Effect of Triiodothyronine Administration on the Kidney During Haemorrhagic Shock and Resuscitation

Apoptosis, measured via caspase activity, can be used to assess renal tissue damage in haemorrhagic shock. We investigated whether Triiodothyronine could attenuate apoptosis and protect against haemorrhagic shock-induced renal injury.

Haemorrhagic shock was induced in swine until the mean arterial pressure (MAP) was 35-40 mmHg for 40 minutes. Animals were randomly assigned to a control group (n=5), Group-F (Fluid resuscitation, n=6), and Group-T3 (Fluid plus Triiodothyronine, n=6). The swine were resuscitated for 1 hour aiming to MAP restoration (±10% from baseline) and were followed up for another 360 minutes. Haemodynamic parameters, fluids, acid-base status, plasma urea nitrogen, creatinine levels and caspase activity in the kidney were measured.

Haemodynamic parameters did not differ significantly amongst the three groups. Group-T3 required less normal saline (Group-T3: 1083±204 mL versus F: 2500±547 mL, p=0.001) and hydroxyethyl starch (Group-T3: 558±102 mL versus F: 916±204 mL, p=0.004) during resuscitation. Additionally, Group-T3 swine experienced less acidosis following haemorrhage/resuscitation with a pH of 7.39 versus a pH of 7.26 in Group-F (p=0.004) at 360 minutes. Urea remained within normal limits in all groups, but creatinine levels were elevated at 6 hours in Group-F as compared to Group-T3 (p=0.019). Apoptosis, assessed by renal caspase-3 activity, was increased in Group-T3 (132±174 pmol minute^-1 g^-1) and reduced in Group-F (32±18 pmol minute^-1 g^-1) as compared to the control group, but without statistical significance (p=0.245 between Group-T3 and Group-F).

Administration of Triiodothyronine in a swine model of haemorrhagic shock seems to interfere with renal cell apoptosis. The exact mechanism needs to be further investigated in future research.