Effects of synchronized retroperfusion on the coronary arterial pressure-flow relationship.
OBJECTIVE
We compared the effects of diastolic coronary sinus pressure elevation due to synchronized retroperfusion (SRP) with systolic coronary sinus pressure elevation due to coronary sinus occlusion on the coronary pressure-flow relationship under similar mean coronary sinus pressure values.


METHODS
Using isolated, perfused canine hearts, coronary perfusion of the left anterior descending artery was reduced gradually, setting the mean coronary sinus pressure to 14.2 +/- 5.7 mmHg (mean +/- s.d.) under control conditions, 30.3 +/- 4.9 mmHg under SRP with lower retrograde perfusion flow [SRP(L)], 30.7 +/- 4.6 mmHg under coronary sinus partial occlusion [CSPO], 51.9 +/- 7.9 mmHg under SRP with higher retrograde perfusion flow [SRP(H)] and 49.0 +/- 7.9 mmHg under coronary sinus complete occlusion [CSCO]. Zero-flow pressure and the slopes of pressure-flow relationship were determined in each condition.


RESULTS
The mean values of the slopes did not significantly differ among the interventions. The mean control value of zero-flow pressure was 17.4 +/- 4.3 mmHg. Zero-flow pressure of SRP(L) was 20.0 +/- 3.5 mmHg, which was not a significant increase, whilst zero-flow pressure of CSPO was 22.9 +/- 3.4 mmHg, a significant increase compared with control (P < 0.05). Zero-flow pressure of SRP(H) and CSCO was 26.0 +/- 4.5 and 31.3 +/- 6.7 mmHg, respectively, and both were significantly higher than control (P < 0.01). Zero-flow pressure of SRP(H) was, however, significantly lower than CSCO (P < 0.05).


CONCLUSIONS
SRP, which causes diastolic coronary sinus pressure elevation, does not greatly affect coronary arterial inflow, compared with coronary sinus occlusion which causes systolic coronary sinus pressure elevation. These results suggest that the blood volume contained in the heart during systole plays a role in determining coronary inflow. Therefore, SRP intervention, which does not interfere with venous outflow during systole, may ameliorate injured myocardium during ischaemia without seriously affecting coronary inflow supply.
Mitsugi
M
M
First Department of Internal Medicine, Fukushima Medical College, Japan.
Saito
T
T
Saitoh
S
S
Sato
M
M
Maruyama
Y
Y
D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D003331:Coronary Vessels; D003971:Diastole; D004285:Dogs; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology; D010477:Perfusion