Altitude-induced changes in plasma thyroxine, 3,5,3'-triiodothyronine, and thyrotropin in rats

1982 ◽  
Vol 53 (2) ◽  
pp. 313-315 ◽  
Author(s):  
J. M. Connors ◽  
L. G. Martin

We have studied the thyroid function of high-altitude-acclimated (6,900 m for 5 wk) and nonaltitude-acclimated control (198 m) rats. After 5 wk of high-altitude exposure the plasma concentrations of both thyroxine (T4) and triiodothyronine (T3) were lower than those in control rats (4.7 +/- 0.3 vs. 3.3 +/- 0.2 microgram/dl and 96 +/- 5 vs. 74 +/- 6 ng/dl, respectively). The plasma thyrotropin (TSH) concentration was elevated in the high-altitude-acclimated rats compared with controls (52 +/- 4 vs. 29 +/- 3 micrograms/dl, respectively). Gross anatomical (thyroid wt/body wt) and histological observations of thyroid tissue were consistent with elevated plasma TSH concentrations. These results suggest that the fall in the plasma concentrations of T4 and T3 during acclimation to severe hypoxia is due to a primary block of thyroid secretion and not to a fall in plasma TSH levels.

2001 ◽  
Vol 280 (1) ◽  
pp. R149-R155 ◽  
Author(s):  
Rochelle Buffenstein ◽  
Ryan Woodley ◽  
Cleopatra Thomadakis ◽  
T. Joseph M. Daly ◽  
David A. Gray

Cold acclimation induces very divergent responses in thyroid function in reptiles and mammals reflective of their different thermoregulatory modes. Naked mole-rats, unlike other small mammals, are unable to effectively employ endothermy and are operatively poikilotherms. We therefore investigated changes in their thyroid status with chronic cold exposure. Under simulated burrow conditions, free thyroxine (T4; 0.39 ± 0.09 ng/dl) and thyroid stimulating hormone (TSH; 1.12 ± 0.56 μIU/ml) levels fell within the reptilian range, one order of magnitude lower than mammalian levels. However, cold induced typical mammalian responses: free T4levels (0.55 ± 0.09 ng/dl) and thyroid follicular cell height were significantly greater. Although TSH levels (1.28 ± 0.83 μIU/ml) were not significantly elevated, thyrotrophs exhibited ultrastructural signs of increased secretory activity. Low thyroid hormone concentrations may contribute substantially to the unusual thermoregulatory mode exhibited by naked mole-rats.


2006 ◽  
Vol 91 (2) ◽  
pp. 530-534 ◽  
Author(s):  
Marcus Dörr ◽  
Daniel M. Robinson ◽  
Henri Wallaschofski ◽  
Christian Schwahn ◽  
Ulrich John ◽  
...  

Background: Elevated plasma fibrinogen levels are associated with an increased risk of cardiovascular events. Decreased serum TSH predicts vascular mortality, which hypothetically could be explained in part by alterations in the blood coagulation system. Objective: The objective of this study was to investigate the association between thyroid function and plasma fibrinogen levels in a general population. Design: The population-based Study of Health in Pomerania was performed in a previously iodine-deficient area in Germany, including 4310 subjects, aged 20–79 yr. Data for 3804 individuals without thyroid disease were analyzed. Analysis revealed an association between thyroid function status and plasma fibrinogen concentration. Results: Elevated fibrinogen levels (>3.25 g/liter) were observed in 14 subjects with increased serum TSH levels (32.6%), 973 euthyroid subjects (28.9%), 158 subjects with decreased serum TSH levels (40.7%), and six individuals with overt hyperthyroidism (54.4%). Logistic regression analysis revealed decreased serum TSH as an independent risk factor for elevated fibrinogen levels (odds ratio, 1.42; 95% confidence interval, 1.12–1.80). Conclusions: Thyroid function is associated with plasma fibrinogen. Decreased serum TSH is an independent risk factor for elevated plasma fibrinogen levels as a possible explanation for the high cardiovascular mortality among affected subjects.


