Triiodothyronine supplementation in a sheep model of intensive care
Triiodothyronine (T3) concentrations in plasma decrease during acute illness and it is unclear if this contributes to disease. Clinical and laboratory studies of T3 supplementation in disease have revealed little or no effect. It is uncertain if short term supplementation of T3 has any discernible e...
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Published in | Experimental and therapeutic medicine Vol. 28; no. 2; p. 321 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
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Spandidos Publications
01.08.2024
Spandidos Publications UK Ltd D.A. Spandidos |
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Abstract | Triiodothyronine (T3) concentrations in plasma decrease during acute illness and it is unclear if this contributes to disease. Clinical and laboratory studies of T3 supplementation in disease have revealed little or no effect. It is uncertain if short term supplementation of T3 has any discernible effect in a healthy animals. Observational study of intravenous T3 (1 µg/kg/h) for 24 h in a healthy sheep model receiving protocol-guided intensive care supports (T3 group, n=5). A total of 45 endpoints were measured including hemodynamic, respiratory, renal, hematological, metabolic and endocrine parameters. Data were compared with previously published studies of sheep subject to the same support protocol without administered T3 (No T3 group, n=5). Plasma free T3 concentrations were elevated 8-fold by the infusion (pmol/l at 24 h; T3 group 34.9±9.9 vs. No T3 group 4.4±0.3, P<0.01, reference range 1.6 to 6.8). There was no significant physiological response to administration of T3 over the study duration. Supplementation of intravenous T3 for 24 h has no physiological effect on relevant physiological endpoints in healthy sheep. Further research is required to understand if the lack of effect of short-term T3 may be related to kinetics of T3 cellular uptake, metabolism and action, or acute counterbalancing hormone resistance. This information may be helpful in design of clinical T3 supplementation trials. |
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AbstractList | Triiodothyronine (T3) concentrations in plasma decrease during acute illness and it is unclear if this contributes to disease. Clinical and laboratory studies of T3 supplementation in disease have revealed little or no effect. It is uncertain if short term supplementation of T3 has any discernible effect in a healthy animals. Observational study of intravenous T3 (1 µg/kg/h) for 24 h in a healthy sheep model receiving protocol-guided intensive care supports (T3 group, n=5). A total of 45 endpoints were measured including hemodynamic, respiratory, renal, hematological, metabolic and endocrine parameters. Data were compared with previously published studies of sheep subject to the same support protocol without administered T3 (No T3 group, n=5). Plasma free T3 concentrations were elevated 8-fold by the infusion (pmol/l at 24 h; T3 group 34.9±9.9 vs. No T3 group 4.4±0.3, P<0.01, reference range 1.6 to 6.8). There was no significant physiological response to administration of T3 over the study duration. Supplementation of intravenous T3 for 24 h has no physiological effect on relevant physiological endpoints in healthy sheep. Further research is required to understand if the lack of effect of short-term T3 may be related to kinetics of T3 cellular uptake, metabolism and action, or acute counterbalancing hormone resistance. This information may be helpful in design of clinical T3 supplementation trials. Triiodothyronine (T3) concentrations in plasma decrease during acute illness and it is unclear if this contributes to disease. Clinical and laboratory studies of T3 supplementation in disease have revealed little or no effect. It is uncertain if short term supplementation of T3 has any discernible effect in a healthy animals. Observational study of intravenous T3 (1 [micro]g/kg/h) for 24 h in a healthy sheep model receiving protocol-guided intensive care supports (T3 group, n=5). A total of 45 endpoints were measured including hemodynamic, respiratory, renal, hematological, metabolic and endocrine parameters. Data were compared with previously published studies of sheep subject to the same support protocol without administered T3 (No T3 group, n=5). Plasma free T3 concentrations were elevated 8-fold by the infusion (pmol/l at 24 h; T3 group 34.9 [+ or -] 9.9 vs. No T3 group 4.4 [+ or -] 0.3, P<0.01, reference range 1.6 to 6.8). There was no significant physiological response to administration of T3 over the study duration. Supplementation of intravenous T3 for 24 h has no physiological effect on relevant physiological endpoints in healthy sheep. Further research is required to understand if the lack of effect of short-term T3 may be related to kinetics of T3 cellular uptake, metabolism and action, or acute counterbalancing hormone resistance. This information may be helpful in design of clinical T3 supplementation trials. Key words: thyroid, liothyronine, triiodothyronine, critical illness, intensive care, metabolic, animal model Triiodothyronine (T3) concentrations in plasma decrease during acute illness and it is unclear if this contributes to disease. Clinical and laboratory studies of T3 supplementation in disease have revealed little or no effect. It is uncertain if short term supplementation of T3 has any discernible effect in a healthy animals. Observational study of intravenous T3 (1 [micro]g/kg/h) for 24 h in a healthy sheep model receiving protocol-guided intensive care supports (T3 group, n=5). A total of 45 endpoints were measured including hemodynamic, respiratory, renal, hematological, metabolic and endocrine parameters. Data were compared with previously published studies of sheep subject to the same support protocol without administered T3 (No T3 group, n=5). Plasma free T3 concentrations were elevated 8-fold by the infusion (pmol/l at 24 h; T3 group 34.9 [+ or -] 9.9 vs. No T3 group 4.4 [+ or -] 0.3, P<0.01, reference range 1.6 to 6.8). There was no significant physiological response to administration of T3 over the study duration. Supplementation of intravenous T3 for 24 h has no physiological effect on relevant physiological endpoints in healthy sheep. Further research is required to understand if the lack of effect of short-term T3 may be related to kinetics of T3 cellular uptake, metabolism and action, or acute counterbalancing hormone resistance. This information may be helpful in design of clinical T3 supplementation trials. |
