2003年6月
Lysophosphatidylcholine-induced myocardial damage is inhibited by pretreatment with poloxamer 188 in isolated rat heart
Molecular and Cellular Biochemistry
- ,
- 巻
- 248
- 号
- 1-2
- 開始ページ
- 209
- 終了ページ
- 215
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1023/A:1024165125139
Lysophosphatidylcholine (LPC) accumulates in myocardial tissues and coronary sinus during ischemia, and plays important role in the development of ischemia-reperfusion injury and ischemic ventricular arrhythmia. The aim of this study was to examine whether pretreatment of poloxamer 188 (P-188), a nonionic and non-toxic surfactant, can prevent the cardiac dysfunction induced by exogenous LPC perfusion in Langendorff perfused rat heart model. LPC (6 μM) significantly (p <
0.05) decreased heart rate (HR) and left ventricular developed pressure (LVDP) from 274.3 ± 23.2 to 175.0 ± 42.9/min and from 115.9 ± 11.3 to 26.7 ± 7.1 mmHg, respectively. The LPC-induced reduction of HR and LVDP did not recover by washout of LPC. Pretreatment with P-188 (1 mM for 30 min) inhibited completely the LPC-induced decreases of HR and LVDP. The pretreatment with P-188 also prevented the LPC-induced increases of left ventricular end-diastolic pressure (LVEDP) and GOT release, significantly (p <
0.05). The coronary perfusion pressure (CPP) rose (p <
0.01) by the LPC perfusion from 71.9 ± 5.3 to 121.9 t 13.0 mmHg, significantly, but pretreatment of P-188 did not affect the LPC-induced vasoconstriction. Our results suggest that exogenous LPC causes irreversible cardiac injury by the sarcolemmal membrane disruption followed by Ca overload, and this LPC-induced cardiac injury, probably, can be prevented by the pretreatment with poloxamer 188.
0.05) decreased heart rate (HR) and left ventricular developed pressure (LVDP) from 274.3 ± 23.2 to 175.0 ± 42.9/min and from 115.9 ± 11.3 to 26.7 ± 7.1 mmHg, respectively. The LPC-induced reduction of HR and LVDP did not recover by washout of LPC. Pretreatment with P-188 (1 mM for 30 min) inhibited completely the LPC-induced decreases of HR and LVDP. The pretreatment with P-188 also prevented the LPC-induced increases of left ventricular end-diastolic pressure (LVEDP) and GOT release, significantly (p <
0.05). The coronary perfusion pressure (CPP) rose (p <
0.01) by the LPC perfusion from 71.9 ± 5.3 to 121.9 t 13.0 mmHg, significantly, but pretreatment of P-188 did not affect the LPC-induced vasoconstriction. Our results suggest that exogenous LPC causes irreversible cardiac injury by the sarcolemmal membrane disruption followed by Ca overload, and this LPC-induced cardiac injury, probably, can be prevented by the pretreatment with poloxamer 188.
- リンク情報
-
- DOI
- https://doi.org/10.1023/A:1024165125139
- CiNii Articles
- http://ci.nii.ac.jp/naid/80016064289
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/12870676
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0037966165&origin=inward
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=0037966165&origin=inward
- ID情報
-
- DOI : 10.1023/A:1024165125139
- ISSN : 0300-8177
- CiNii Articles ID : 80016064289
- PubMed ID : 12870676
- SCOPUS ID : 0037966165