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PubMed1982

The effects of diazoxide upon fetal and maternal hemodynamics and fetal brain function and metabolism.

The effects of maternal infusion of Diazoxide (D) were evaluated in two groups of experiments: Nine ewes and their five nonhypoxic fetuses; the remaining four fetuses were excluded because of the development of hypoxia prior to the study. D was directly administered intravenously (IV) to the six fetuses. In group 1 maternal and fetal observations were made at 0, 5, 15, 30, and 45 minutes. A 60-minute observation was also made for the maternal infusion studies. Maternal infusion of 5 mg/kg maternal weight significantly reduced maternal pH from the control value at 5 minutes. Maternal metabolic acidosis was indicated by concomitant significant reductions in base deficit (BD) and total bicarbonate (HCO3), both of which remained low for all subsequent time periods. Maternal lactic acid concentration also increased at 15 minutes, although not significantly. Maternal PO2 also fell significantly at 5 minutes, remaining significantly low for the remaining observations. A profound maternal hypotension was elicited at 5 minutes. All following observations for maternal blood pressure (MBP) were also significantly low. Fetal carotid arterial (FCA) pH declined significantly from the control period value at 15 minutes, remaining significantly low for the remaining observations. FCA O2% saturation (O2%) also witnessed a significant decline from baseline for all observations. FCA serum lactate level rose at 15 minutes; however, this was not deemed significant. No significant changes were seen in fetal brain metabolic rate of oxygen or glucose. Fetal electroencephalogram (EEG) revealed a definite hypoxic change in a majority of cases. In group 2, the effects of a direct fetal IV administration of 30 mg D (mean dose = 7.97 mg/kg fetal weight) were studied in six experiments. No significant changes in fetal acid base status or fetal blood pressure (FBP) were witnessed for the 45 minutes under scrutiny. Fetal heart rate (FHR) showed a short transient rise from baseline at 5 and 15 minutes, returning to normal thereafter. A slight significant decrease in O2% saturation and O2 content were seen only for the 5-minute observation. There were no significant changes of fetal brain function and metabolism observed following D administration to the fetus. The significant fetal hypoxia and acidosis witnessed through the maternal infusion but not in the direct fetal bolus administration were probably owing to profound maternal hypotension resulting in deterioration of uteroplacental perfusion and fetal "gas exchange."

Animals↗
PubMed1981

[Changes in plasma volume and electrolytes after treatment of therapy-resistant hypertension with diazoxide and furosemide].

10 patients (5 females, 5 males, average age 50.2 +/- 5.8 years) with a therapy-resistant hypertension were for 10 days treated with injections of diazoxide and furosemide (hypertonalum and furesis). A significant decrease of the blood pressure as well as a decrease of sodium and potassium in the serum occurred, where as the electrolyte content of te 24-hour collection urine was influenced in homogeneously. The blood and plasma volume, respectively, was also significantly reduced. Heart rate and blood sugar significantly increased, urea-N, creatinine, hematocrit and hemoglobin did not increase significantly. The new regulation of the blood pressure to an oral antihypertensive permanent therapy continued 4 weeks to 6 months.

Blood Glucose↗
PubMed1995

Prophylaxis of genetically determined diabetes by diazoxide: a study in a rat model of naturally occurring obese diabetes.

The study was carried out using a new rat model of naturally occurring obese, nonketotic diabetes, Otsuka Long-Evans Tokushima Fatty rat (Kawano et al., Diabetes 41: 1422-1428, 1992), which closely resembles obese noninsulin-dependent diabetes in human. At the age of 3.5 wk, body weight, glucose tolerance and plasma insulin level after glucose load were normal in Otsuka Long-Evans Tokushima Fatty rats, indicating the animals are at nonobese, prediabetic phase. At this age, however, glucose-stimulated insulin release by pancreatic islets in vitro was abnormally exaggerated whereas the islet insulin content and glucose metabolism by the islet cells were normal. Administration of diazoxide (0.2% in diet), an inhibitor of insulin secretion, to Otsuka Long-Evans Tokushima Fatty rats from the age of 4 to 12 wk completely prevented the development of obesity and insulin resistance, which was accompanied by marked improvement of glucose tolerance and disappearance of exaggerated B cell response to glucose in vitro. This is the first report of successful pharmacological prevention of genetically determined obese diabetes.

Animals↗
PubMed1976

Neonatal pancreatic beta-cell hyperplasia: report of a case with failure of diazoxide and benefit of early subtotal pancreatectomy.

