苯妥英钠促进心肌梗死后大鼠心室基质金属蛋白酶活性及胶原沉积

目的 研究苯妥英钠对急性心肌梗死(AMI)后大鼠心室基质金属蛋白酶(MMPs)活性和胶原合成的影响及其促进心肌梗死后组织修复的机制.方法 用Wistar大鼠建立AMI模型,将大鼠分成苯妥英钠组、对照组和假手术组,在造模后处死动物,取心室,一部分用组织学方法分析;另一部分采用Gelatin Zymography测定MMPs活性.结果 苯妥英钠组14 d时梗死区厚度大于对照组,非梗死区心肌横断面积小于对照组;AMI后梗死区胶原容积分数苯妥英钠组高于对照组;AMI后苯妥英钠组Ⅰ/Ⅲ型胶原高于对照组(P＜0.05);心室梗死区MMPs活性相对于假手术组明显上调(P＜0.05).结论 苯妥英钠可促进AMI后早期梗死区胶原的合成,MMP-2和MMP-9可能参与了此机制.     

肥厚心肌胶原及基质金属蛋白酶的活性变化

探讨压力负荷增高性心肌肥厚时心肌胶原网络及心肌细胞外基质金属蛋白酶（ ＭＭＰｓ）活性的变化。腹主动 脉部分结扎术致大鼠压力负荷增高性心肌肥厚,ＶＧ染色和图像处理观察心肌胶原网络,酶谱法（Ｚｙｍｏｇｒａｐｈｙ）测定 心肌ＭＭＰｓ活性。结果：手术组大鼠术后２周即出现明显心肌肥厚,术后４周左室肥厚程度进一步加重。与假手术组 比较,左室心肌总胶原容积百分比（ＣＶＥ－Ｔ）于术后２周即增高（Ｐ＜０．０５）,术后４、８周大鼠ＣＶＦ－Ｔ和无小血管视野 ＣＶＦ（ＣＶＦ－ＮＶ）均明显增高（Ｐ＜０．０１）,手术组大鼠左室心肌组织ＭＭＰ－１活性明显低于相应假手术大鼠,但经胰蛋 白酶激活后其活性反而高于假手术大鼠。结论：压力负荷增高性心肌肥厚时伴有心肌胶原网络的重构,心肌组织内 ＭＭＰ－１活性调节异常可能与心肌胶原网络重构的形成有关。     

心室重构及心衰时基质金属蛋白酶的活性变化

心室重构引起心肌纤维化和进行性心室扩张 ,最终导致心力衰竭。在心肌中存在能降解有所心脏基质成分的基质金属蛋白酶 (MMPs) ,是重构过程中引起心脏基质降解和心肌纤维化的主要因素。在心室重构和心力衰时MMPs的活性升高 ,使纤维胶原降解、细胞外基质重构和进行性心室扩张。研究MMPs的活性变化对限制心室重构和延缓心衰进展的治疗方面具有指导意义     

基质金属蛋白酶在心肌缺血大鼠心室间质重构中的作用

目的:探讨大鼠心肌缺血后心肌间质基质金属蛋白酶(MMPs)活性变化与心室间质重构的关系。方法:用异丙肾上腺素(ISP)复制大鼠心肌缺血模型,用酶谱法测定心肌间质MMPs活性,氯胺T法测定胶原含量,免疫组化法测定I/III胶原比例,电镜观察心肌超微结构。结果:心肌缺血组(M组)MMP-2活性在1、2、4周分别是对照组(C组)的5.8倍、2.3倍(P＜0.01)和1.7倍(P＜0.05),MMP-9活性则分别是对照组的4.9倍、1.9倍(P＜0.01)和1.4倍(P＜0.05)。胶原含量、I/III胶原比例在2周、4周时均显著高于对照组。电镜见缺血组心肌细胞坏死、间质胶原大量增生、结构紊乱。结论:心肌缺血后心肌间质内MMPs活性升高,可能是心室重构的重要原因。     

基质金属蛋白酶及其抑制物与子宫内膜癌的研究进展

基质金属蛋白酶（MMPs）及其抑制物（TIMPs）在细胞外基质（ECM）的降解中起重要作用,国内外大量研究表明,ECM降解是恶性子宫内膜浸润子宫内膜和开始转移的重要提示。某些类型MMPs在子宫内膜癌中的表达明显增加,由此提出MMPs及TIMPs在子宫内膜癌的诊断和治疗中有较大的研究空间。因此就MMPs及TIMPs与子宫内膜癌的关系及研究情况进行如下综述。     

