Deoxygenated blood minimizes adherence of sonicated albumin microbubbles during cardioplegic arrest and after blood reperfusion: Experimental and clinical observations with myocardial contrast echocardiography

Abstract

Both administration of cardioplegic solution and blood reperfusion result in endothelial dysfunction. The transit rate of albumin microbubbles during myocardial contrast echocardiography may reflect endothelial injury. Accordingly, we performed myocardial contrast echocardiography in 12 dogs undergoing cardiopulmonary bypass and measured the myocardial transit rate of microbubbles injected into the aortic root during delivery of cardioplegic solutions containing arterial and venous blood and delivery of pure crystalloid cardioplegic solution. The myocardial transit rate of 99mTc-labeled red blood cells was measured and perfusates were sampled for biochemical analysis at each stage. The microbubble transit rate was markedly prolonged during delivery of crystalloid cardioplegic solution and improved significantly during infusion of blood cardioplegic solution (p < 0.001); venous compared with arterial blood in the solution resulted in a greater rate (p < 0.001). The microbubble transit rate did not correlate with pH, oxygen tension or carbon dioxide tension values, or K+ concentration. The red blood cell transit rate remained constant regardless of the cardioplegic perfusate infused. Myocardial contrast echocardiography was also performed in 12 patients undergoing coronary artery bypass who underwent sequential arterial and venous reperfusion after cardioplegic arrest. The microbubble transit rate was faster with venous than arterial blood reperfusion (p = 0.01), although this gain was diminished when arterial blood reperfusion preceded venous blood reperfusion (p = 0.05). Our results indicate that endothelial dysfunction after cardioplegic arrest may be ameliorated by reperfusion with venous rather than arterial blood.

Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload

“…Ostensibly, the early generation of ROS could be reduced during the postconditioning procedure by limiting the actual supply of substrate oxygen (substrate limitation) or by attenuating the enzymes involved in oxidant generation such as xanthine oxidase or endothelial NAD(P)H oxidase. A limitation of substrate oxygen as a mechanism of attenuating the ROS generation by postconditioning would be consistent with studies that report a reduction of postischemic or posthypoxic injury by low levels of oxygen perfusates (4,5,24,34). The level of hypoxia achieved during the 3-h index hypoxia was sufficient to elicit cellular damage, which was expressed as a number of hallmark pathological markers.…”

Microbubble Persistence in the Microcirculation During Ischemia/Reperfusion and Inflammation Is Caused by Integrin- and Complement-Mediated Adherence to Activated Leukocytes

“…3,21 Previous studies have described normal appearance (wash-in) rates but delayed decay (wash-out) rates of albumin microbubbles after I-R. 3 These results are consistent with the microbubble/leukocyte interactions observed in the present study. We previously postulated that the disruption of the negatively charged glycocalyx, resulting from oxygenderived free radical formation after I-R, 22 could promote attachment of anionic albumin microbubbles to the endothelial surface.…”

Targeted renal therapies through microbubbles and ultrasound☆

“…Similar results were obtained in the myocardium immediately after cardioplegic arrest in dogs, although here microbubbles were directly injected into the myocardium through arterial injection [33]. The mechanisms for microbubble phagocytosis by leukocytes are initiated through the binding of microbubbles to activated leukocytes adherent to the microvascular wall [34].…”