Occurrence of hyperglycemia and hypoglycemia in premature and malnourished premature infants during glucose infusion in the first 48 hours of life.
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Blood Glucose↗
Biomedical subjects
M Tuncer
Publications and source records attributed to M Tuncer.
Comparison of the effect of endothelium on the responses to sumatriptan in rabbit isolated iliac, mesenteric and carotid arteries.
The contractions induced by the 5-hydroxytryptamine (5-HT) and 5-HT1-like receptor agonist sumatriptan in open ring segments of rabbit iliac, mesenteric and common carotid arteries were studied isometrically in vitro. The alteration of the responses by removal of the endothelium and by inhibitors of nitric oxide synthase and cyclooxygenase was investigated. 5-HT induced concentration-dependent contractions of all these three arterial segments. Sumatriptan did not induce any contraction of quiescent mesenteric and iliac arteries, but when a moderate tone was given with a threshold concentration of prostaglandin F2 alpha, it elicited contractions of both arteries (Emax values for sumatriptan in mesenteric and iliac arteries were 84.7% and 29.7% of the phenylephrine maximal effect and EC50 values were 0.22 +/- 0.14 and 0.33 +/- 0.06 microM, respectively). Sumatriptan had no contractile effect at all in carotid arteries in which 5-HT-induced contractions seemed to be mediated by 5-HT2 receptors only. Removal of the endothelium did not affect the responses to 5-HT in iliac, mesenteric and carotid arteries. The contractions induced by sumatriptan were not influenced by removal of the endothelium in the mesenteric artery, while sumatriptan responses were potentiated in the endothelium-denuded preparations of the iliac artery (Emax = 50.8% of the phenylphrine maximal effect; EC50 = 0.46 microM). L-NG-monomethyl arginine (100 microM), a nitric oxide synthase inhibitor, also potentiated the sumatriptan responses in the endothelium-intact segments of the iliac artery. Indomethacin (0.1 microM), a cyclooxygenase inhibitor, did not affect the sumatriptan responses. These results suggest that sumatriptan-induced contractions of the rabbit iliac, but not mesenteric artery, were depressed by itself through the release of nitric oxide upon stimulation of 5-HT1-like receptors located on the endothelium, whereas neither on vascular smooth muscle nor on endothelium, 5-HT1-like receptors were present in the rabbit carotid artery.
Animals↗
Direct vascular smooth muscle contractile effect of cyclosporin A and its vehicle in rabbit isolated arteries.
cyclosporin A is a widely used immunosuppressant agent which has direct vascular effects such as contraction of the arterial smooth muscle and potentiation of other vasoconstrictor agents. In rabbit isolated arterial segments, the contractile effects of a cyclosporin A preparation (Sandimmun; 10(-6) M) and its solvent (Cremophor-EL) were investigated. Both caused an increase in the basal tension of arterial segments after an incubation period of 1 hour. Several substances were tested to antagonize the contractile activity of the cyclosporin A preparation and its solvent. Prednisolone and quinacrine (phospholipase A2 inhibitors), indomethacin (cyclooxygenase inhibitor), verapamil (calcium antagonist), phentolamine (alpha-adrenoceptor blocker), captopril (angiotensin-converting enzyme inhibitor) and prazosin (alpha 1-adrenoceptor-blocking agent) decreased the contractile responses to the cyclosporin A preparation and its solvent in a comparable manner. These findings indicate that the solvent of the cyclosporin A preparation is responsible for the contractile effect of this latter preparation and that this contractile activity cannot be explained by a single mechanism.
Animals↗
Characterization of 5-hydroxytryptamine receptors in rabbit isolated iliac artery.
