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Low-flow reperfusion after myocardial ischemia enhances leukocyte accumulation in coronary microcirculation
1College of Medicine, University of Arizona, Tucson 85724, USA.
Insights
Reducing coronary blood flow during heart reperfusion increases leukocyte accumulation in capillaries and venules. This enhanced leukocyte buildup may worsen early reperfusion injury following myocardial ischemia.
Area of Science:
- Cardiovascular Physiology
- Immunology
- Pathophysiology
Background:
- Leukocyte accumulation in the heart during early reperfusion after myocardial ischemia is not fully understood.
- Investigating the role of reduced coronary blood flow during reperfusion is crucial for understanding early reperfusion injury.
Purpose of the Study:
- To examine the effects of reduced coronary blood flow during reperfusion on leukocyte accumulation in coronary capillaries and postcapillary venules.
- To determine the relationship between leukocyte adhesion and venular shear rate after ischemia.
Main Methods:
- Isolated rat hearts underwent 30 minutes of no-flow ischemia followed by reperfusion.
- Leukocyte deposition was observed using intravital microscopy in capillaries and venules.
- Blood cell velocity and shear rate were measured in venules.
Main Results:
- Reduced reperfusion flow (10% of full flow) significantly increased leukocyte accumulation in both capillaries and venules.
- Leukocyte trapping in capillaries increased with reduced flow, while venular adhesion was not significant at full or 50% flow.
- Leukocyte margination in venules showed a significant inverse correlation with venular shear rate.
Conclusions:
- Reduced coronary reflow after ischemia enhances leukocyte trapping in capillaries.
- Leukocyte adhesion in venules is inversely related to shear rate.
- Increased leukocyte accumulation may contribute to early myocardial reperfusion injury.
Abstract:
During early reperfusion after myocardial ischemia, the mechanisms responsible for leukocyte accumulation in the heart are unclear. We examined the effects of reducing coronary blood flow during reperfusion on leukocyte accumulation in coronary capillaries and postcapillary venules. Isolated rat hearts were perfused for 30 min and then subjected to 30 min of 37 degrees C, no-flow ischemia. The deposition of fluorescently labeled leukocytes was observed directly in coronary capillaries and venules using intravital microscopy after 5, 20, and 35 min of reperfusion. Blood cell velocity was measured in venules after 5 min of reperfusion (R5), and shear rate (s-1) was calculated. Four groups were studied: nonischemic control (NIC) hearts and postischemic hearts reperfused at full flow (I/R100) and at 50 and 10% of full flow (I/R50 and I/R10, respectively). In I/R100 hearts, there was a significant increase in leukocyte trapping in capillaries compared with the NIC group (R5: 5.7 +/- 0.6 vs. 2.0 +/- 0.4 leukocytes/capillary field, respectively; P < 0.05). However, the increase in leukocyte adhesion to venules was not statistically significant compared with NIC (R5: 3.2 +/- 0.4 vs. 1.5 +/- 0.6 leukocytes/100-micron venule, respectively; P < 0.2). In I/R50 hearts, a further increase in leukocyte accumulation occurred in the capillaries but not in the venules. However, in I/R10 hearts, there was a statistically significant increase in both capillaries (R5: 9.2 +/- 0.8; P < 0.05) and venules (R5: 4.4 +/- 0.5; P < 0.05). When leukocyte margination in coronary venules was examined as a function of venular shear rate, a significant correlation (r = 0.99, P < 0.05) was found. These results suggest that, after ischemia, a reduction in reflow enhances leukocyte trapping in capillaries and that leukocyte adhesion in venules is inversely related to shear rate. Enhanced leukocyte accumulation may in turn increase the leukocyte contribution to early reperfusion injury in the heart.