Ci. Pantos et al., Hyperthyroidism is associated with preserved preconditioning capacity but intensified and accelerated ischaemic contracture in rat heart, BAS R CARD, 94(4), 1999, pp. 254-260
Background: The present study was undertaken to define the effects of thyro
xine administration on ischaemic preconditioning (PC) and the ischaemic con
tracture. Methods: Hyperthyroidism was induced by administration of L-thyro
xine in rats (THYR) while normal animals served as controls (NORMa). Isolat
ed rat hearts were perfused in a Langendorff preparation. NORMa control (n
= 16) and THYR control (n = 9) hearts underwent 20 min of ischaemia and 45
min reperfusion while NORMa PC (n = 16) and THYR PC (n = 14) were subjected
to PC before ischaemia. Additional normal hearts were subjected to 30 min
of ischaemia with and without PC, NORMb control, n = 8 and NORMb PC, n = 6.
Postischaemic recoveries of left ventricular (LV) developed pressure were
expressed as % of the initial value (LVDP%). Severity of contracture was me
asured by the time (Tmax) and magnitude (Cmax) of peak contracture. Results
: LVDP% was significantly higher after PC, both in NORMa and THYR rats. In
NORMa control hearts, ischaemic contracture had not yet reached a plateau a
t 20 min of ischaemia. Contracture appeared earlier in THYR control and PC
than in NORMa control and PC groups. Tmax was 22.1 (0.9) vs 16.8 (1.4) min
for NORMb control and PC, p < 0.05 and 12.5 (1.0) vs 9.3 (1.1) min for THYR
control and PC hearts, p < 0.05. Tmax was earlier in both THYR groups comp
ared to NORMb groups, p < 0.05. Cmax was significantly higher in both THYR
groups compared to both NORMb groups. Conclusion: Ischaemic contracture is
both accelerated and accentuated in thyroxine treated hearts while precondi
tioning capacity is preserved. Preconditioning and thyroxine administration
shorten Tmax in an additive way, whereas Cmax in hyperthyroid hearts did n
ot further increase by preconditioning.