[
Abstract]
[
Full Text PDF] （in Japanese / 2229KB）
[Members Only And Two Factor Auth.] J.Jpn. Surg. Soc.. 89(10): 1587-1593, 1988
Original article
THE EFFECT OF TRIIODOTHYRONINE (T3) AND REVERSE TRIIODO-THYRONINE (rT3) ON CANINE HEMORRHAGIC SHOCK
The euthyroid sick (“low T
3") syndrome occurs in circulatory collapse and could influence survival. To evaluate the role of T
3 and rT
3 in shock, 36 mongrel dogs were subjected to hemorrhagic shock. In 13 dogs 15μg/kg of T
3 was given after 60 min of hypotension and 15μg/kg of rT
3 was administered IV 30min before hemorrhage in 10 dogs. An equal volurne of saline was injected in 13 dogs for control study. These dogs were bled rapidly into a reservoir to a mean arterial pressure (MAP) of 40mmHg. After 60 min of hypotension the reservoir line was clamped for 30 min. The shed blood was then reinfused over 30 min. T
3 administration caused significant increases during the clamped period in cardiac output, stroke volume, MAP, right and left ventricular stroke work and systemic vascular resistance, with a decrease in pulmoanry vascular resistance (PVR), In the group receiving rT
3 the only significant hemodynamic-metabolic differences were PVR and mean arterial pH. In the control group, 6 of 13 dogs died, whereas 9 of 10 dogs given rT
3 died (p＜0.03) and only one of 13 T
3 dogs died (p＜0.05). This study strongly suggests that T
3 improves survival by acting on cardiovascular receptors or via the hypothalamic-pituitary-thyroid axis and that exogeneous rT
3 is detrimental during the stress of shock and may play a biologically causative role in the sick euthyroid syndrome.
To read the PDF file you will need Adobe Reader installed on your computer.