脓毒症大鼠心脏基质金属蛋白酶及其抑制物基因的表达变化

目的：探讨脓毒症大鼠心脏中基质金属蛋白酶（MMP）及其组织抑制物（TIMP）的基因表达谱变化及其与脓毒症导致的心脏损伤的关系。方法：雄性3月龄Wistar大鼠20只，随机均分为2组，分别以盲肠结扎针刺法建立脓毒症动物模型或行假手术作为对照组。术后24 h快速摘取心脏，以Langendorff 离体鼠心灌注法测量大鼠心功能参数，其后做心脏病理检查，并以寡核苷酸基因芯片检测基质金属蛋白酶及其抑制物基因在2组大鼠心脏组织中的表达差异。结果：脓毒症大鼠心脏无明显病理改变，但心功能明显下降，表明大鼠心脏处于抑制状态；基因芯片结果显示：20个MMP基因中14个表达上调3倍以上，包括胶原酶MMP8、明胶酶（MMP2和MMP9）、基质溶解素（MMP3、MMP7及MMP10）和膜型金属蛋白酶（MMP15、MMP17和MMP24）等；4个TIMP基因中仅TIMP3基因表达上调。结论：脓毒症时心脏组织中多种MMP基因表达上调、MMP/TIMP基因表达失衡，可能导致心肌抑制和ECM重构，是脓毒症诱发心脏损伤的重要分子机制。     

基质金属蛋白酶系统与卵巢生殖周期中的组织重建

基质金属蛋白酶（MMPs）及其天然组织型抑制物TIMPs是调节许多生理和病理过程中细胞外基质有序降解和重塑的重要分子。在卵巢的一个生殖周期中,从卵泡的发育成熟、排卵到黄体的形成和退化以及卵泡闭锁都受到MMPs/TIMPs家族的精确调控。文章就MMPs家族在卵巢生殖周期中的功能和调控作一综述,并简要介绍MMPs系统与多囊卵巢综合征发病关系的研究进展。     

家兔慢性冬眠心肌MMP-2、MMP-9和TIMP-2表达与胶原重构

目的观察家兔慢性冬眠心肌(CHM)心肌间质胶原纤维变化及基质金属蛋白酶-2,9(MMP-2、MMP-9)及其抑制剂(TIMP-2)的表达。方法27只家兔随机分为模型组(CHM,n=15)及假手术组(SHAM,n=12)。观察心肌间质胶原容积百分比(ICVF)、Ⅰ型和Ⅲ型胶原纤维比例、计算Ⅰ/Ⅲ型胶原纤维比例记分(CRS);免疫组化染色及Western blot观察MMP-2、MMP-9及TIMP-2表达。结果与SHAM组相比,CHM组ICVF显著增加(P<0.01);Ⅰ/Ⅲ胶原比例增高;CRS显著增加(P<0.01);MMP-2及MMP-9的表达明显增多(P<0.01),TIMP-2的表达明显减少(P<0.01)。结论在CHM过程中,MMPs/TIMPs比例失平衡,可能是CHM间质胶原重构的机制之一。     

金属蛋白酶及其抑制物与糖尿病肾病

基质金属蛋白酶（MMPs)和金属蛋白酶组织抑制剂（TIMPs)是细胞外基质（ECM）合成与降解代谢平衡调节中两个重要的酶系，它们的调节在导致糖尿病肾病的发生发展中起重要作用。检测血清MMPs和TIMPs水平变化能早期诊断糖尿病肾病，应用干预措施有利于糖尿病肾病的早期防治。     

