Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reported failure of serum TSH to rise in response to the low serum T3 of severe systemic illness may be due to the known stress inhibition of TSH secretion. We therefore measured TSH and total and free thyroid hormones during the course of recovery from severe illness. During recovery, TSH increased at a time when T3 was rising but still below normal (mean TSH during recovery, 6.5 +/- 0.8 SEM microU/ml, n = 41 vs. normal, 2.5 +/- 0.2 SEM microU/ml; n = 31; P less than 0.001), TSH concentrations were negatively correlated with total and free T3 and less strongly correlated with total T4 but not with free T4. Average TSH concentrations were also significantly elevated in severely ill patients with hypothermia that was unrelated to cold exposure (mean TSH, 5.6 +/- 1.3 microU/ml; n = 11; P less than 0.005). The T3 concentrations in these sera were lower than those of other severely ill patients. Thus, during recovery from severe illness and during hypothermia not induced by cold, the relationship between serum T3 and TSH is qualitatively similar to that seen in primary hypothyroidism and may imply a pituitary response to a deficiency of thyroid hormone.
 ...
PMID:The relationship between serum triiodothyronine and thyrotropin during systemic illness. 707 98

Female rats were killed 15 days, 2 months, and 4 months after surgical thyroidectomy that was followed by injection of 100 microCi 131I. The concentrations of T3 and T4 were measured in tissues (liver, kidney, brain, heart, and hindleg muscle) specific RIAs. Results were compared to those found in intact rats. Thyroidectomy resulted in severe hypothyroidism by 2 and 4 months after the operation, as assessed by undetectable levels of T4 and T3 in unextracted plasma, high circulating TSH, hypothermia, stasis of body weight increase, and depletion of pituitary GH content. Concentrations of T4 and T3 in plasma, as determined after extraction and concentration, were very low, being less than 5% of the normal value by the earliest observation period (15 days). In contrast, although tissue concentrations and total organ contents also decreased after thyroidectomy, they were still clearly detectable 4 months after thyroidectomy. The rates of decrease of T4 and T3 concentrations in most tissues were markedly slower than expected from their rapid decrease in plasma. Some tissues still contained 20% of the normal level 2-4 months after ablation of the thyroid. Tissue levels of thyroid hormones were hardly detectable in rats thyroidectomized 6 months before, having decreased in most tissues to less than 5% of the normal value. Several animals from this group had died. It is concluded that tissues from severely hypothyroid thyroidectomized rats may contain higher concentrations of T4 and T3 than previously thought. The idea that thyroid hormone is not essential for life, based on the assumption that thyroidectomized animals survive without thyroid hormones, might have to be reevaluated.
 ...
PMID:Presence of L-thyroxine and 3,5,3'-triiodo-L-thyronine in tissues from thyroidectomized rats. 726 25

A patient with mild hypothyroidism underwent a repair of abdominal aortic aneurysm. Although the serum TSH level of this patient was very high and T4, free T4 levels were low, T3 level remained within normal ranges. Inhalation anesthesia with continuous epidural block was selected and there was no complication such as hypotension or hypothermia during perioperative period. Recently, several reports demonstrate that the preoperative supplemental therapy of the thyroid hormone should not be necessary in the case of mild hypothyroidism. Moreover, the biological potency of T3 is higher than that of T4. Thus, in patients whose T3 level is kept within normal ranges even if serum T4 level is low and serum TSH level is high, we may say that they are in euthyroid state. We think these patients can be anesthetized safely.
 ...
PMID:[Anesthetic management of a patient with mild hypothyroidism]. 807 61

Myxedema coma is the most severe form of hypothyroidism and is characterized by extreme hypothermia, bradycardia, central hypoventilation and hypoxia. Common causes are intercurrent diseases, interruption of thyroid hormone treatment, or an overdose of sleeping pills or sedatives. The diagnosis is usually readily established on the basis of very high serum TSH and low T4 levels. Consideration must also be given to an extra-thyroidal influence on the hormone levels. Intensive care treatment involving intravenous high-dose L-thyroxine and the reversal of hypoxia improve the prognosis of the serious disease.
 ...
PMID:[Coma in myxedema--a rare complication of hypothyroidism. Possible iatrogenic factors should be taken into account]. 908 99

