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Biomedical subjects

M Gilbert

Publications and source records attributed to M Gilbert.

At least 253 records · Page 14Linked to original sources
PubMed1978

Modification of methylmercury neurotoxicity by vitamin E.

The protective effect of vitamin E on the neurotoxicity of methylmercury was investigated by means of light and electron microscopy. Young male golden hamsters were exposed to 2.0 ppm methylmercury chloride with or without concurrent administration of vitamin E (2.0 ppm). No toxic symptoms were observed in the vitamin E-protected animals while all the animals given methylmercury alone developed severe symptoms of methylmercury poisoning. Light microscopy revealed no significant neural damage by mercury in those animals exposed to methylmercury/vitamin E while significant neuronal necrosis could be demonstrated in both the cerebellum and calcarine cortex of the methylmercury-treated animals. Besides some accumulation of lysosomes, electron microscopy also demonstrated remarkable intactness of the cellular organelles in the nerve cells without neuronal necrosis. It appears that vitamin E has a strong protective potential against the toxicity of methylmercury.

Animals↗
PubMed1977

Toxicity to fish of flame retardant fabrics immersed in their water. Part I.

A number of commercial and candidate flame retardants were studied with regard to their toxicity to fish when released from fabrics immersed in their water. Immersion of laundered or unlaundered flame retardant 100% polyester or polyester blend fabrics used in children's sleepwear in water containing goldfish resulted in release of the anticholin-esterase flame retardant TDBPP (tris (2, 3-dibromopropyl) phosphate) and death of all fish within 24 hours. TDBPP undergoes loss of HBr in water and production of a metabolite.

Animals↗
PubMed1977

Fetal metabolic response to maternal fasting in the rat.

To determine the fetal response to altered maternal fuel supply, the effects of prolonged maternal fasting, begun 24-96 h before term, were examined and compared with values from normally fed term animals. Fetal weight decreased only after 48 h of maternal fasting. Prolonged maternal fasting was associated with low blood glucose, high blood ketone bodies, and decreased gluconeogenic substrate in the fetus. Plasma insulin was decreased, whereas plasma glucagon was increased in the fetus of fasted mothers. Infusion of [2-3H]glucose into the mother to constant specific activity gave a ratio of maternal to fetal glucose activity of 1.0 in fed and 1.56 in fasted mothers. Fetal liver from fasted mothers showed both increase in activity of key gluconeogenic enzymes (glucose-6-phosphatase and phosphoenolpyruvate carboxykinase) and increased conversion in vitro of lactate, alanine, serine, and glycerol in glucose by liver slices. It is inferred that maternal fasting induces fetal substrate alterations and hormonal changes appropriate to premature appearance of hepatic gluconeogenesis. The priority for endogenous fuel provision in this state leads to impaired fetal growth.

Amino Acids↗
PubMed1977

Glycerol metabolism in the pregnant and virgin rats.

The parameters of in vivo glycerol kinetic curves were determined after a single injection of glycerol-1-14 C in pregnant and in virgin rats. The half-life of glycerol was found to be 9 min in pregnant rats and 17 min in virgin rats. There was no significant difference between the absolute turnover rates. The glycerol plasma space cannot be appreciated. The distribution volume expressed in milliliter of plasma appeared to be very high indicating that glycerol was not distributed only in the plasma. Glycerol was found to be a precursor of glucose and this conversion seemed to proceed more rapidly in the pregnant rat than in the virgin rat.

Animals↗
PubMed1977

Hyperglycemia and glycogen storage in the rabbit fetal liver. Role of age and hormonal status.

A 2-hour glucose infusion to pregnant rabbits resulted in fetal hyperglycemia. The question was studied whether this hyperglycemia would induce an increase in the concentration of glycogen in the fetal liver. The result depended upon the age of the fetus. In 24- or 25-day-old fetuses hyperglycemia did not increase the liver glycogen. On the contrary, on day 26, 27 and 28, the glycogen content in the liver was approximately twice as high as in controls. However, in fetuses which were decapitated on day 24 and studied on day 26, the maternal glucose infusion did not increase the glycogen stores. But in those fetuses decapitated on day 25 hyperglycemia provoked glycogen deposition. The activity of liver glycogen synthetase (active form alpha and total form a + b) increased between days 24 and 28 in control fetuses. Some increase of the alpha form already occurs between days 24 and 25. In fetuses decapitated on day 23, the alpha form was found almost as low on day 31 as it was on day 23. The incapacity of the liver of fetuses under 26 days of age or of those decapitated before day 25 to store glycogen under conditions of hyperglycemia probably results from a low glycogen synthetase activity.

