| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
114-267 |
DRI_Background |
denotes |
Hydroxyl radicals (OH) are involved in the pathogenesis of reperfusion injury and are observed in acute heart failure, stroke, and myocardial infarction. |
| T2 |
268-489 |
DRI_Background |
denotes |
Two different subcellular defects are involved in the pathogenesis of OH injury, deranged calcium handling, and alterations of myofilament responsiveness, but their temporal impact on contractile function is not resolved. |
| T3 |
490-608 |
DRI_Approach |
denotes |
Initially, after brief OH exposure, there is a corresponding marked increase in diastolic calcium and diastolic force. |
| T4 |
609-709 |
DRI_Approach |
denotes |
We followed these parameters until a new steady-state level was reached at ~45 min post-OH exposure. |
| T5 |
710-845 |
DRI_Background |
denotes |
At this new baseline, diastolic calcium had returned to near-normal, pre-OH levels, whereas diastolic force remained markedly elevated. |
| T6 |
846-967 |
DRI_Background |
denotes |
An increased calcium sensitivity was observed at the new baseline after OH-induced injury compared with the pre-OH state. |
| T7 |
968-1119 |
DRI_Challenge |
denotes |
The acute injury that occurs after OH exposure is mainly due to calcium overload, while the later sustained myocardial dysfunction is mainly due to the |
| T8 |
1150-1165 |
DRI_Challenge |
denotes |
responsiveness. |