Hypothermic hyperkalemic circulatory arrest has been widely used for myocardial protection during heart surgery. Recent data showed that administration of triiodo-L-thyronine (T3) postoperatively enhanced ventricular function. The effect of hyperkalemic arrest in conjunction with thyroid hormone on the plasma membrane enzyme sodium/potassium-adenosine triphosphatase (Na/K-ATPase), was determined in cultured neonatal rat atrial and ventricular myocytes. Exposure of ventricular myocytes to hyperkalemic medium (50 mM KCl) in the absence of T3 increased expression of the Na/K-ATPase catalytic subunit mRNAs, alpha1 and alpha3 isoforms, by 1.9- and 1.5-fold, respectively (p<0.01), which were accompanied by similar increases (1.4- and 1.8-fold) in protein content. Addition of T3 to the hyperkalemic cultures attenuated these increases in Na/K-ATPase mRNA isoforms to levels of expression observed in cells treated with T3 (10(-8) M) alone. Similarly, expression of the alpha1 mRNA isoform in atrial myocytes was increased (p<0.05) by hyperkalemic conditions, and T3 treatment attenuated this effect. In contrast, although expression of the Na/K-ATPase beta1 mRNA in both atrial and ventricular myocytes was significantly increased by hyperkalemia, addition of T3 did not prevent the hyperkalemic response, and in atrial myocytes T3 significantly increased beta1 mRNA expression 1.8-fold. These results show that expression of cardiac Na/K-ATPase is regulated by T3 and hyperkalemia in an isoform and chamber specific manner, and suggest that use of hyperkalemic cardioplegia during heart surgery may alter plasma membrane ion function.
 ...
PMID:Regulation of Na/K-ATPase gene expression by thyroid hormone and hyperkalemia in the heart. 1003 77

We tested the effect of chronic leptin treatment on fasting-induced torpor in leptin-deficient A-ZIP/F-1 and ob/ob mice. A-ZIP/F-1 mice have virtually no white adipose tissue and low leptin levels, whereas ob/ob mice have an abundance of fat but no leptin. These two models allowed us to examine the roles of adipose tissue and leptin in the regulation of entry into torpor. Torpor is a short-term hibernation-like state that allows conservation of metabolic fuels. We first characterized the A-ZIP/F-1 animals, which have a 10-fold reduction in total body triglyceride stores. Upon fasting, A-ZIP/F-1 mice develop a lower metabolic rate and decreased plasma glucose, insulin, and triglyceride levels, with no increase in free fatty acids or beta-hydroxybutyrate. Unlike control mice, by 24 hr of fasting, they have nearly exhausted their triglycerides and are catabolizing protein. To conserve energy supplies during fasting, A-ZIP/F-1 (but not control) mice entered deep torpor, with a minimum core body temperature of 24 degrees C, 2 degrees C above ambient. In ob/ob mice, fasting-induced torpor was completely reversed by leptin treatment. In contrast, neither leptin nor thyroid hormone prevented torpor in A-ZIP/F-1 mice. These data suggest that there are at least two signals for entry into torpor in mice, a low leptin level and another signal that is independent of leptin and thyroid hormone levels. Studying rodent torpor provides insight into human torpor-like states such as near drowning in cold water and induced hypothermia for surgery.
 ...
PMID:Torpor in mice is induced by both leptin-dependent and -independent mechanisms. 1058 55

A 49-year-old man with herpes simplex encephalitis at age 22 was admitted with hypotension (90/60 mm Hg) and hypothermia (33.7 degrees C). His blood pressure was 80-90/50-60 mm Hg, with temperatures averaging 35 degrees C, for at least 3 years before admission. Evaluation of his hypothermia and hypotension revealed a low free triiodothyronine, low normal thyrotropin, luteinizing hormone < 2 mIU/L, follicle stimulating hormone <3 mIU/L, and low testosterone of 1.39 ng/dL. A baseline cortisol of 13.9 microg/dL was stimulated to 41.8 microg/dL with corticotropin, indicating he had partial anterior hypopituitarism with an intact pituitary-adrenal axis. Posterior pituitary function was normal. MRI revealed a "bright" posterior pituitary on a T1-weighted image, further indicating a normal posterior pituitary. Extensive decreased T1-weighting on MRI in the right and left temporal lobes was consistent with encephalomalacia. With thyroid hormone replacement, his blood pressure increased to 110/70 mm Hg with a temperature of 37 degrees C.
 ...
PMID:Post-herpes encephalitic anterior pituitary insufficiency with hypothermia and hypotension. 1106 53

