PubMed Health⌕ Search

Biomedical subjects

R A Becker

Publications and source records attributed to R A Becker.

At least 37 records · Page 2Linked to original sources
PubMed1982

Hypermetabolic low triiodothyronine syndrome of burn injury.

The free tetraiodothyronine index (FT4I) and free triiodothyronine index (FT3I) in burn patients represented the serum levels of free (dialyzable) T4 and free T3, respectively. FT4I and FT3I were lower with greater burn size and were lower in nonsurvivors than expected for the burn size. there was no compensatory elevation of basal or releasing hormone-stimulated thyrotrophin (TSH) concentrations. Reverse T3 was higher with greater burn size. T3 treatment restored FT3I but did not affect mortality or resting metabolic rate (MR) measured in survivors, compared with placebo therapy. Whereas the hypermetabolic response to burn injury appeared t be independent of thyroid hormones, MR was correlated positively with burn size and with elevated plasma norepinephrine and epinephrine concentrations for several weeks after injury. Lack of augmented TSH concentrations, absence of low plasma reverse T3, and presence of hypermetabolism suggest that the reduced plasma free T3 does not indicate functional hypothyroidism, but may represent an adaptation to the assumption of metabolic control by the sympathetic nervous system.

Adolescent↗
PubMed1982

Cortisol and corticotrophin in burned patients.

In a study of 36 men burned in a fire, based on sequential early morning samples, plasma cortisol concentration was elevated in proportion to burn size. Plasma corticotrophin (ACTH) was not correlated with burn size, suggesting that factors other than ACTH contribute to the elevated cortisol. Cortisol levels did not fall on the days preceding death in nonsurvivors. During 24-hr sampling, burned patients exhibited a fitted cortisol curve mean that was elevated in proportion to burn size, a rhythm amplitude that was significantly less than that in uninjured controls, and a normal peak time. Metabolic rate, rectal temperature, and urinary catecholamine excretion were also elevated in proportion to burn size. Although plasma cortisol was positively correlated with metabolic rate and with temperature, this appeared to result from a common relationship of these variables with burn size. On the other hand, urinary catecholamine values significantly reduced the residual variance of metabolic rate and temperature after accounting for variance related to burn size. Cortisol appears to be less prominent than catecholamines as a possible mediator of the elevated thermogenesis.

Adolescent↗
PubMed1982

A prospective study of circulating prolactin during primigravid pregnancy.

A prospective, cross-sectional study of 164 primigravid patients was conducted to determine the role of prolactin in the pathogenesis of pregnancy induced hypertension. Clinically normal patients had peripheral venous blood sampled from the lateral and recumbent positions monthly in the morning during their last two trimesters in labor and six weeks postpartum. One-third of the patients had 24 hour urine collections. Homologous double antibody radioimmunoassays were performed to determine prolactin levels. The data were analyzed according to pregnancy outcome: pregnancy-induced hypertension or normotensive throughout pregnancy. Acute positional change did not influence prolactin level. Prolactin levels were significantly elevated in the hypertensive outcome group only at 37-39 weeks and were not correlated with sodium excretion. We conclude that circulating prolactin does not play a significant role in pathogenesis of pregnancy-induced hypertension, but perhaps the elevated levels may be reflecting pathophysiologic changes.

Blood Specimen Collection↗
PubMed1981

Methylation of liver DNA guanine in hydrazine hepatotoxicity: dose-response and kinetic characteristics of 7-methylguanine and O6-methylguanine formation and persistence in rats.

