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P Kesler

Publications and source records attributed to P Kesler.

6 recordsLinked to original sources
PubMed1980

Nature of suppressed TSH secretion during undernutrition: effect of fasting and refeeding on TSH responses to prolonged TRH infusions.

TSH responses to 4-hr continuous TRH infusions of approximately 0.8 microgram/min were assessed during feeding (1500 Kcal), fasting, and refeeding (1500 Kcal) intervals in 9 euthyroid obese subjects. The total area under the TSH response curve was 1854 +/- 322 muU/ml . 4-hr during feeding, decreased to 1359 +/- 199 muU/ml . 4-hr (p less than 0.01) on the 10th day of fasting, and remained low, being 1405 +/- 185 muU/ml . 4-hr, despite refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) for 5 days. Baseline serum T3 concentrations were 167 +/- 11 ng/dl during feeding, 86 +/- 8 ng/dl during fasting, and 119 +/- 12 ng/dl during refeeding. The observed decreases in TSH release appeared to correlate with decreased biologic action on the thyroid gland since the net rise in T3 during the infusion was less in fasting and refeeding than in the control (fed) period. Basal serum rT3 levels were 42 +/- 5 ng/dl during feeding, rose as expected to 56 +/- 5 ng/dl during fasting (p less than 0.005), and were completely restored to normal during refeeding (36 +/- 5 ng/dl). These data suggest that: (1) TSH responsiveness to prolonged TRH infusion is diminished during fasting and does not return to control (fed) values despite 5 days of refeeding a 1500 Kcal diet; (2) net T3 increases observed during the TRH infusion are greater in the fed period than in the fasting or refeeding periods; and (3) 5 days of refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) did not return the T3 to its original fed value whereas rT3 was completely restored to control values. Lastly, since the TSH response was lower both during the early and late phases of the infusion, the decrease in delta TSH to a bolus of TRH during fasting appears to represent one manifestation of a more general suppression of TSH neogenesis associated with caloric deprivation.

Adult↗
PubMed1979

The effect of T3 and reverse T3 administration on muscle protein catabolism during fasting as measured by 3-methylhistidine excretion.

Since recent studies have indicated that measurement in urine of the amino acid, 3-methylhistidine, accurately reflects the extent of muscle catabolism, and because it has been suggested that thyroid hormones may influence muscle breakdown, especially during fasting, the effect of T3 and reverse T3 (rT3) administration on the excretion of 3-methylhistidine was examined in obese subjects during fasting. The mean (+/- SE) 3-methylhistidine excretion in patients fed an egg protein diet (devoid of meat protein) was 256 +/- 35 mumoles/day and decreased to 190 +/- 14 mumoles/day during fasting. T3 administration (100 microgram/day x 5 days) increased 3-methylhistidine excretion to 304 +/- 37 mumoles/day during its ingestion and to 485 +/- 46 mumoles/day in the T3 posttreatment interval. T3 doses of 10 microgram every 4 hr (q4h) for the first 6 days of fasting also appeared capable of increasing 3-mehis excretion whereas 5 microgram T3 q4h administered during the first 6 days of fasting did not increase 3-mehis excretion. Reverse T3 administration (80 microgram q6h) during fasting was associated with a mean 3-methylhistidine of 130 +/- 13 mumoles/day, a value no higher than in patients fasted alone. These observations suggest that: (1) skeletal muscle catabolism decreases during fasting: and (2) pathophysiologic doses of T3 (60 microgram/day or more), but not reverse T3, enhance muscle catabolism during fasting.

Adult↗
PubMedDate not supplied

The effect of hemodialysis on oxygen transport in chronic uremics.

Previous studies from our laboratory suggested a decrease in tissue oxygen delivered during hemodialysis of chronic uremic patients due to an increase in hemoglobin-oxygen affinity, i.e. decrease in P50. This current study was designed to determine whether the changes in cardiac index and/or tissue oxygen extraction could compensate for increases in hemoglobin-oxygen affinity previously observed, so that total tissue delivery was unchanged during hemodialysis. This study demonstrated in patients during a 6-hour hemodialysis that: 1) no change occurs in hemoglobin-oxygen affinity expressed as P50, with unchanging plasma inorganic phosphate and red blood cell pH; 2) increased extraction of oxygen from tissue, measured via (A-V) O2 difference compensates for decreased oxygen delivery due to decreased cardiac output, and although there was no demonstrable change in hemoglobin-oxygen affinity, it would appear that increased tissue extraction of oxygen via other mechanisms should be easily able to compensate for previously reported changes in P50.

Adult↗
PubMedDate not supplied

[Thalamic dementia due to infarct of the left thalamus and genum of the right internal capsule].

INTRODUCTION AND OBJECTIVES: Thalamic dementia is the clinical consequence of a disorder of both thalami. It is generally secondary to bilateral paramedial thalamic infarcts due to disorders of small blood vessels or cardioembolism. We report a case of dementia of acute onset involving the left thalamus and the genum of the right internal capsule. CLINICAL CASE: A 33 year old man, HIV positive, category B2, admitted to hospital for tuberculous meningitis presented with the acute onset of somnolence, followed by marked bradypsychism, personality changes, marked disorder of executive explicit memory without associated praxic, gnosic or language disorders. Ocular motility remained normal. There was left central facial paralysis with inverse emotive voluntary dissociation. The other cranial nerves were normal. There was left hemiparesia with extensor plantar reflex. No other alterations. Cerebral MR imaging was compatible with paramedial infarcts of the left thalamus and genum of the right internal capsule. CONCLUSIONS: Thalamic dementia generally occurs in bilateral paramedian thalamic disorders. There are cases of disorders of executive memory secondary to infarcts of the genum of the internal capsule due to interruption of the thalamotemporal pathways and a contralateral paramedial thalamic lesion.

Adult↗