Biomedical subjects

I Cakici

Publications and source records attributed to I Cakici.

26 records · Page 2Linked to original sources

PubMed1994

Hypoglycaemic effect of Momordica charantia extracts in normoglycaemic or cyproheptadine-induced hyperglycaemic mice.

The hypoglycaemic effect of orally administered extracts of Momordica charantia L. fruits was examined in normoglycaemic or cyproheptadine-induced hyperglycaemic mice. The aqueous extract reduced the fasting glucose levels of hyperglycaemic or normoglycaemic mice. However, the ethanol extract did not affect the fasting or nonfasting glucose levels significantly in both groups of mice. There was no significant difference between the glucose-loaded and glucose-loaded plus aqueous extract given group. On the other hand, oral glucose-loading of the cyproheptadine-induced hyperglycaemic animals reduced the fasting glucose levels significantly. These results showed that aqueous extract of M. charantia fruits has a hypoglycaemic activity without improving the tolerance to glucose in cyproheptadine-induced diabetic mice.

Animals↗

PubMed1993

Epithelium-dependent responses of serotonin in a co-axial bioassay system.

Serotonin (10(-6) - 10(-4) M) produced relaxations in a concentration-dependent (at 10(-6) and 10(-5) M concentrations) manner followed by a contraction (at 10(-4) M concentration) in a co-axial system, which consisted of guinea-pig trachea as a donor organ for epithelial derived-relaxing factor(s) and phenylephrine-precontracted rat anococcygeus muscle as assay tissue. Serotonin produced a concentration-dependent contraction only in precontracted rat anococcygeus muscle mounted alone or mounted co-axially within epithelium-denuded trachea. Indomethacin (10(-6) M) significantly inhibited the initial relaxations (from 25.1 +/- 7.8 to 7.8 +/- 5.0% and from 35.6 +/- 8.7 to 10.4 +/- 8.3% at 10(-6) and 10(-5) M concentrations of serotonin), but did not affect the contraction. Imipramine (10(-8) M) and hydrocortisone (3 x 10(-5) M) reduced the initial relaxations (from 20.5 +/- 1.6 to 3.8 +/- 1.5% and from 32.1 +/- 6.4 to 18.9 +/- 3.9% at 10(-6) M and 10(-5) M concentrations of serotonin, respectively) and also converted the serotonin (10(-4) M)-induced contraction to a relaxation. In the co-axial system with trachea from guinea-pigs previously sensitized with i.p. injected egg-ovalbumin, the serotonin-induced biphasic response was converted to a contractile response only after ovalbumin challenge. Histopathologic changes were observed in the epithelium of challenged tracheas taken from sensitized guinea-pigs and alterations of serotonin-induced epithelium-dependent responses were attributed to the morphological and/or functional damage of tracheal epithelium caused by ovalbumin challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Antinociceptive effects of H1- and H2-antihistaminics in mice.

1. Two methods were used to study the analgesic effects of subcutaneous injections of antihistaminics in mice: the p-benzoquinone(PBQ)-writhing test and caudal compression test. 2. Mepyramine, lupitidine (SKF 93479), and famotidine produced significant antinociceptive effects dose-dependently, during both the PBQ-writhing and caudal compression tests. 3. However, ranitidine did not reveal any antinociceptive effect. 4. Icotidine (SKF 93319) produced significant antinociception and also augmented the analgesic effect of morphine, on the caudal compression test. 5. However, mepyramine, famotidine, and lupitidine did not affect morphine-induced analgesia on the caudal compression test and displayed a nonsignificant potentiation on morphine-induced analgesia in the PBQ-writhing test.

Analgesics↗

PubMed1992

Biphasic effect of histamine on spontaneously beating rat atria.

1. Effect of histamine (HA) (10(-4)-10(-2) M) on spontaneously beating rat atrium was investigated. HA produced a biphasic effect which is composed of an initial negative chronotropy followed by a positive chronotropic phase, at each single dose. 2. At a submaximal dose of HA (3 x 10(-3) M) we have investigated the effects of some antagonists on the biphasic effect profile. 3. Propranolol (10(-7) M) depressed the secondary phase by abolishing the biphasic pattern of the effect of HA leading it to a monophasic one (negative chronotropy). 4. On the other hand, combination with atropine (10(-7) M) was shown to reduce the negative inotropic effect (in the secondary phase) which was produced by HA in the presence of propranolol. 5. The initial negative chronotropic phase was significantly enhanced by propranolol and reduced by pheniramine (10(-6) M). 6. Pheniramine also potentiated the positive chronotropy at the secondary phase of the response, but cimetidine (10(-4) M) has no significant effect on both phases. 7. Theophylline (10(-4) M) abolished the initial negative chronotropic phase, but did not influence the secondary phase. Dipyridamole (10(-5) M) did not affect the secondary phase of the response of HA, but increased the initial negative chronotropic effect.