Fischer 344 or Sprague Dawley rats were fasted overnight and given orally 30--90 mg hydrazine/kg body wt. The presence of 7-methylguanine and O6-methylguanine in liver DNA was demonstrated 5 and 24 h after hydrazine administration using two different analytical techniques. Methylation levels changed little with dose except for the highest dose (ca. LD50) at which the levels doubled. In a time-response study, rats were given 90 mg hydrazine/kg body wt. and killed 0.25 to 96 h later. Both 7-methylguanine and O6-methylguanine were detected quantitatively in liver DNA from rats as early as 15 min after hydrazine administration. After maximum levels of methylguanines had formed, 7-methylguanine was removed from DNA at a rate of approximately 50% in 47 h; the half-life of O6-methylguanine in liver DNA was approximately 13 hr. Three or four, but not one or two, daily administrations of 3 mg hydrazine/kg body wt. also produced detectable levels of 7-methylguanine in rat liver DNA. Neither 7-methylguanine or O6-methylguanine was detected in comparable amounts of liver DNA from control animals. The study confirms the observation that hydrazine administration results in the formation of methylated guanines in liver DNA.

Animals↗
PubMed1981

Visceral blood flow following thermal injury.

To determine if visceral blood flow was altered by thermal injury, effective renal blood flow (ERBF) was measured by para-aminohippurate clearance in five control subjects and 13 nonbacteremic burn patients (mean burn size: 50% total body surface, range: 24.5-83.5) 6-25 days after burn injury. Splanchnic blood flow (SBF) and cardiac output were determined in a matched group of ten patients by indocyanine green clearance and dilution techniques, respectively. Renal and splanchnic oxygen consumptions (VO2) were calculated from regional arteriovenous O2 differences and blood flows. ERBF was not significantly elevated in these patients (780 +/- 68 ml/min x m2, mean +/- SE, versus 552 +/- 37 in controls). SBF, at 1463 +/- 96 ml/min x m2, was twice normal and 19% of the cardiac index (7764 +/- 393 ml/min x m2). Individual variations in ERBF and SBF were unrelated to burn size or the time after injury, but ERBF varied with 24-hour sodium excretion. Renal and splanchnic VO2 were twice normal levels at 33 +/- 6 and 66 +/- 4 ml/min, respectively. These results indicate that an increase in ERBF is not an obligatory response to burn injury, but is dependent on sodium load and/or vascular volume. Conversely, SBF is consistently increased by thermal injury and contributes to the rise in cardiac output after injury. While the increase of SBF is appropriate for the rise in local VO2, the cause of the apparent splanchnic vasodilation is unknown.

Abdomen↗
PubMed1980

Increased renal perfusion and kidney size in convalescent burn patients.

Renal blood flow was elevated in convalescent burn patients shortly before discharge (992 +/- 112 mL/min/sq m in burn patients vs 551 +/- 37 mL/min/sq m in normal subjects; mean +/- SE). Autopsy studies demonstrated that renal enlargement was a constant feature of patients after a prolonged hospital course; the kidneys of 28 patients who died after 60 days of hospitalization weighed 241 +/- 10 g vs 153 +/- 8 g in control subjects. The increase in renal weight was primarily related to cellular hypertrophy and hyperplasia. These physiological and morphological findings in thermally injured patients may be a form of renal work hypertrophy following increased protein catabolism accompanying severe injury.

Adult↗
PubMed1980

Plasma norepinephrine, epinephrine, and thyroid hormone interactions in severely burned patients.

In this prospective study of thyroid catecholamine interactions, 15 severely burned patients were divided into two groups. Nine patients receiving 200 micrograms/day of triiodothyronine constituted the T3-treated group. Eight additional patients constituted the untreated group. Mean serum concentrations of T3 were significantly lower in the untreated group than in the treated group. Mean serum thyroxine (T4) concentrations were significantly higher in the untreated group than in the treated group. The mean plasma norepinephrine concentration in the untreated group was significantly greater than that of the treated group. In the untreated group, log plasma norepinephrine correlated inversely with serum T3. Similarly, in the untreated group, log plasma epinephrine correlated inversely with serum T3. Metabolic rates were not different between groups. These data suggest that a reciprocal relationship exists between plasma concentration of T3 and both norepinephrine and epinephrine in untreated burn patients and that treatment with the metabolically active hormone, triiodothyronine, does not alter the level of hypermetabolism accompanying thermal injury.

Adult↗
PubMed1980

Free T4, free T3, and reverse T3 in critically ill, thermally injured patients.