Animals↗
PubMed1977

Origin and metabolic fate of plasma glycerol in the rat and rabbit fetus.

On day 21.5 a pregnant rat received a single injection of [1-14C]glycerol. The purpose was to study the transfer of glycerol through the placenta from the maternal to fetal plasma. From 3-20 min after injection the specific activity of glycerol in maternal and fetal plasma was measured. The results indicate that the mother can provide this molecule to the fetus. Similar results were obtained with the rabbit on day 28 of pregnancy. The possibility of the conversion of plasma glycerol to glucose has been investigated in the rat and rabbit fetus. This molecule was chosen chiefly to see whether the gluconeogenic pathway was functioning in the fetus above the triose phosphate step. At two stages of fetal development the capacity of the fetus to incorporate [1-14C]glycerol into glucose plus glycogen has been shown in the two species. In the rat fetus the conversion of [1-14C]glycerol to [14C]glucose increases from 19.5 to 21.5 days of gestation. For the rabbit this parameter increases from 25 to 28 days of gestation. On day 25 in the rabbit and day 19.5 in the rat the liver glycogen was labeled, but it did not accumulate the [14C]glucose from [1-14C]glycerol during the time that we have studied. In contrast, on day 28 in the rabbit and day 21.5 in the rat the incorporation of radioactivity increased as function of the time. However, the relative importance of glycerol as precursor of the glucose plus glycogen in the fetus remains to be elucidated.

Animals↗
PubMed1976

The effects of narcotics on fetal acid base status.

This paper reports two randomized control trials on the effects of nalorphine, pethidine, morphine and heroin on fetal and maternal acid base status. The drugs decreased pH and increased pCO2 in the mother, and decreased pH and base excess in the fetus. The changes in the fetus were independent of the changes in the mother. In equivalent dosages, nalorphine increased maternal pCO2 more than pethidine and morphine. The effects of heroin were found to be greater than that of other drugs, and we suggest that heroin should be avoided where the fetus is already at risk.

Acid-Base Equilibrium↗
PubMed1976

Electrophysiologic effects of propranolol on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered propranolol (0.1 mg/kg) on three parameters of sinus node function were examined in ten symptomatic patients with sinus node dysfunction. The patients ranged in age from 26 to 79 years. Symptoms ranged from fatigue to frank syncope. Sinoatrial (SA) block and sinus pauses were observed in one patient; sinus pauses alone were observed in three patients. Five (5/10) patients had intraatrial block; three (3/10) patients had atrioventricular block; four (4/10) patients had an intraventricular conduction disturbance. At the time of electrophysiologic study, two patients had a control spontaneous sinus cycle length that exceeded 1000 msec. Following propranolol, the mean spontaneous cycle length increased by 17.4% (924 to 1085 msec, P less than 0.005) and spontaneous second degree SA block reappeared in the one patient. The maximum escape cycle ranged from 116% to 229% of the prepacing spontaneous cycle length and was considered to be prolonged in two of ten patients. Propranolol had no significant effect on the maximum escape cycle/prepacing cycle length X 100 (%). The estimated sinoatrial conduction time (SACT) was determined in seven patients and ranged in value from 120 to 238 mes. Propranolol increased the mean value of the estimated SACT from 179 to 213 msec, P less than 0.025. Propranolol may cause marked bradyarrhythmias in some patients with sinus node dysfunction, and should be used with caution in these patients.

Adult↗
PubMed1976

Effect of environmental temperature on glucose-induced insulin response in the newborn rat.

Blood glucose and plasma insulin and glucagon concentrations were determined in full-term rats delivered by cesarean section and exposed to 37 degrees C. or 24 degrees C. environmental temperature during the first hours of extrauterine life. When newborn rats were maintained at thermal neutrality (37 degrees C.), a transient period of hypoglycemia of two hours occurred, associated with a rapid fall in plasma insulin and a rise in plasma glucagon concentrations. During cold exposure (24 degrees C.), the blood glucose level remained stable over the four hours studied; the decrease of plasma insulin was sluggish while the rise of plasma glucagon was unchanged. In newborn rats maintained at 37 degrees C., an intraperitoneal glucose load one hour after delivery produced a marked rise in blood glucose and plasma insulin concentrations one hour later. The distribution of experimental points suggested a sigmoidal dose-response curve. By contrast in newborn rats kept at room temperature (24 degrees C.) the same glucose load did not induce any increase in plasma insulin in spite of hyperglycemia. However, phentolamine resulted in pronounced plasma insulin rise in hypothermic newborns in response to glucose administration. From these observations it is concluded that the in-vivo unresponsiveness of the beta cells to glucose at birth, reported by others, is mainly due to the experimental conditions.