Animals↗

PubMed1989

Temperature-dependent specific desensitization in the rat anococcygeus muscle to angiotensin II.

The effect of angiotensin II (A II) on isolated rat anococcygeus muscle was investigated. A II, when used submaximally (4 X 10(-9) mol/l), produced a rapid contraction of the rat anococcygeus muscle. However, a profound tachyphylaxis developed with repeated administrations. This tachyphylaxis is specific in nature, since the tissue responded normally to noradrenaline even after the establishment of a complete tachyphylaxis to the peptide. Incubation with phentolamine or indometacin had no effect on the A II-induced tachyphylaxis. On the other hand, a marked prevention of tachyphylaxis was obtained by lowering the bath temperature to 31 or 25 degrees C. These results indicate that neither noradrenaline nor prostaglandin release participate in the development of tachyphylaxis to A II in rat anococcygeus muscle, and this tachyphylaxis can be prevented by lowering the temperature of the bath solution.

Angiotensin II↗

PubMed1987

Digoxin-induced cardiac toxicity in the anaesthetized guinea-pigs and effect of heparin infusion.

We have examined the effects of heparin infusion on the arrhythmias induced by digoxin. Digoxin treatment consisted of 0.6 mg kg-1 given i.v. 15 min after the beginning of heparin infusion. Heparin infusions (1.7 IU, 3.4 IU and 6.8 IU kg-1 min-1) were begun 15 min before digoxin injection and continued for another 30 min. ECG, blood pressure, heart rate and arrhythmias were recorded starting 15 min before and continuing for 60 min after the digoxin injection. Heparin at the infusion rates of 3.4 IU and 6.8 IU kg-1.min-1 reduced significantly the arrhythmia scores. On the other hand, heparin did not significantly alter the arterial blood pressure and heart rate values affected by digoxin.

Animals↗

PubMedDate not supplied

Effects of cyclooxygenase and lipoxygenase inhibitors on digoxin-induced arrhythmias and haemodynamics in guinea-pigs.

Effects of cyclooxygenase and lipoxygenase inhibitors of digoxin-induced arrhythmias and haemodynamics were studied in guinea-pigs. ECG, mean arterial blood pressure heart rate, pressure rate index and arrhythmias were recorded, starting 15 min before digoxin administration and continuing for 30 min afterwards. The cyclooxygenase inhibitor aspirin (50 mg kg-1) and the dual cyclooxygenase/lipoxygenase inhibitor BW 755C (0.25-10.0 mg kg-1) were found to produce a significant protection against the arrhythmias, whereas aspirin (100 mg kg-1) and CGS 8515 were found to be ineffective. SK&F 104 353, a potent and selective peptidoleukotriene receptor antagonist significantly attenuated the arrhythmias and mortality in a dose-dependent manner. It is concluded that production of both cyclooxygenase and lipoxygenase metabolites could favour the occurrence and/or the maintenance of digoxin-induced cardiac toxicity.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

PubMedDate not supplied

Synergism between UK 38485 and ICI 185282 against digoxin-induced arrhythmias in guinea-pigs.

In this study, the combination of a thromboxane synthetase inhibitor (UK 38485) and a thromboxane receptor antagonist (ICI 185282) was tested for an interaction of potential therapeutic importance and the effect of acetylsalicylic acid pretreatment on this combination was evaluated in digoxin-induced arrhythmias in guinea-pigs. Drug treatments at the dose combinations used (ICI 185282: 0.2 mg/kg + 0.2 mg/kg/hr + UK 38485 0.1 mg/kg/hr and ICI 185282: 2 mg/kg + 2 mg/kg/hr + UK 38485 1 mg/kg/hr) markedly reduced the incidence of ventricular fibrillation, mortality rate and arrhythmia score. Pretreatment with acetylsalicylic acid plus drug combination resulted in a dose-dependent increase in mortality rate and arrhythmia score. The increase in mean arterial blood pressure, observed after digoxin administration, was inhibited by the combination therapy. Although heart rate values were increased, the computed pressure-rate index remained unchanged when compared with the control group. These data suggest that the combined treatment with a thromboxane synthetase inhibitor and a thromboxane receptor antagonist provides a better protection against digoxin intoxication than with either agent alone. Furthermore, the results illustrate that formation of cyclooxygenase metabolites of arachidonic acid plays an important role in this action.

Animals↗