ETA2023 Poster Presentations Thyroid Physiology in Periphery & Development Basic (9 abstracts)
Combined triiodothyronine and preconditioning improves cardiac diastolic dysfunction in ex vivo rat hearts subjected to normothermic perfusion: a new method for donor heart preservation
Iordanis Mourouzis 1 , Dimitris Anagnostopoulos 2 , Vassiliki Brozou 2 , Dimitris Kounatidis 2 , Dimitris Giannoulis 2 , Theodosios Saranteas 2 , Georgia Kostopanagiotou 3 & Constantinos Pantos 4
1National and Kapodistrian University of Athens, Pharmacology, Athens, Greece; 2National and Kapodistrian University of Athens, Medical School, Pharmacology, Greece; 3National and Kapodistrian University of Athens, Medical School; 4National and Kapodistrian University of Athens, Pharmacology, Greece
Objectives: Machine perfusion may become a platform for cardioprotective approaches, enabling repair and reconditioning of donor hearts. Ischemic preconditioning (PC) is a powerful means of cardioprotection. Triiodothyronine (T3) is shown to repair the injured myocardium and recently this cardioprotective action was demonstrated in an ex vivo rat heart normothermic perfusion model. This study investigated potential effects of low-flow PC with and without T3 administration in an ex vivo rat heart model.
Methods: Rat hearts were perfused in Langendorff apparatus with constant flow. Control isolated hearts were subjected to normothermic perfusion (NP) with Krebs-Henseleit for 6h (NP, n =9). Another group of hearts, after stabilization for 30min, was perfused with normal flow for 30 min followed by 5 cycles of preconditioning (40 min of low flow perfusion and 20 min normal flow perfusion) with either vehicle (PC, n =11) or 60nM T3 (PC+T3, n =10) in the perfusate. T3 or vehicle administration started at the end of stabilization period (30min). Left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), perfusion pressure (PP), as an indirect index of microvascular function and % change of these parameters from baseline values were measured.
Results: Changes in LVEDP and PP are shown in table as Mean (SD). LVEDP at the end of perfusion was significantly increased from the baseline in both NP and PC groups. The magnitude of this change was significantly less in PC hearts vs NP. In PC+T3 hearts, LVEDP at the end of perfusion was similar to baseline. PP at the end of perfusion was significantly increased from the baseline in all groups, however this increase was significantly less in both PC and PC+T3 hearts vs NP. LVDP at the end of perfusion was significantly reduced from baseline in all groups and no difference between the groups was observed.
| LVEDP (mmHg) | PP (mmHg) | |||||
| End of stabilization (30 min) | End of perfusion (360min) | % Change | End of stabilization (30 min) | End of perfusion (360min) | % Change | |
| NP | 7.6 (0.3) | 21.8 (7.0)* | 188 (94)% | 69 (5) | 153 (47) | 120 (63)% |
| PC | 7.7 (0.4) | 13.4 (7.8)* # | 73 (98)% # | 68 (6) | 105 (22)* # | 58 (35)% # |
| PC+T3 | 7.6 (0.3) | 8.3 (4.6) # | 8 (58)% # | 66 (4) | 90 (19)* # | 39 (27)% # |
| * P < 0.05 vs Baseline, paired samples t-test, # P < 0.05 vs NP, OneWay ANOVA | ||||||
Conclusion: PC limits cardiac and microvascular dysfunction and T3 added to PC prevents the increase in LVEDP after prolonged perfusion. These data may have important therapeutic implications for normothermic perfusion of marginal human donor hearts.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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