Myocardial fluid balance

Mehlhorn, Uwe; Geissler, Hans J.; Laine, Glen A.; Allen, Steven J.

doi:10.1016/s1010-7940(01)01031-4

Cited by 121 publications

(113 citation statements)

References 65 publications

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“…The cardiac lymphatic system modulates myocardial fluid homeostasis between fluid filtration into the myocardial interstitium from blood capillaries and its removal via the lymphatic system (Mehlhorn et al, 2001). In the process of myocardial remodeling, the viable cardiomyocytes around the infarcted area produce cytoprotective proteins and cytokines which enhance the healing of the affected lesion (Ishikawa et al, 2000(Ishikawa et al, , 2005.…”

Section: Discussionmentioning

confidence: 99%

Endothelial progenitor cell transplantation decreases lymphangiogenesis and adverse myocardial remodeling in a mouse model of acute myocardial infarction

Park

Yoon

et al. 2011

Exp Mol Med

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Cardiac lymphatic system in the remodeling after acute myocardial infarction (AMI) has been overlooked. We wanted to investigate the role of bone marrow-derived endothelial progenitor cells (EPCs) and their contribution to lymphatic distribution in myocardial remodeling after AMI. Mouse (C57bl/6J) MI models were created by ligation of the left anterior descending coronary artery and were treated with phosphate buffered saline (PBS) or EPCs. Real-time RT-PCR with 2-to 4-week myocardial tissue samples revealed that lymphangiogenetic factors such as vascular endothelial growth factor (VEGF)-C (8.5 fold, P ＜ 0.05), VEGF-D (6.1 fold, P ＜ 0.05), Lyve-1 (15 fold, P ＜ 0.05), and Prox-1 (11 fold, P ＜ 0.05) were expressed at significantly higher levels in the PBS group than the EPC group. The PBS group also showed a significantly higher density of lymphatic vessels in the peri-infarction area. Echocardiography showed that from 2 weeks after the treatment, left ventricle (LV) dimensions at both systole and diastole were significantly smaller in the EPC group than in the PBS group (P ＜ 0.01) and LV fractional shortening was higher in the EPC group accordingly (P ＜ 0.01). Lymphangiogenic markers increased in a mouse MI model. EPC transplantation decreased lymphangiogenesis and adverse ventricular remodeling after AMI. These novel findings suggest that new lymphatic vessels may be formed in severely damaged myocardium, and may be involved in adverse myocardial remodeling after AMI.

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Section: Discussionmentioning

confidence: 99%

Endothelial progenitor cell transplantation decreases lymphangiogenesis and adverse myocardial remodeling in a mouse model of acute myocardial infarction

Park

Yoon

et al. 2011

Exp Mol Med

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“…We also show evidence for AQP-1 expression by rat and human cardiac myocytes and AQP-4 by mouse cardiac myocytes. Because only small changes in myocardial water content are associated with significant impairment of cardiac function (21,31,41), detailed examination of myocardial water handling and the role of AQPs may reveal potential avenues for therapeutic intervention.…”