A newborn infant with pancreatic beta-cell hyperplasia had persistent hypoglycemia due to hyperinsulinism. After medical management, including the use of diazoxide and constant glucose infusions had proved ineffective, a subtotal pancreatectomy was curative. Cumulative experience seems to indicate that there should be little delay in performing a subtotal pancreatectomy when aggressive medical management cannot maintain normoglycemia in a neonate.

Diazoxide↗
PubMed1996

Diazoxide and cyclothiazide convert AMPA-induced dark cell degeneration of Purkinje cells to edematous damage in the cerebellar slice.

Using the in vitro cerebellar slice preparation from young rats (8-12 days old), AMPA produced in addition to dark cell degeneration (DCD), an edematous type of toxicity (edematous damage; ED) in a minority (35%) of Purkinje cells. The intent of this study was to evaluate whether AMPA receptor desensitization is a primary factor that governs the type of toxicity induced by AMPA in the in vitro cerebellar slice preparation. Both the competitive and noncompetitive AMPA antagonists CNQX and GYKI 52466, respectively, blocked ED when given during the entire protocol (30 min AMPA exposure followed by 90 min of recovery). Cyclothiazide (100 microM) and diazoxide (500 microM), two antagonists of AMPA receptor desensitization reversed DCD and unveiled a fulminating ED. Lowering Na+ and lowering Cl- proved effective in blocking ED, whereas removal of Ca2+ proved to be ineffective. Kainate (KA) (30-100 microM) produced only 50% as much ED as AMPA. This study indicates that AMPA can elicit more than one type of degeneration in the same neuronal population and that a primary governing factor in determining which toxicity is expressed seems to be the ability of AMPA receptors to desensitize.

Animals↗
PubMed1996

[Polycystic ovary and diazoxide. In vivo study].

The suppression of hyperinsulinism with diazoxide (300 mg/d during 30 days) in a young woman with PCOS and hirsutism, hyperinsulinism and insulinoresistance was followed by a modification of plasma androgens. Testosterone (T) and free testosterone (fT) were reduced after ten days and then increased but always remained below the baseline level. DHEAS had increased 200% by day 10, and 3 alpha-adiol G to three times its basal value by day 20. These modifications were constant during the treatment. fT decrease was secondary to reduction of hyperinsulinism which was followed by an increase of TeBG and a modest and transient reduction of androgen theca cells production. DHEAS increase was due to hyperinsulinism suppression which stimulated adrenal 17-20 lyase activity. 3 alpha-adiol G increase was concomittant, and can be considered as an index of adrenal androgen secretion.

Adolescent↗
PubMed1976

Side effects of diazoxide.

Diazoxide given for hypertensive crises caused severe complications in two patients. Hypotension, anginal syndrome, cerebral ischemia, and right hemiplegia developed in one patient, and myocardial infarction in the other.

Acute Disease↗
PubMed1976

[Leucine-sensitive hypoglycaemia and its treatment with diazoxide (author's transl)].

A seven months old infant suffered from convulsions due to leucine-sensitive hypoglycaemia. The convulsions could not be stopped by a diet lacking in leucine, but ceased after additional application of diazoxide; hypoglycaemia was no longer observed the mental development of the child is hoped to be normal.

Amino Acid Metabolism, Inborn Errors↗
PubMed1998

The diazoxide derivative 7-chloro-3-methyl-3,4-dihydro-2H-1,2,4-benzothiadiazine-S,S-dioxide augments AMPA- and GABA-mediated synaptic responses in cultured hippocampal neurons.

The diazoxide derivative 7-chloro-3-methyl-3,4-dihydro-2H-1,2,4-benzothiadiazine-S,S-dioxide (IDRA21) enhances memory and learning in rodents, most likely by potentiating AMPAergic synaptic activity. We examined IDRA21's effect upon AMPAergic synaptic currents and whole-cell glutamate currents in cultured rat hippocampal neurons to determine whether IDRA21 was a partial modulator of AMPA receptor desensitization and deactivation. Comparable to cyclothiazide, IDRA21 prolonged AMPAergic autaptic currents (5.6 times control, EC50 150 microM) and slowed the rate of AMPA deactivation (3 times control) following 1-ms applications of 1 mM glutamate to excised, outside-out membrane patches. IDRA21 also augmented autaptic GABA currents by 27 +/- 8.1%, although it had two opposing effects, reducing the peak amplitude versus prolonging autaptic GABA currents. IDRA21 (200 microM) inhibited whole-cell GABA currents elicited by exogenously applied 1 mM GABA by 41 +/- 11%. At sufficient concentrations, IDRA21 reduced AMPA receptor desensitization and slowed the rate of deactivation, most consistent with full agonist activity with lower potency compared to cyclothiazide. IDRA21 slightly augments GABAergic synaptic currents.

Animals↗