Relation of thyroid state to myocardial catecholamine concentration

1963 ◽  
Vol 205 (6) ◽  
pp. 1270-1274 ◽  
Author(s):  
George S. Kurland ◽  
Rupert P. Hammond ◽  
A. Stone Freedberg

The myocardial catecholamine content was measured in euthyroid, thyrotoxic, and hypothyroid rabbits. Male rabbits were made thyrotoxic by injection of l-thyroxine, or were rendered hypothyroid by injection of I131. Body weight, basal metabolic rate, serum protein-bound iodine, and appearance were used as criteria of thyroid state. Myocardial norepinephrine and epinephrine concentrations were measured, after alumina column chromatography, by a modification of the trihydroxyindole method. Fluorescence spectra and paper chromatographic analyses confirmed the identity of the trihydroxyindole-fluorescing material, and revealed no extraneous fluorescing substances. In the heart of the euthyroid rabbit, epinephrine concentration averaged 0.3 ± .2 (sd) µg/g in the atrium, and 0.06 ± .03 µg/g in the ventricle. Norepinephrine concentration averaged 2.9 ± .4 µg/g in the atrium, and 2.2 ± .3 µg/g in the ventricle. In thyrotoxicosis, atrial epinephrine and norepinephrine concentrations were decreased, ventricular epinephrine was unchanged, and ventricular norepinephrine was decreased. In hypothyroidism, atrial epinephrine and norepinephrine were decreased and ventricular epinephrine was unchanged, but in the hypothyroid ventricle, norepinephrine content was markedly increased.

1996 ◽  
Vol 84 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Malcolm Daniel ◽  
Edmond I Eger ◽  
Richard B. Weiskopf ◽  
Mariam Noorani

Background A rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses. Methods To test this hypothesis, five healthy male volunteers were studied three times. After induction of anesthesia with 2 mg.kg-1 propofol, anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. On separate occasions, in random order, either no propofol or 2 mg.kg-1 propofol was administered either 2 or 5 min before increasing end-tidal desflurane concentration from 4% to 8%. Results Without propofol pretreatment, the increase to 8% desflurane transiently increased heart rate (from 63 +/- 3 beats/min to 108 +/- 5 beats/min, mean +/- SEM; P < 0.01), mean arterial pressure (from 73 +/- 1 mmHg to 118 +/- 6 mmHg; P < 0.01), and epinephrine concentration (from 14 +/- 1 pg.ml-1 to 279 +/- 51 pg.ml-1; P < 0.05). There was no significant change in norepinephrine concentration (from 198 +/- 37 pg.ml-1 to 277 +/- 46 pg.ml-1). The peak plasma epinephrine concentration was attenuated by each propofol pretreatment (158 +/- 35 pg.ml-1, propofol given 2 min before, and 146 + 41 pg.ml-1, propofol given 5 min before; P < 0.05), but neither propofol pretreatment modified the cardiovascular or norepinephrine responses. Conclusions Although able to blunt the increase in epinephrine concentration, propofol 2 mg.kg-1 propofol does no attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.


1987 ◽  
Vol 70 (6) ◽  
pp. 1031-1032
Author(s):  
Yuuko S Endoh ◽  
Ryozo Yamaoka ◽  
Nobuo Sasaki

Abstract A liquid chromatographic (LC) method is described for the quantitative determination of sulfamoyldapsone (2-sulfamoyl-4,4'-diaminodiphenyl sulfone) in swine muscle, liver, kidney, and fat. Sulfamoyldapsone was extracted from tissues with acetonitrile saturated with n-hexane. The extract was washed with n-hexane saturated with acetonitrile, concentrated, and cleaned up by alumina column chromatography. Sulfamoyldapsone was separated on an ODS column by using acetonitrile-methanol-water (6 + 18 + 76) and was detected at 292 nm. Overall average recovery of sulfamoyldapsone added to tissues at levels of 0.1 and 0.5 /μg/g was 93.3% ± 6.0. Detection limit was 0.02 μg/g in these tissues.