To characterize the 5-hydroxytryptamine (5-HT) receptors, the contractile effects of both 5-HT and the 5-HT1-like receptor agonist sumatriptan were investigated in isolated open ring preparations of the rabbit common iliac artery. 5-HT induced concentration-dependent contractions. Sumatriptan did not induce any contraction of unstimulated preparations, whereas it elicited concentration-dependent contractions in preparations given a moderate tone with a threshold concentration of prostaglandin F2 alpha. In vessel segments precontracted with prostaglandin F2 alpha, Emax values for 5-HT and sumatriptan reached about 85% and 30% of the phenylephrine maximal effect, respectively. The mean EC50 values for sumatriptan and 5-HT were 3.34 microM and 1.5 microM, respectively. Pargyline, cocaine or normetanephrine were without significant effect on the contractions induced by 5-HT or sumatriptan. The 5-HT3 receptor antagonist tropisetron (1 microM) had no effect on 5-HT- and sumatriptan-induced contractions. The 5-HT2 receptor antagonist ketanserin (0.1-1 microM) produced parallel displacements to the right of the 5-HT and phenylephrine concentration-effect curves, without significant reduction in the maximum responses. The pA2 values were 7.85 +/- 0.19 and 7.9 +/- 0.16, respectively. Ketanserin had no effect on the sumatriptan concentration-effect curves. The nonselective 5-HT receptor antagonists methysergide (0.3 microM) and methiothepin (0.01 microM) shifted the concentration-response curve to sumatriptan to the right (mean pKB values of 6.91 and 8.68, respectively). The pA2 value for prazosin against 5-HT (9.98 +/- 0.43) was not significantly different from the value against phenylephrine (9.27 +/- 0.20). These results suggest that the sumatriptan-induced contraction is mediated by a 5-HT1-like receptor, whereas an additional mechanism, probably an alpha 1-adrenoceptor stimulation, plays a role in the contraction induced by 5-HT in the rabbit iliac artery.
Animals↗
Cyclosporin A and Cremophor-EL augment renal vascular responses to various agonists and nerve stimulation.
The acute actions of cyclosporin A and its solvent Cremophor-EL on the rise of perfusion pressure induced by periarterial stimulation were studied in the rabbit isolated kidney. Thirty-second stimulations were used and the parameters were 1-25 Hz, 5 msec duration, and 15 V. The responses to periarterial stimulation were frequency-dependent. Noradrenaline (0.01-20 microgram) induced similar effects when given into the renal artery. Clonidine (10(-7)M), added to the perfusion medium, inhibited the responses to periarterial stimulation without altering the effect of noradrenaline. Cyclosporin A (10(-7)-4 x 10(-5)M), added to the perfusion medium, potentiated the responses both to periarterial stimulation and exogenously given noradrenaline and restored the responses to clonidine (10(-7)M). The effects of cyclosporin A and Cremophor-EL on the responses to various contractile agonists (potassium chloride, phenylephrine, serotonin and angiotensin II) were also studied in the rabbit isolated renal artery. The results suggest that cyclosporin A may exert a direct action on the vasculature rather than an action on the vascular adrenergic neurotransmission of the rabbit kidney.
Animals↗
Bernard-Soulier-like functional platelet defect in myelodysplastic syndrome and in acute myeloblastic leukemia associated with trilineage myelodysplasia.
Platelet function was studied in a child with myelodysplastic syndrome (MDS: refractory anemia with an excess of blasts) and a child with acute myeloblastic leukemia (AML-M6) associated with trilineage myelodysplasia (TMDS). An acquired Bernard-Soulier-like platelet defect was considered in both patients with the findings of prolonged bleeding time and abnormally large platelets that failed to aggregate in response to ristocetin. In contrast to findings in von Willebrand's disease, the abnormal response of platelets to ristocetin could not be corrected by the addition of normal flesh plasma. The detection of abnormal platelet aggregation response to ristocetin may be a useful diagnostic finding for clonal disorders causing impaired platelet function in MDS and coexistent TMDS associated with AML. Further studies of ristocetin-induced platelet aggregation in a large number of these patients are required.
Adolescent↗
Streptococcus equinus peritonitis in a CAPD patient.
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Humans↗