Diabetes ◽  
1992 ◽  
Vol 41 (9) ◽  
pp. 1160-1164 ◽  
Author(s):  
J. C. Levy ◽  
J. L. Morton ◽  
M. Davenport ◽  
A. Beloff-Chain ◽  
R. C. Turner

Hypertension ◽  
2013 ◽  
Vol 61 (4) ◽  
pp. 793-799 ◽  
Author(s):  
Paolo Salvi ◽  
Miriam Revera ◽  
Andrea Faini ◽  
Andrea Giuliano ◽  
Francesca Gregorini ◽  
...  

2016 ◽  
Vol 23 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Daniel A. Nation ◽  
Mark W. Bondi ◽  
Ellis Gayles ◽  
Dean C. Delis

AbstractObjectives: Cognitive dysfunction from high altitude exposure is a major cause of civilian and military air disasters. Pilot training improves recognition of the early symptoms of altitude exposure so that countermeasures may be taken before loss of consciousness. Little is known regarding the nature of cognitive impairments manifesting within this critical window when life-saving measures may still be taken. Prior studies evaluating cognition during high altitude simulation have predominantly focused on measures of reaction time and other basic attention or motor processes. Memory encoding, retention, and retrieval represent critical cognitive functions that may be vulnerable to acute hypoxic/ischemic events and could play a major role in survival of air emergencies, yet these processes have not been studied in the context of high altitude simulation training. Methods: In a series of experiments, military aircrew underwent neuropsychological testing before, during, and after brief (15 min) exposure to high altitude simulation (20,000 ft) in a pressure-controlled chamber. Results: Acute exposure to high altitude simulation caused rapid impairment in learning and memory with relative preservation of basic visual and auditory attention. Memory dysfunction was predominantly characterized by deficiencies in memory encoding, as memory for information learned during high altitude exposure did not improve after washout at sea level. Retrieval and retention of memories learned shortly before altitude exposure were also impaired, suggesting further impairment in memory retention. Conclusions: Deficits in memory encoding and retention are rapidly induced upon exposure to high altitude, an effect that could impact life-saving situational awareness and response. (JINS, 2017, 23, 1–10)


1986 ◽  
Vol 9 (5) ◽  
pp. 367-370 ◽  
Author(s):  
C. P. Reilly ◽  
R. G. Symons ◽  
M. L. Wellby

2017 ◽  
Vol 102 (11) ◽  
pp. 4235-4241 ◽  
Author(s):  
Meg Henze ◽  
Suzanne J Brown ◽  
Narelle C Hadlow ◽  
John P Walsh

Abstract Context Thyroid function testing often uses thyrotropin (TSH) measurement first, followed by reflex testing for free thyroxine (T4) if TSH is outside the reference range. The utility of different TSH cutoffs for reflex testing is unknown. Objective To examine different TSH cutoffs for reflex free T4 testing. Design, Setting, and Patients We analyzed concurrent TSH and free T4 results from 120,403 individuals from a single laboratory in Western Australia (clinical cohort) and 4568 Busselton Health Study participants (community cohort). Results In the clinical cohort, restricting free T4 measurement to individuals with TSH <0.3 or >5.0 mU/L resulted in a 22% reduction in free T4 testing compared with a TSH reference range of 0.4 to 4.0 mU/L; using TSH cutoffs of 0.2 and 6.0 mU/L resulted in a 34% reduction in free T4 testing. In the community cohort, the corresponding effect was less: 3.3% and 4.8% reduction in free T4 testing. In the clinical cohort, using TSH cutoffs of 0.2 and 6.0 mU/L, elevated free T4 would go undetected in 4.2% of individuals with TSH levels of 0.2 to 0.4 mU/L. In most, free T4 was marginally elevated and unlikely to indicate clinically relevant hyperthyroidism. Low free T4 would go undetected in 2.5% of individuals with TSH levels of 4 to 6 mU/L; in 94%, free T4 was marginally reduced and unlikely to indicate clinically relevant hypothyroidism. Conclusions Setting TSH cutoffs at 0.1 to 0.2 mU/L less than and 1 to 2 mU/L greater than the reference range for reflex testing of free T4 would reduce the need for free T4 testing, with minimal effect on case finding.


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