1988 ◽  
Vol 64 (1) ◽  
pp. 11-16 ◽  
Author(s):  
M. Kjaer ◽  
H. Galbo

Epinephrine responses to hypoglycemia and to identical relative work loads have been shown to be higher in endurance-trained athletes than in untrained subjects. To test the hypothesis that training increases the adrenal medullary secretory capacity, we studied the effects of glucagon (1 mg/70 kg iv), acute hypercapnia (inspired O2 fraction = 7%), and acute hypobaric hypoxia (inspired Po2 = 87 Torr), respectively, on the epinephrine concentration in arterialized hand vein blood in eight endurance-trained athletes [T, O2 uptake = 66 (62-70) ml.min-1.kg-1] and seven sedentary males [C, O2 uptake = 46 (41-50)]. In response to identical increments in glucagon concentrations, plasma epinephrine increased more in T than in C subjects [0.87 +/- 0.11 vs. 0.38 +/- 0.14 (SE) nmol/l, P less than 0.05]. In response to hypercapnia [arterial PCO2 = 56 +/- 0.7 Torr (T) and 55 +/- 0.4 (C), P greater than 0.05], the increment in epinephrine was significant in T (0.38 +/- 0.11 nmol/l) but not (P less than 0.1) in C subjects (0.22 +/- 0.11). Hypoxia [arterial PO2 = 42 +/- 2 Torr (T) and 41 +/- 2 (C), P greater than 0.05] increased epinephrine in T (0.22 +/- 0.10 nmol/l, P less than 0.05) but not in C subjects (0.01 +/- 0.07). The plasma norepinephrine concentration never changed, whereas heart rate always increased, the increase being higher (P less than 0.05) in T than in C subjects only during hypercapnia. The results indicate that training increases the capacity to secrete epinephrine.


1961 ◽  
Vol 201 (4) ◽  
pp. 723-728 ◽  
Author(s):  
Dorothy A. Piatnek ◽  
Robert E. Olson

A hyperthyroid state was induced and maintained in 17 dogs for 2–10 months by the administration of massive amounts of thyroid hormone. The great tolerance of this species to such large doses was striking. The clinical signs characteristic of hyperthyroidism in other mammals were observed including significantly increased caloric intake, oxygen consumption, heart rate, and body temperature. The laboratory findings included polycythemia, markedly increased levels of protein-bound iodide (PBI), increased turnover rates of l-thyroxine, and a decreased urinary excretion of inorganic iodide. Unlike other species the hyperthyroid dogs did not demonstrate marked reductions in body weight or serum cholesterol. Salivariectomy neither hastened nor enhanced the onset of exogenous hyperthyroidism in the dog. Measurements of the rate of disappearance of I131 l-thyroxine from the plasma and the rate of appearance of radioactive iodide in the urine indicated that the salivary glands in the intact dog are effective sites of deiodination and iodide excretion. This activity, however, is not the sole regulator of the level of circulating thyroid hormone and thus of the thyroid state.


1987 ◽  
Vol 70 (4) ◽  
pp. 706-707 ◽  
Author(s):  
Tomoko Nagata ◽  
Masanobu Saeki

Abstract A liquid chromatographic (LC) method is described for determination of olaquindox residues in swine tissues. The drug is extracted from tissues with acetonitrile, and the extract is evaporated to dryness. This residue is cleaned up by alumina column chromatography. LC analysis is carried out on a Nucleosil C18 column, and olaquindox is quantitated by ultraviolet detection at 350 nm. The average recoveries of olaquindox added to tissues at levels of 0.2, 0.1, and 0.05 ppm were 74.0, 68.6, and 66.3%, respectively. The detection limit was 2 ng for olaquindox standard and 0.02 ppm in tissues.


1982 ◽  
Vol 53 (4) ◽  
pp. 891-894 ◽  
Author(s):  
P. Lijnen ◽  
R. Fagard ◽  
J. Staessen ◽  
A. Amery

Plasma prostaglandins (PGE and PGF alpha), catecholamine concentration, and plasma renin activity (PRA) were measured during an uninterrupted graded exercise test on the bicycle ergometer in 11 hypertensive patients. Blood was withdrawn from the brachial and pulmonary arteries after 30 min of recumbent rest, after 15 min of rest sitting, and at the final work load of the exercise test, which averaged 143 +/- 16.5 W. Exercise did not provoke a significant change in these plasma PGE or PGF alpha concentrations, whereas a rise (P less than 0.001) in arterial PRA and (nor)epinephrine concentration was observed. It is thus unlikely that PGE or PGF alpha is an important determinant of PRA release during exercise, although circulating levels of PGE and PGF alpha do not necessarily reflect release rate or activity in the kidney.


1994 ◽  
Vol 86 (4) ◽  
pp. 441-446 ◽  
Author(s):  
M. J. Soares ◽  
L. S. Piers ◽  
P. S. Shetty ◽  
A. A. Jackson ◽  
J. C. Waterlow

