Given the current T3 climate in the UK, we'd better hope that the authors of this paper know something we don't! They say "using commercially available and inexpensive T3"! Ho, bloomin' ho.
All too likely to end up both not available and hugely expensive.
I love the word "safely" in there.
Front Physiol. 2017 Apr 12;8:225. doi: 10.3389/fphys.2017.00225. eCollection 2017.
Modified Low-Dose Triiodo-L-thyronine Therapy Safely Improves Function Following Myocardial Ischemia-Reperfusion Injury.
Rajagopalan V1,2, Zhang Y2, Pol C2, Costello C2, Seitter S2, Lehto A2, Savinova OV2, Chen YF2, Gerdes AM2.
1 Department of Basic Sciences, New York Institute of Technology-College of Osteopathic MedicineJonesboro, AR, USA.
2 Department of Biomedical Sciences, New York Institute of Technology-College of Osteopathic MedicineOld Westbury, NY, USA.
Background: We have shown that thyroid hormones (THs) are cardioprotective and can be potentially used as safe therapeutic agents for diabetic cardiomyopathy and permanent infarction. However, no reliable, clinically translatable protocol exists for TH treatment of myocardial ischemia-reperfusion (IR) injury. We hypothesized that modified low-dose triiodo-L-thyronine (T3) therapy would confer safe therapeutic benefits against IR injury.
Methods: Adult female rats underwent left coronary artery ligation for 60 min or sham surgeries. At 2 months following surgery and T3 treatment (described below), the rats were subjected to functional, morphological, and molecular examination.
Results: Following surgery, the rats were treated with T3 (8 μg/kg/day) or vehicle in drinking water ad libitum following IR for 2 months. Oral T3 significantly improved left ventricular (LV) contractility, relaxation, and relaxation time constant, and decreased beta-myosin heavy chain gene expression. As it takes rats ~6 h post-surgery to begin drinking water, we then investigated whether modified T3 dosing initiated immediately upon reperfusion confers additional improvement. We injected an intraperitoneal bolus of T3 (12 μg/kg) upon reperfusion, along with low-dose oral T3 (4.5 μg/kg/day) in drinking water for 2 months. Continuous T3 therapy (bolus + low-dose oral) enhanced LV contractility compared with oral T3 alone. Relaxation parameters were also improved compared to vehicle. Importantly, these were accomplished without significant increases in hypertrophy, serum free T3 levels, or blood pressure.
Conclusions: This is the first study to provide a safe cardiac therapeutic window and optimized, clinically translatable treatment-monitoring protocol for myocardial IR using commercially available and inexpensive T3. Low-dose oral T3 therapy supplemented with bolus treatment initiated upon reperfusion is safer and more efficacious.
cardiac physiology; heart function; ischemia-reperfusion injury; therapeutic protocol; thyroid hormones