环孢霉素A诱导大鼠心肌纤维化和对基质金属蛋白酶及其抑制剂表达的影响

目的:研究环孢霉素A(CsA)诱导的大鼠心肌损伤及心肌纤维化的程度,检测基质金属蛋白酶(MMP) 2和MMP9及其组织抑制物(TIMP) 2和TIMP1表达的变化,为探寻CsA诱导心肌纤维化的发生机制提供理论依据。方法:64只健康雌性6～8周龄Wistar大鼠随机分为4组:对照组、低剂量CsA组、中剂量CsA组和高剂量CsA组,分别腹腔注射生理盐水、5 mg·kg~(-1)·d~(-1)CsA、12. 5 mg·kg~(-1)·d~(-1)CsA和25 mg·kg~(-1)·d~(-1)CsA,分别在第1、2、3周时处死大鼠。利用HE染色观察心肌组织形态结构,Masson染色观察心肌胶原沉积情况,免疫组织化学和Western blot法检测MMP2、MMP9、TIMP2和TIMP1蛋白的表达情况。结果:HE染色可见,随着CsA作用时间的延长和剂量的增加,心肌组织形态结构损伤严重,逐渐出现心肌灶状坏死及纤维化。Masson染色结果亦可见心肌纤维化程度随着时间和剂量的增加逐渐加重。免疫组织化学及Western blot检测结果显示,在CsA导致大鼠心肌纤维化的过程中,同一时点MMP2和TIMP2随CsA剂量增加表达显著增高(P 0. 05)。第1周MMP2高表达,随着时间的延长表达逐渐减低; TIMP2则随时间延长表达逐渐增高(P 0. 05)。与对照组相比MMP9和TIMP1表达则减低。各用药组MMP9第1周低表达,第2周表达增高,第3周表达减低(P 0. 05);同一时点,CsA对于MMP9表达变化的差异无统计学显著性。TIMP1随CsA剂量增加表达增高(P 0. 05)。结论:CsA可引起大鼠心肌损伤及间质纤维化,随着用药时间的延长和剂量的增加,纤维化程度逐渐加重。CsA诱导的大鼠心肌纤维化与MMPs/TIMPs表达的改变及MMPs/TIMPs的失衡有关。     

Ghrelin抑制大鼠心肌梗死后心室重构

目的:探讨Ghrelin对大鼠心肌梗死后心室重构的影响及其机制。方法:结扎SD大鼠前降支造成急性心肌梗死(AMI)模型,并设假手术组。结扎24h后,存活大鼠给予Ghrelin(100μg/kg)或生理盐水皮下注射,每天两次。4周后,超声心动图和血流动力学方法检测心功能,实时定量PCR检测梗死心肌白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)mRNA表达,Western-blot检测核转录因子-κB(NF-κB)活性。结果:与假手术组相比,AMI模型组左室收缩内径(LVESD)、左室舒张内径(LVEDD)、左室舒张末压力(LVEDP)都明显增加(P<0.01);而左室收缩压(LVSP)、压力变化值最大值(dp/dtmax)、左室短轴缩短率(FS)都显著降低(P<0.01)。与AMI模型组相比,Ghrelin治疗组LVEDP、LVEDD以及LVESD明显变小(P<0.01),而dp/dtmax及FS显著增加(P<0.01)。梗死后心肌IL-1β、TNF-αmRNA表达增强,Ghrelin治疗后IL-1β、TNF-αmRNA表达明显降低(P<0.01)。AMI模型组心肌核蛋白P65表达明显增加,而胞浆蛋白I-κBα含量显著减少(P<0.01),Ghrelin治疗明显降低梗死心肌核蛋白P65表达(P<0.01),同时增加胞浆蛋白I-κBα含量(P<0.01)。结论:Ghrelin能够抑制心肌梗死后心室重构,改善心功能,可能与其抑制炎症介质表达及NF-κB活性有关。     

