No hypoperfusion is produced in the epicardium during application of myocardial topical negative pressure in a porcine model

Abstract

Background: Topical negative pressure (TNP), commonly used in wound therapy, has been shown to increase blood flow and stimulate angiogenesis in skeletal muscle. We have previously shown that a myocardial TNP of -50 mmHg significantly increases microvascular blood flow in the myocardium. When TPN is used in wound therapy (on skeletal and subcutaneous tissue) a zone of relative hypoperfusion is seen close to the wound edge. Hypoperfusion induced by TNP is thought to depend on tissue density, distance from the negative pressure source, and the amount negative pressure applied. When applying TNP to the myocardium, a significant, long-standing zone of hypoperfusion could theoretically cause ischemia, and negative effects on the myocardium. The current study was designed to elucidate whether hypoperfusion was produced during myocardial TNP.

Methods: Six pigs underwent median sternotomy. Laser Doppler probes were inserted horizontally into the heart muscle in the LAD area, at depths of approximately, 1-2 mm. The microvascular blood flow was measured before and after the application of a TNP. Analyses were performed before left anterior descending artery (LAD) occlusion (normal myocardium) and after 20 minutes of LAD occlusion (ischemic myocardium).

Results: A TNP of -50 mmHg induced a significant increase in microvascular blood flow in normal myocardium (**p = 0.01), while -125 mmHg did not significantly alter the microvascular blood flow. In ischemic myocardium a TNP of -50 mmHg induced a significant increase in microvascular blood flow (*p = 0.04), while -125 mmHg did not significantly alter the microvascular blood flow.

Conclusion: No hypoperfusion could be observed in the epicardium in neither normal nor ischemic myocardium during myocardial TNP.

Figure 1

Microvascular blood flow measured using laser Doppler velocimetry in normal myocardium exposed to topical negative pressures of A) -50 mmHg, and B) -125 mmHg. The measurements were performed in six pigs at a depth of 1–2 mm in the myocardium. Significance was defined as *p < 0.05, **p < 0.01, ***p < 0.001 and p > 0.05 (not significant, n.s.). Values are presented as means ± the standard error on the mean (SEM).

Figure 2

Microvascular blood flow measured using laser Doppler velocimetry in the myocardium before and after 5, 10, 15, and 20 minutes of occlusion of the left anterior descending artery (LAD). Note the decrease in microvascular blood flow, from 311.7 ± 106.2 PU before, to 84.2 ± 29.9 PU after 20 minutes' occlusion of the LAD, in the area studied. Significance was defined as *p < 0.05, **p < 0.01, ***p < 0.001 and p > 0.05 (not significant, n.s.). Values are presented as means ± the standard error on the mean (SEM).

Figure 3

Microvascular blood flow measured using laser Doppler velocimetry in ischemic myocardium exposed to topical negative pressures of A) -50 mmHg, and B) -125 mmHg. The measurements were performed in six pigs at a depth at 1–2 mm in the myocardium. Significance was defined as *p < 0.05, **p < 0.01, ***p < 0.001 and p > 0.05 (not significant, n.s.). Values are presented as means ± the standard error on the mean (SEM).