Section: Discussionmentioning

confidence: 99%

Cardiac aquaporin expression in humans, rats, and mice

Butler¹,

Au²,

Yang³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Water accumulation in the heart is important in ischemia-reperfusion injury and operations performed by using cardiopulmonary bypass, with cardiac dysfunction associated with myocardial edema being the principal determinant of clinical outcome. As an initial step in determining the role of aquaporin (AQP) water channels in myocardial edema, we have assessed the myocardial expression of AQPs in humans, rats, and mice. RT-PCR revealed expression of AQP-1, -4, -6, -7, -8, and -11 transcripts in the mouse heart. AQP-1, -6, -7, and -11 mRNAs were found in the rat heart as well as low levels of AQP-4 and -9. Human hearts contained AQP-1, -3, -4, -5, -7, -9, -10, and -11 mRNAs. AQP-1 protein expression was confirmed by Western blot analysis in all three species. AQP-4 protein was detected in the mouse heart but not in the rat or human heart. To determine the potential functional consequences of myocardial AQP expression, water permeability was measured in plasma membrane vesicles from myocardial cells of wild-type versus various AQP knockout mice. Water permeability was reduced by AQP-1 knockout but not by AQP-4 or AQP-8 knockout. With the use of a model of isolated rat heart perfusion, it was found that osmotic and ischemic stresses are not associated with changes in AQP-1 or AQP-4 expression. These studies support a possible functional role of AQP-1 in myocardium but indicate that early adaptations to osmotic and ischemic stress do not involve transcriptional or posttranslational AQP-1 regulation. aquaporin knockout; cardiac myocyte; cardiopulmonary bypass OUR INTEREST IN CARDIAC AQUAPORINS (AQPs) stems from the recognition that myocardial edema is associated with a significant reduction in cardiac performance in a number of clinically important situations. Ischemia and reperfusion are associated with the development of myocardial edema, with expansion of both interstitial and cellular compartments. The resulting systolic and diastolic dysfunctions are the most important prognostic factors in patient survival after an acute ischemic event or "planned" ischemia, as occurs during cardiac surgery. Procedures involving cardiopulmonary bypass bring additional osmotic stress due to hemodilution and increased vascular permeability (32,40,42

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“…Myocardial edema formation represents a major clinical problem and leads to vessel collapse, stunning of the myocardium, induction of arrhythmias, and impaired cardiac function. Edema occurs in response to ischemia/reperfusion, inflammation, organ transplant rejection, or cardioplegic arrest during surgical interventions such as coronary artery bypass grafting 3. Following myocardial infarction (MI), vascular permeability (VP) across the microvascular endothelium is increased, resulting in persistent postischemic vasogenic edema 2, 4.…”

Section: Introductionmentioning

confidence: 99%

Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice

Stieger

Daniel

Thölen

et al. 2017

JAHA

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BackgroundFollowing myocardial infarction (MI), peri‐infarct myocardial edema formation further impairs cardiac function. Extracellular RNA (eRNA) released from injured cells strongly increases vascular permeability. This study aimed to assess the role of eRNA in MI‐induced cardiac edema formation, infarct size, cardiac function, and survival after acute MI and to evaluate the therapeutic potential of ribonuclease 1 (RNase‐1) treatment as an eRNA‐degrading intervention.Methods and ResultsC57BL/6J mice were subjected to MI by permanent ligation of the left anterior descending coronary artery. Plasma eRNA levels were significantly increased compared with those in controls starting from 30 minutes after ligation. Systemic application of RNase‐1, but not DNase, significantly reduced myocardial edema formation 24 hours after ligation compared with controls. Consequently, eRNA degradation by RNase‐1 significantly improved the perfusion of collateral arteries in the border zone of the infarcted myocardium 24 hours after ligation of the left anterior descending coronary artery, as detected by micro–computed tomography imaging. Although there was no significant difference in the area at risk, the area of vital myocardium was markedly larger in mice treated with RNase‐1 compared with controls, as detected by Evans blue and 2,3,5‐triphenyltetrazolium chloride staining. The increase in viable myocardium was associated with significantly preserved left ventricular function, as assessed by echocardiography. Moreover, RNase‐1 significantly improved 8‐week survival following MI.ConclusionseRNA is an unrecognized permeability factor in vivo, associated with myocardial edema formation after acute MI. RNase‐1 counteracts eRNA‐induced edema formation and preserves perfusion of the infarction border zone, reducing infarct size and protecting cardiac function after MI.

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Myocardial fluid balance

Cited by 121 publications

References 65 publications

Endothelial progenitor cell transplantation decreases lymphangiogenesis and adverse myocardial remodeling in a mouse model of acute myocardial infarction

Endothelial progenitor cell transplantation decreases lymphangiogenesis and adverse myocardial remodeling in a mouse model of acute myocardial infarction

Cardiac aquaporin expression in humans, rats, and mice

Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice

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