Since the introduction of neonatal mass screening for congenital hypothyroidism (CH), numerous cases have been detected. It is of interest that even severely hypothyroid neonates rarely exhibit bradycardia, hypothermia, or inactivity, which have been recognized as typical signs of CH. Regarding neonates and young infants, few reported data are available on the effects of thyroid hormones on energy expenditure. Plasma free fatty acids (FFAs), markers for lipolysis, play essential roles in maintaining physiologic homeostasis. To study fuel utilization in CH neonates, we measured heart rates, plasma FFA, and thyroid hormones before and after levothryoxine (LT4) replacement therapy. Fifty-five screen-detected CH neonates and 29 age-matched normal neonates for controls were enrolled. The CH neonates were divided into two groups according to serum thyroid hormone levels: a mildly hypothyroid group (n = 37), serum thyrotropin (TSH) less than 100 microIU/mL and free thyroxine (FT4) 0.6 ng/dL or more; and a severely hypothyroid group (n = 18), TSH 100 microIU/mL or more and FT4 less than 0.6 ng/dL. Twenty-four of the 55 patients had their heart rates measured by electrocardiography. Fasting blood samples were taken from the subjects during physical movements. Serum levels of TSH, FT4, FFA, and other blood chemicals, measured on an autoanalyzer system in our hospital, were compared before and after LT4 substitution therapy. The following results were obtained. The mean plasma FFA values before LT4 replacement were 208.5 +/- 89.4 microEq/L in the mildly hypothyroid group, 228.5 +/- 114.7 microEq/L in the severely hypothyroid group, and 213.9 +/- 97.7 microEq/L in controls. No statistical differences were noted among the three values. Two months after LT4 replacement therapy, at the age of 3 months, plasma FFA concentrations significantly increased in both groups compared with those before the therapy. Control infants also showed a significant increase in plasma FFA concentrations from 1 to 3 months of age. There were no significant differences in plasma FFA concentrations among the three groups at the age of 3 months. No significant correlations were found between plasma FFA and serum thyroid hormones. From these results it is suggested that in neonates and young infants, thyroid hormones do not play major roles in mobilization of fats through the adrenergic regulation of lipolysis for energy supply. This may be one of the reasons for the unexpectedly mild signs and symptoms in the screen-detected hypothyroid neonates.
 ...
PMID:Plasma free fatty acids in neonates with congenital hypothyroidism. 1127 1

Myoglobin (Mb) gene expression, Citrate Synthase (CS) and Succinate Dehydrogenase (SDH) activities of Soleus (S) and Extensorum Digitalis Longus (EDL) muscles were studied in intact, thyroidectomized and T3-treated (25 microg/100g, BW, ip, 15 days) rats. The fiber type composition of S muscle was also evaluated and used as control of the T3-induced effects. In the S muscle, the T3 treatment increased the Mb mRNA and protein expression, as well as the CS and SDH activity. These changes occurred parallel to the expected increase in type II (fast) and decrease in type I (slow)-fibers in S muscle. In the hypothyroid state, the Mb mRNA was decreased, while the Mb expression and CS activity tended to decrease. In contrast the SDH activity was increased, probably due to the enhanced motor activity that occurs as a short-term response to the hypothermia induced by hypothyroidism. In the EDL, the alterations were milder than those in S muscle in both thyroid states. These findings show that Mb gene expression is induced by T3. This is concomitant with the enhancement of Krebs Cycle enzyme activities and provides additional evidence that thyroid hormone increases the aerobic potential of skeletal muscles, as well as the speed of muscle contraction.
 ...
PMID:Thyroid hormone stimulates myoglobin expression in soleus and extensorum digitalis longus muscles of rats: concomitant alterations in the activities of Krebs cycle oxidative enzymes. 1144 1

Hypothyroid status is believed to cause various metabolic changes in infants. However, it is interesting that even severely hypothyroid neonates, detected during mass neonatal screening, rarely show bradycardia, hypothermia, or inactivity. To study cardiac functions of screen-detected neonates with congenital hypothyroidism (CH), we recorded the electrocardiograms (ECG) of 53 screen-detected CH neonates before levothyroxine (LT4) replacement therapy, and 15 age-matched normal neonates for controls. The 53 CH neonates were divided into two groups according to initial serum thyroid hormone levels: a mildly hypothyroid group (n = 37), serum thyroid-stimulating hormone (TSH) less than 100 microIU/mL and free thyroxine (FT4) 0.6 ng/dl or more; and a severely hypothyroid group (n = 16), TSH 100 microIU/mL or more and FT4 less than 0.6 ng/dL. TSH, FT4, and other blood chemicals were measured on an autoanalyzer (Hitachi 7170). After blood sampling, the ECG was recorded during induced sleep by oral administration of triclofos sodium syrup. ECG parameters, including HR, PR, QRS, QT time and corrected QT time (QTc) were automatically obtained, using an auto-ECG analyzing system. The following results were obtained. No CH patients showed abnormal ECG findings. There was no significant difference of the mean heart rates (HRs) between the mildly hypothyroid (147.5 +/- 16.3 beats per minute) and the control group (148.3 +/- 12.1 beats per minute). The mean HR in the severely hypothyroid group (134.0 +/- 17.9 beats per minute, p = 0.007) was significantly low compared with the normal control group. However, all values were within normal ranges. QTc in the severely hypothyroid group (0.414 +/- 0.015, p = 0.033) was significantly shorter than in the control group (0.440 +/- 0.052). No statistical differences of PR, QRS, and QT time were noted among the three groups. All ECG parameters were within normal ranges. HR positively correlated with FT4 and log (FT4), and negatively with TSH and log (TSH). From these results we conclude that the deficiency of thyroid hormones does not affect ECG findings of congenitally hypothyroid neonates. This may be consistent with the unexpectedly mild signs and symptoms of screen-detected hypothyroid neonates.
 ...
PMID:Effects of thyroid hormone deficiency on electrocardiogram findings of congenitally hypothyroid neonates. 1152 69


<< Previous 1 2 3 4 5 6 Next >>