1. Two groups of adult men were studied in Bangalore, India, under identical conditions: the ‘normal weight’ subjects (mean body mass index 20.8 kg/m2) were medical students of the institute with access to habitual energy and protein intakes ad libitum. The other group, designated ‘undernourished’, were labourers on daily wages (mean body mass index 16.7 kg/m2). 2. In an earlier study we obtained lower absolute values for both basal metabolic rate and protein synthesis in the undernourished subjects; however, when the data were expressed on a body weight or fat-free mass basis, a trend towards higher rates of protein synthesis, as well as higher basal metabolic rate, was evident. The suggestion was made that such results reflected the relatively higher energy intakes per kg body weight of the undernourished subjects on the day of study. The objective of the present study was therefore to control for the dietary intake during the measurement of whole body protein turnover. 3. In the present study dietary intakes were equated on a body weight basis; however, expressed per kg fat-free mass, the normal weight subjects had received marginally higher intakes of energy and protein. The results, however, were similar to those of the previous study. In absolute terms, basal metabolic rate, protein synthesis and breakdown were lower in the undernourished subjects. When expressed per kg body weight or per kg fat-free mass, the undernourished subjects had higher basal metabolic rates than the well-nourished subjects, whereas no differences were seen in the rate of protein synthesis or breakdown. 4. Estimates of muscle mass, based on creatinine excretion, indicated that the undernourished subjects had a higher proportion of non-muscle to muscle mass. Nitrogen flux (Q) was determined from 15N abundance in two end products, urea (Qu) and ammonia (Qa). The ratio Qu/Qa was increased in the undernourished subjects and was significantly correlated with the ratio of non-muscle to muscle mass (r = 0.81; P < 0.005). These results fit in with our earlier suggestion of a greater proportion of non-muscle (visceral) mass in undernourished subjects. 5. The present data suggest that there are no changes in the rate of protein synthesis or breakdown in chronic undernutrition when results are expressed, conventionally, per kg fat-free mass. It can be theoretically shown, however, that there could be a 15% reduction in the rate of turnover of the visceral tissues in chronic undernutrition. This, together with the reduced urinary nitrogen excretion, would contribute to nitrogen economy in these individuals.


2006 ◽  
Vol 190 (2) ◽  
pp. 407-414 ◽  
Author(s):  
Kely de Picoli Souza ◽  
Francemilson Goulart da Silva ◽  
Maria Tereza Nunes

The neonatal period (NP) is a critical phase of the development in which the expression pattern of most genes is established. Thyroid hormones (TH) play a key role in this process and, alterations in its availability in the NP may lead to different patterns of gene expression, which might reflect in the permanent expression of several genes in the adulthood. GH gene expression in the pituitary is greatly dependent on TH in the early postnatal life; thus, modifications of thyroid state in NP might lead to alterations in GH gene expression as well as to physiological repercussions in the adult life. This study aimed to investigate this possibility by means of the induction of a neonatal hyperthyroidism in rats (4 μg of 3,5,3′-triiodo-l-thyronine (T3)/100 g body weight, s.c.) for 5, 15 or 30 days, and further evaluation of GH gene expression, as well as its physiological consequences in adult rats subjected to a transient hyperthyroidism in the first 30 days of life. GH mRNA level was shown to be increased in T3-treated rats for 5 days; when the treatment was extended to 15 or 30 days, the GH mRNA levels were similar to the control group. Moreover, rats treated with T3 for 30 days and killed when 90 days old, i.e., 60 days at the end of the T3 treatment, showed decreased GH mRNA content, body weight, bone mineral density, and lean body mass. In conclusion: (1) T3 effects on GH gene expression depend on the period of life in which the hyperthyroidism is set and on the length of T3 treatment in the NP and (2) transient neonatal hyperthyroidism leads to a lower GH mRNA expression in adult life accompanied by physiological repercussions indicative of GH deficiency.


1992 ◽  
Vol 263 (1) ◽  
pp. E23-E27
Author(s):  
K. Oyama ◽  
J. Padbury ◽  
A. Martinez ◽  
B. Chappell ◽  
H. Stein ◽  
...  

There have been little data on catecholamine sulfoconjugation in developing animals or humans. We studied the differences in free and sulfoconjugated catecholamines at birth in newborn sheep. Baseline concentrations of sulfoconjugated norepinephrine and epinephrine were the predominant form of circulating catecholamine, representing 77 +/- 4 and 65 +/- 12% of total circulating catecholamines, respectively. At birth the free epinephrine concentration increased 10-fold (49 +/- 27 to 653 +/- 21 pg/ml, respectively), and plasma free norepinephrine concentration rose 4-fold (307 +/- 92 to 1,178 +/- 389 pg/ml). In contrast, there was only a transient twofold increase in the sulfoconjugated epinephrine. There was no increase in the sulfoconjugated form of norepinephrine. These data demonstrate that, while the near-term newborn sheep has a well-developed mechanism for sulfoconjugation of circulating catecholamines, this does not occur rapidly. During the logarithmic increases of circulating catecholamines at birth, there are not commensurate increases in the concentration of sulfoconjugated norepinephrine or epinephrine. Thus sulfoconjugation does not appear to represent a significant mechanism for inactivation of the high circulating levels of catecholamines seen at birth.


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