Histamine is released from the heart during ischaemia‐reperfusion injury. As histamine has cardiac effects, we investigated the role of histamine in ischaemia‐reperfusion injury of isolated rat hearts. A Langendorff‐model with 30 min global (37 oC) 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 H1‐ and H2‐receptor blockade with cimetidine (10 μM, n= 10), chlorpheniramine (10 μm, n= 8), terfenadine (10 μM, n= 8), and promethazin (10 μM, 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. H2‐blockade did not modify the changes in left ventricular pressures, coronary flow, or heart rate induced by ischaemia. Three different Hj‐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 H1‐blockers alone. Coronary flow was increased during reperfusion in two of the groups with Hj‐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 Hj‐receptor blockers.
|Number of pages||12|
|Journal||Acta Physiologica Scandinavica|
|Publication status||Published - Apr 1994|
- myocardial injury
- rat heart
ASJC Scopus subject areas