Age Factors↗
PubMed1975

[Control of glycogen biosynthesis in fetal rat liver].

We have studied through the late foetal period of the rat, the evolution of two enzymes involved in glycogen metabolism of the liver : UDPG glycogen synthetase (a and b forms) and branching enzyme. The activities were measured during the development of normal foetuses and of foetuses experimentally deprived of corticosteroids. In normal foetus the activity of glycogen synthetase and the branching enzyme increased progressively between days 18 and 21 ; but the percentage of glycogen synthetase a increased promptly between days 18 and 19. This variation coincides with the beginning of glycogen accumulation in the liver. In foetuses submitted to corticosteroid shortage, the activity of each enzyme, and the amount of glycogen in the liver, were reduced at term. Cortisol given to the decapited foetus restores subnormal glycogen storage and normal activity of branching enzyme. The activity of synthetase a was slightly increased but remained very low ; only synthetase b was restored to normal. It seems that there is no relationship between the synthesis of glycogen, in the foetal rat liver, and the activity of synthetase a.

Adrenal Cortex Hormones↗
PubMed1975

Wolff-Parkinson-White syndrome. The problem, evaluation, and surgical correction.

Physiological studies of the type we have described, when performed in patients with the WPW syndrome, can yield diagnostic information regarding the mechanism of arrhythmia, demonstrate functional properties of therapeutic import, facilitate therapeutic decision-making about drug regimens and presumptively localize the site of pre-excitation as a basis for possible surgical intervention. Based on our experience, we feel that in selected patients, surgical correction of the WPW syndrome is entirely feasible, and can be accomplished in the majority of patients in whom free wall A-V connections are present. The continuing challenge of identification and correction of septal accessory pathways directs our present work with the WPW syndrome.

Adolescent↗
PubMed1975

Digitalis and the sick sinus syndrome. Clinical and electrophysiologic documentation of severe toxic effect on sinus node function.

Digoxin, in a common clinical dose and at a low serum level, brought out severe manifestations of sinus node dysfunction in a patient who had previously undergone successful mitral valve replacement. This report presents the results of extensive clinical and electrophysiologic studies of this patient before and after a digoxin challenge. In the absence of cardiac glycoside, the only demonstrable abnormalities of sinus node function were mild resting sinus bradycardia and failure to respond to atropine administration. Responses to isoproterenol administration, programmed premature atrial stimulation, and overdrive pacing at several cycle lengths were normal. Following the administration of intravenous digoxin, 1.025 mg/24 hrs, the resting sinus cycle length increased and the response to overdrive pacing became markedly abnormal. The latter was followed by sinus pauses in excess of six seconds, even at relatively slow overdrive pacing rates. The electrophysiologic and clinical implications of these data are discussed. It is suggested that despite previous reports that digitalis preparations are relatively well tolerated by patients with sick sinus syndrome, caution should be used when administering these drugs to this group of patients.

Arrhythmia, Sinus↗
PubMed1975

[Energy metabolism in the perinatal period (author's transl)].

Neonatal hypoglycemia is of frequent occurrence in fasted newborn babies or animals but the origin of this hypoglycemia is not fully understood. Studies performed in newborn rats have shown that liver glycogenolysis and gluconeogenesis occur immediately after birth and that the increase in the activities of key regulatory enzymes (phosphorylase, glycogen synthetase and phosphoenolpyruvate carboxykinase) results probably from the rise of plasma glucagon and the fall of plasma insulin induced by the "stress" of birth. When the liver glycogen stores have been exhausted, i.e. between 6 and 16 hours after birth, a profound hypoglycemia develops in fasting newborn rats. The inability of hepatic gluconeogenesis to produce sufficient glucose to meet the energy requirement of the newborn tissues results from a lack of fat-derived (free fatty acids and ketone bodies) and gluconeogenic (lactate, amino acids) substrates. The stage of appearance and the mechanisms regulating gluconeogenesis in other species including human are discussed.

Adenosine Triphosphate↗