A prospective study of thyroid function was performed in 25 thermally injured patients. These patients are divided into two groups. The first group contains five patients with greater than 50% burn size studied longitudinally during the first 15 days following thermal injury. Significant suppression of serum concentrations of 3,5,3'-triiodothyronine (T3) and elevation of serum concentrations of 3,3',5'-triiodothyronine (rT3) were seen. The free thyroxine index and serum TSH concentrations remained within the normal range. To assess the clinical significance of these alterations in peripheral thyroid hormone concentrations, a second group of 20 patients was studied. We measured the free serum levels of T4 (FT4) and T3 (FT3) in ten patients, mean age 34 years, mean burn size 56%, studied during a period of clinical deterioration, and in ten patients of comparable age and burn size who were clinically stable. Both FT4 and T3 values were significantly lower in the unstable patients (p < 0.01). All FT3 values for the unstable patients (M +/- SE), 193 +/- 14 pg/dl, were below the normal range for FT3 of 230 to 669 pg/dl, and significantly lower than those observed in the stable patients (M +/- SE), 430 +/- 59 pg/dl (p < 0.001). This correlation of biochemical hypothyrodisim with clinical deterioration may have functional significance for the critically ill trauma patient.

Adolescent↗
PubMed1977

Prospective study of angiotensin II response to positional change in pregnancy-induced hypertension.

The response of endogenous angiotensin II levels to positional change, lateral to supine recumbency, was investigated in a prospective study of 55 primigravid patients during the last half of pregnancy. Blood samples were obtained in the lateral and supine recumbent positions. The mean supine angiotensin II level was significantly higher between 29 and 34 weeks' gestation in those patients destined to develop pregnancy-induced hypertension than in those who remained normotensive (P less than 0.05). As gestation advanced, the mean per cent relative change of angiotensin II from the lateral to the supine position altered from negative to positive in those patients destined to develop pregnancy-induced hypertension, whereas it remained negative in those patients who remained normotensive. These findings are discussed in relation to pathophysiologic alterations in the development of pregnancy-induced hypertension.

Angiotensin II↗
PubMed1977

Effects of pentoxifylline on cerebral ultrastructure of normal and ischemic gerbils.

Normal gerbils and those made ischemic for 15 to 60 minutes by bilateral common carotid artery occlusion were studied ultrastructurally after administration of the vasoactive drug pentoxifylline. In both groups, hypertrophy of neuronal mitochondria was found in the hippocampus and cerebral cortex. Planimetry of electron micrographs revealed a statistically significant increase in average mitochondrial size of drug-treated animals compared with untreated ischemic gerbils and normal controls; the treated ischemic group showed the greatest increase. Incubated cortical slices from normal gerbils that were given the drug 5 hours before they were killed showed a significant increase in oxygen consumption compared with controls.

Animals↗
PubMed1974

Experimental acute lead encephalopathy in the juvenile rhesus monkey.

Lead subacetate (0.5g) and 1000 units of vitamin D were given three times a week to four newly-weaned rhesus monkeys. In addition, two animals received only the vitamin D. The poisoned animals had an increase in the urinary excretion of delta-aminolevulinic acid, an elevated content of lead in the blood, and a fall in hemoglobin concentration. Between 6 and 18 weeks the animals suddenly developed ataxia, nystagmus, generalized weakness, and convulsions. At this time the animals were killed by perfusion of fixative and the brain prepared for light and electron microscopic studies. Definite morphological evidence of disease was confined to the central nervous system, except for one animal which showed the characteristic renal inclusions of lead poisoning. All animals showed PAS-positive globules associated with blood vessels and an exudative edema involving the white matter of the cerebral hemispheres and cerebellum. Ultra-structurally, this appeared as a granular precipitate within an expanded extracellular space. Alterations of nerve fibers were not seen in the white matter but axonal swelling was observed in the cerebral cortex. The perikaryon and neuropil appeared normal. The control animals showed no significant cerebral changes.

Acute Disease↗