Desai Ketaki V, Laine Glen A, Stewart Randolph H, Cox Charles S, Quick Christopher M, Allen Steven J, Fischer Uwe M
Michael E. DeBakey Institute, Texas A&M University, College Station, Texas 77843-4466, USA.
Am J Physiol Heart Circ Physiol. 2008 Jun;294(6):H2428-34. doi: 10.1152/ajpheart.00860.2007. Epub 2008 Mar 28.
Myocardial interstitial edema forms as a result of several disease states and clinical interventions. Acute myocardial interstitial edema is associated with compromised systolic and diastolic cardiac function and increased stiffness of the left ventricular chamber. Formation of chronic myocardial interstitial edema results in deposition of interstitial collagen, which causes interstitial fibrosis. To assess the effect of myocardial interstitial edema on the mechanical properties of the left ventricle and the myocardial interstitium, we induced acute and chronic interstitial edema in dogs. Acute myocardial edema was generated by coronary sinus pressure elevation, while chronic myocardial edema was generated by chronic pulmonary artery banding. The pressure-volume relationships of the left ventricular myocardial interstitium and left ventricular chamber for control animals were compared with acutely and chronically edematous animals. Collagen content of nonedematous and chronically edematous animals was also compared. Generating acute myocardial interstitial edema resulted in decreased left ventricular chamber compliance compared with nonedematous animals. With chronic edema, the primary form of collagen changed from type I to III. Left ventricular chamber compliance in animals made chronically edematous was significantly higher than nonedematous animals. The change in primary collagen type secondary to chronic left ventricular myocardial interstitial edema provides direct evidence for structural remodeling. The resulting functional adaptation allows the chronically edematous heart to maintain left ventricular chamber compliance when challenged with acute edema, thus preserving cardiac function over a wide range of interstitial fluid pressures.
心肌间质水肿是由多种疾病状态和临床干预导致的。急性心肌间质水肿与心脏收缩和舒张功能受损以及左心室腔硬度增加有关。慢性心肌间质水肿的形成会导致间质胶原沉积,进而引起间质纤维化。为了评估心肌间质水肿对左心室和心肌间质力学性能的影响,我们在犬类动物中诱导了急性和慢性间质水肿。通过升高冠状窦压力来产生急性心肌水肿,而通过慢性肺动脉结扎来产生慢性心肌水肿。将对照动物的左心室心肌间质和左心室腔的压力-容积关系与急性和慢性水肿动物进行比较。还比较了非水肿动物和慢性水肿动物的胶原含量。与非水肿动物相比,产生急性心肌间质水肿会导致左心室腔顺应性降低。在慢性水肿情况下,主要的胶原类型从I型转变为III型。慢性水肿动物的左心室腔顺应性显著高于非水肿动物。慢性左心室心肌间质水肿继发的主要胶原类型变化为结构重塑提供了直接证据。由此产生的功能适应性使慢性水肿心脏在受到急性水肿挑战时能够维持左心室腔顺应性,从而在广泛的间质液压力范围内保持心脏功能。