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Biomedical subjects

H Hamakawa

Publications and source records attributed to H Hamakawa.

58 records · Page 4Linked to original sources
PubMed1976

[Pharmacological effects of [(octahydro-2-azocinyl)methyl] guanidine(guanazodine): its action mechanism and hypotensive effect].

Cardiovascular effects of guanazodine, a new antihypertensive drug, in anesthetized dogs, rabbits and rats and also isolated atria and arteries were compared with those of guanethidine and bethanidine. Guanazodine caused a sustained decrease in the systemic blood pressure of spontaneously hypertensive rats, renal hypertensive dogs and normal cats. No tachyphylaxis developed when the drug was administered orally to the rats once a day for 10 days. The heart rate decreased. Guanazodine relaxed the cat nictitating membrane, attenuated the positive chronotropic response to sympathetic nerve stimulation in anesthetized dogs and in isolated rabbit aorta to transmural electrical stimulation. Guazazodine potentiated the pressor response to noradrenaline but attenuated the response to tyramine in anesthetized cats. The noradrenaline content of rat hearts was significantly reduced 4 hr or later after the injection of guanazodine, while the content in brains and adrenal glands was unaffected. The LD50 of guanazodine injected intravenously to male rats was 136 +/- 11 mg/kg which was approximately 4 times the value of guanethidine and 7 times the value of bethanidine. It may be concluded that the hypotensive effect of guanazodine is related to adrenergic neuron blocking action, the noradrenaline-depleting action in peripheral tissues is similar to the effect of guanethidine and bethanidine, and that the extent and the duration of the hypotension induced by guanazodine are approximately the same as those with guanethidine but appreciably greater than those with bethanidine. Toxicity and side effects appear to be less with guanazodine than with guanethidine and bethanidine.

Adrenal Glands↗
PubMedDate not supplied

Inhibition of telomerase activity as a measure of tumor cell killing by cisplatin in squamous cell carcinoma cell line.

BACKGROUND: Telomerase is a ribonucleoprotein enzyme which is involved in the maintenance of chromosome ends. Telomerase activity is frequently associated with malignant phenotypes, and it can be considered a ubiquitous tumor marker. In this study we describe an approach for developing in vitro chemosensitivity assays based on the assessment of telomerase activity in squamous cell carcinoma to treatment with anticancer drugs. METHODS: We used A431/CDDP1 and A431/CDDP2, two previously established cisplatin (CDDP)-resistant A431 sublines. These cell lines were not multidrug resistant but specifically resistant to the CDDP drug family. The telomeric repeat amplification protocol (TRAP assay) was used to measure telomerase activity in CDDP-resistant cell lines and to examine the effect of CDDP and other anticancer drugs on enzyme levels. We next analyzed the relations between telomerase activity and cytotoxic effects of CDDP in human squamous cell carcinoma (HSC2, HSC3, HSC4 and KB cell lines). RESULTS: The telomerase activity of A431/CDDP1 and A431/CDDP2 was significantly higher than that of the parent A431 cell (A431/P) treated with CDDP and carboplatin at IC(50). On the other hand, telomerase activity in these cell lines was not influenced by treatment with 5-fluorouracil, bleomycin, Adriamycin or taxol. The regression line derived from the quantitative analysis of the telomeric ladder versus IC(50) of CDDP concentrations was analyzed. Telomerase activity was found to be positively correlated with the IC(50) values for CDDP. CONCLUSIONS: The results of the present studies on in vitro squamous cell carcinoma cell lines indicate that telomerase activity inhibition can be used as a marker of tumor cell killing by CDDP. Therefore, the present investigation provides a rational basis for an in vitro chemosensitivity assay based on telomerase activity evaluation.

Antineoplastic Agents↗
PubMedDate not supplied

Effects of cold preservation on the lung mechanical properties in rats.

In lung transplantation, cold preservation is an important process. However, the mechanical changes in the airway and tissue during cold preservation, especially before reperfusion, are unknown. To test the hypothesis that the mechanical changes in the airway and lung parenchyma start during cold preservation, we investigated the mechanical properties of the rat lung as a whole organ and in excised lung strips. In the 0 h group, the lungs were not preserved. In the 9 and 24 h group, the lungs were preserved for 9 and 24 h at 4 degrees C. After preservation, we evaluated the static compliance (Csta) of the whole lung as obtained from the pressure volume curves (n=5 in each group). Also, we measured the input impedance taken by a computer-controlled small-animal ventilator (n=9 in each group). All data were analyzed using a homogeneous linear model, which includes airway resistance (Raw), tissue elastance (H), and tissue resistance (G). Hysteresivity (eta) was calculated as G/H. Moreover, the tissue elasticity (Eqs) obtained from the quasi-static stress-strain curves was compared. There was no significant difference in Csta among the three groups. Raw was significantly lower in the 24 h group than in the 0 h group (p<0.01). Eqs was significantly higher in the preserved groups than in the 0 h group (p<0.01). These results demonstrated that the changes in the three mechanical properties of the airway and the tissue started within 9 h of preservation.

Animals↗