ArticleNumber | 321 |
Audience | Academic |
Author | Torpy, David Kuchel, Tim Maiden, Matthew Clarke, Iain Nash, Coralie Matthews, Loren Ludbrook, Guy Chacko, Binila Porter, Susan |
AuthorAffiliation | 8 Department of Physiology, Faculty of Science, Monash University, Clayton, Victoria 3800, Australia 11 Preclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Hillcrest, South Australia 5086, Australia 4 Department of Critical Care, Melbourne Medical School, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Parkville, Victoria 3052, Australia 9 School of Agriculture, Food and Ecosystems Science, The University of Melbourne, Parkville, Victoria 3052, Australia 6 Discipline of Medicine, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia 5005, Australia 2 Intensive Care Unit, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia 5 Endocrine and Metabolic Unit, Department of Medicine, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia 1 Discipline of Acute Care Medicine, Adelaide Medic |
AuthorAffiliation_xml | – name: 2 Intensive Care Unit, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia – name: 1 Discipline of Acute Care Medicine, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia 5005, Australia – name: 4 Department of Critical Care, Melbourne Medical School, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Parkville, Victoria 3052, Australia – name: 7 Department of Anaesthesia, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia – name: 10 Department of Critical Care, Christian Medical College, Vellore, Tamil Nadu 632004, India – name: 8 Department of Physiology, Faculty of Science, Monash University, Clayton, Victoria 3800, Australia – name: 9 School of Agriculture, Food and Ecosystems Science, The University of Melbourne, Parkville, Victoria 3052, Australia – name: 3 Intensive Care Unit, Royal Melbourne Hospital, Parkville, Victoria 3052, Australia – name: 6 Discipline of Medicine, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia 5005, Australia – name: 11 Preclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Hillcrest, South Australia 5086, Australia – name: 5 Endocrine and Metabolic Unit, Department of Medicine, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia |
Author_xml | – sequence: 1 givenname: Matthew surname: Maiden fullname: Maiden, Matthew organization: Discipline of Acute Care Medicine, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia 5005, Australia – sequence: 2 givenname: David surname: Torpy fullname: Torpy, David organization: Endocrine and Metabolic Unit, Department of Medicine, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia – sequence: 3 givenname: Guy surname: Ludbrook fullname: Ludbrook, Guy organization: Discipline of Acute Care Medicine, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia 5005, Australia – sequence: 4 givenname: Iain surname: Clarke fullname: Clarke, Iain organization: Department of Physiology, Faculty of Science, Monash University, Clayton, Victoria 3800, Australia – sequence: 5 givenname: Binila surname: Chacko fullname: Chacko, Binila organization: Intensive Care Unit, Royal Adelaide Hospital, Central Adelaide Local Health Network, Adelaide, South Australia 5000, Australia – sequence: 6 givenname: Coralie surname: Nash fullname: Nash, Coralie organization: Discipline of Acute Care Medicine, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia 5005, Australia – sequence: 7 givenname: Loren surname: Matthews fullname: Matthews, Loren organization: Preclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Hillcrest, South Australia 5086, Australia – sequence: 8 givenname: Susan surname: Porter fullname: Porter, Susan organization: Preclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Hillcrest, South Australia 5086, Australia – sequence: 9 givenname: Tim surname: Kuchel fullname: Kuchel, Tim organization: Preclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Hillcrest, South Australia 5086, Australia |
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Keywords | intensive care thyroid critical illness triiodothyronine animal model liothyronine metabolic |
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Snippet | Triiodothyronine (T3) concentrations in plasma decrease during acute illness and it is unclear if this contributes to disease. Clinical and laboratory studies... |
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SubjectTerms | Anesthesia Animals Blood Clinical trials Dosage and administration Electrolytes Health aspects Heart surgery Hematology Hemodynamic monitoring Hemodynamics Hemoglobin Hormones Intensive care Ketamine Measurement Metabolism Methods Ostomy Physiology Plasma Pulmonary arteries Sheep Thyroid gland Thyroid hormones Transplants & implants Triiodothyronine Veins & arteries Ventilators |
Title | Triiodothyronine supplementation in a sheep model of intensive care |
URI | https://www.ncbi.nlm.nih.gov/pubmed/38939174 https://www.proquest.com/docview/3084628571 https://pubmed.ncbi.nlm.nih.gov/PMC11208762 |
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