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  • Electronic Resource  (2)
  • 1995-1999  (2)
  • 1975-1979
  • Gastric inhibitory polypeptide  (1)
  • Prostaglandin I2  (1)
  • 1
    ISSN: 1432-1238
    Keywords: Key words Cardiac arrest ; Cardiopulmonary resuscitation ; Platelet aggregation ; Prostaglandin I2 ; Thromboxane A2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: Hypoxia and ischemia cause endothelial cell damage with consequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was tested. Design: Prospective, observational cohort study. Setting: Emergency Department and general Intensive Care Unit in a city hospital. Interventions: Basic and advanced life support. Patients and participants: Forty-seven out-of-hospital cardiac arrest patients. The patients were classified into two groups, those who were resuscitated (n=18) and those who died (n=29). Measurements and results: Serial levels of platelet aggregation, thromboxane B2 (TXB2), 11-dehydro-TXB2 and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured. The results of measurements and demographic data were compared between the groups. Platelet counts decreased at the end of cardiopulmonary resuscitation (CPR), the decrease of the platelet counts showed statistical significance especially in the patients who died (p〈0.001). Platelet aggregation induced by adenosine diphosphate, epinephrine and collagen decreased to the lower limits of normal during and after CPR. Although high values of TXB2 and 11-dehydro-TXB2 continued throughout the study period in the resuscitated patients, 6-keto-PGF1 alpha decreased to the normal range (22.7±3.6 pg·ml–1, p〈0.05) at 24 h after arrival at the Emergency Department. Conclusions: Platelet activation with the massive formation of thromboxane A2 (TXA2) occurs in patients with out-of-hospital cardiac arrest. Successful resuscitation is not associated with the balanced production of PGI2 against the TXA2 formation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-5233
    Keywords: Gastric inhibitory polypeptide ; Truncated glucagon-like peptide-1 ; Incretin ; Sulfonylurea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Gastric inhibitory polypeptide (GIP) and truncated glucagon like peptide-1 (tGLP-1) are potent gastrointestinal insulinotropic factors (incretin), mostly released after a meal or ingestion of glucose in man and animals. To investigate whether sulfonylurea (SU) affects the secretion of incretin, the modulation of plasma GIP and tGLP-1 levels following glucose ingestion in non-insulin-dependent diabetic type 2 patients with or without SU therapy was studied. A 75-g oral glucose tolerance test (OGTT) was carried out on 9 healthy subjects (controls) and 18 patients with non-obese type 2, 9 of whom were treated by diet alone (NIDDM-diet) and the other 9 with SU (glibenclamide 2.5 mg or gliclazide 40 mg) once a day (NIDDM-SU). Plasma GIP was measured by radioimmunoassay (RIA) with R65 antibody, and GLP-1 was measured by RIA with N-terminal-directed antiserum R1043 (GLP-1NT) and C-terminal-directed antiserum R2337 (GLP-1CT). Following OGTT, plasma glucose, GIP, GLP-1NT, and GLP-1CT in type 2 patients increased more markedly than in controls, despite the lower response of insulin. However, there were no significant differences in plasma levels of these peptides between the NIDDM-diet and NIDDM-SU groups. Therefore, it is unlikely that SU is involved in the high response of GIP and GLP-1s to OGTT in type 2 patients.
    Type of Medium: Electronic Resource
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