Histamine release and its effects in ischaemia‐reperfusion injury of the isolated rat heart
Histamine is released from the heart during ischaemia-reperfusion injury. As histamine has cardiac effects, are investigated the role of histamine in ischaemia-reperfusion injury of isolated rat hearts. A Langendorff-model with 30 min global (37 degrees C) ischaemia followed by 60 min reperfusion wa...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
| Megjelent: |
1994
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| Sorozat: | ACTA PHYSIOLOGICA SCANDINAVICA
150 No. 4 |
| Tárgyszavak: | |
| doi: | 10.1111/j.1748-1716.1994.tb09706.x |
| mtmt: | 1433433 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/31998 |
| Tartalmi kivonat: | Histamine is released from the heart during ischaemia-reperfusion injury. As histamine has cardiac effects, are investigated the role of histamine in ischaemia-reperfusion injury of isolated rat hearts. A Langendorff-model with 30 min global (37 degrees C) ischaemia followed by 60 min reperfusion was employed. The effects of ischaemia alone (n = 10, group 1.1 + n = 10, group 2.1, 2 different series), and ischaemia with H-1- and H-2-receptor blockade with cimetidine (10 mu M, n = 10), chlorpheniramine (10 mu M, n = 8), terfenadine (10 mu M, n = 8), and promethazin (10 mu M, n = 9), or both cimetidine and chlorpheniramine (n = 8), were studied. Histamine was measured in the coronary effluent and cardiac tissue of group 1.1. Release of histamine increased from 6.5 +/- 1 pmol min(-1) before ischaemia to 19 +/- 3 pmol min(-1) at the start of reperfusion. Ischaemia decreased left ventricular developed pressure to 18 +/- 11% (1.1) and 50 +/- 11 % (2.1) of initial value (mean +/- SEM) at the start of reperfusion. Left ventricular end-diastolic pressure increased from 0 to 79 + 8 mmHg (1.1) and 39 + 9 (2.1) mmHg, while left ventricular systolic pressure was unchanged (101 +/- 12% in 1.1 and 101 +/- 10% in 2.1). Severe arrhythmias were induced in 90 (1.1) and 30 (2.1)% of the hearts, while coronary flow decreased during reperfusion. H-2-blockade did not modify the changes in left ventricular pressures, coronary how, or heart rate induced by ischaemia. Three different H-1-blockers increased left ventricular systolic pressure, inhibited the decrease of developed pressure, attenuated the increase of end-diastolic pressure, and totally inhibited reperfusion arrhythmias. The effect of both blockers together was similar to that of H-1-blockers alone. Coronary flow was increased during reperfusion in two of the groups with H-1-blocker compared with ischaemic controls. Increased release of histamine from ischaemic-reperfused rat hearts concurred with depression of left ventricular function and arrhythmias during early reperfusion. Cardiac dysfunction during reperfusion was attenuated by three different H-1-receptor blockers. |
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| Terjedelem/Fizikai jellemzők: | 413-424 |
| ISSN: | 0001-6772 |