplasm. No changes in the fluorescence patterns were observed with respect to moving stages or cell types. The presence of the protein beneath the cell membrane was also confirmed electron micrographically.

Amino Acids↗
PubMed1984

Protective effect of FR35447 on experimental cerebral infarction.

The protective effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline [FR35447] on cerebral infarction was examined in animal models. FR35447 in p.o. doses of 1 mg/kg or more caused a marked reduction of arachidonate-induced cerebral infarction in rats. Since FR35447 (10(-6) M) inhibited platelet aggregation induced by adrenaline plus the divalent cation ionophore A23187, as did yohimbine (10(-6) M), the protective effect of FR35447 is presumed to be due to its blocking activity on the alpha 2 adrenoceptors of platelets. However, additional mechanisms appear to participate in the protective effect of FR35447 on cerebral infarction. A ten-day treatment with FR35447 in p.o. doses of 1 to 10 mg/kg/day decreased serum lipid peroxide levels in vitamin E deficient rats, suggesting that FR35447 may have free radical scavenging activity. Moreover, FR35447 (greater than or equal to 10(-5) M) increased red cell deformability. These effects of FR35447 suggest that it may be useful in preventing or treating cerebral infarction.

Animals↗
PubMed1983

[High dose of methotrexate-leucovorin treatment in advanced non-Hodgkin's lymphoma].

High doses of methotrexate (MTX) and leucovorin (LCV) as a rescue treatment were applied to five patients with non-Hodgkin's lymphoma, refractory to standard combination chemotherapy. Two of 5 patients showed a complete remission, and 2 patients showed a partial remission. One patient with massive pleural effusion showed an improvement by the treatment without any severe side effect under monitoring and controlling the dose of MTX. However, the remission duration of the treatment was short; therefore, additive therapy was required of later. From these results we assumed that the high dose of MTX and LCV could be effective for malignant lymphoma being resistant to other combination therapies.

Adolescent↗