缬沙坦对阿霉素心肌病大鼠的心脏保护作用及机制研究

目的： 探讨AT1受体阻滞剂缬沙坦对阿霉素心肌病(ADR-DCM)大鼠的心脏保护作用及其机制。方法: 雄性Wistar大鼠分3组：(1)阿霉素心肌病组(ADR-DCM，n=25)，阿霉素 2.5 mg/kg，尾静脉注射，每周1次，连续10周；(2)阿霉素心肌病+缬沙坦治疗组(ARB，n=10)， 缬沙坦 30 mg/kg，每天1次，灌胃治疗；(3)正常对照组(CON，n=10)。12周时进行超声和血流动力学检测，氯胺T法检测羟脯氨酸及胶原含量， Western印迹分析检测MMP-2、MMP-9及TIMP-1的表达，明胶酶谱法检测MMPs活性。结果: ARB组死亡率明显低于ADR-DCM组(20% vs 40%，P<0.01)。ADR-DCM组大鼠左室内径大于CON组，心功能明显低于CON组， ARB组左室内径增加程度及心功能各项指标变化低于ADR-DCM组。ADR-DCM组心肌羟脯氨酸及胶原含量高于CON组， ARB组显著低于ADR-DCM组(P<0.01)。ADR-DCM组左室心肌MMP-2、MMP-9蛋白表达及MMPs明胶酶活性明显高于CON组 (P<0.01)，ARB组MMP-2、MMP-9表达及活性明显低于ADR-DCM组(P<0.01)，而TIMP-1的表达在3组间均无显著差异(P>0.05)。结论: 缬沙坦部分通过抑制MMPs表达及活性逆转ADR-DCM左室重构，改善心功能。     

Simulation of systolic and diastolic left ventricular dysfunction in a mock circulation: the effect of arterial compliance

Arterial compliance (AC) is expected to play a major role on cardiac efficacy by acute or long-term mechanisms. The aim of this study was to investigate the purely mechanical effect of AC on left ventricular (LV) performance, for different conditions of LV dysfunction (systolic versus diastolic). A hydraulic, Windkessel model of systemic circulation was used. LV function and aortic flow were simulated using a left ventricular assist device (LVAD). Two cases of LV dysfunction were simulated: Case A, systolic and Case B, diastolic dysfunction. In Case A, AC increased from 1.14 to 2.85 ml mm Hg(-1) leading to an increase in LVAD stroke volume up to 6%, while no significant effect was observed in Case B. LVAD systolic work was decreased by 4% in systolic and by 11% in diastolic LVAD dysfunction. The purely mechanical effect of AC changes on LVAD function was different between systolic and diastolic dysfunction. It might be expected that even an acute reduction in arterial stiffness could enhance LV performance by different means in systolic compared to diastolic dysfunction.     

Simulation of systolic and diastolic left ventricular dysfunction in a mock circulation: the effect of arterial compliance

Arterial compliance (AC) is expected to play a major role on cardiac efficacy by acute or long-term mechanisms. The aim of this study was to investigate the purely mechanical effect of AC on left ventricular (LV) performance, for different conditions of LV dysfunction (systolic versus diastolic). A hydraulic, Windkessel model of systemic circulation was used. LV function and aortic flow were simulated using a left ventricular assist device (LVAD). Two cases of LV dysfunction were simulated: Case A, systolic and Case B, diastolic dysfunction. In Case A, AC increased from 1.14 to 2.85 ml mm Hg &#109 1 leading to an increase in LVAD stroke volume up to 6%, while no significant effect was observed in Case B. LVAD systolic work was decreased by 4% in systolic and by 11% in diastolic LVAD dysfunction. The purely mechanical effect of AC changes on LVAD function was different between systolic and diastolic dysfunction. It might be expected that even an acute reduction in arterial stiffness could enhance LV performance by different means in systolic compared to diastolic dysfunction.     

Assessment of synchronized direct mechanical ventricular actuation in a canine model of left ventricular dysfunction

Direct mechanical ventricular actuation (DMVA) is an experimental procedure that provides biventricular cardiac assistance by intracorporeal pneumatic compression of the heart. The advantages this technique has over other assist devices are biventricular assistance, no direct blood contact, pulsatile blood flow, and rapid, less complicated application. Prior studies of nonsynchronized DMVA support have demonstrated that a subject can be maintained for up to 7 days. The purpose of this study was to determine the acute hemodynamic effects of cardiac synchronized, partial DMVA support in a canine model (RVP) of left ventricular (LV) dysfunction. The study consisted of rapidly pacing seven dogs for 4 weeks to create LV dysfunction. At the conclusion of the pacing period, the DMVA device was positioned around the heart by means of a median sternotomy. The animals were then imaged in a 1.5 T whole body high speed clinical MR system, with simultaneous LV pressure recording. Left ventricular pressure-volume (PV) loops of the nonassisted and DMVA assisted heart were generated and demonstrated that DMVA assist shifted the loops leftward. In addition, assist significantly improved pressure dependent LV systolic parameters (left ventricular peak pressure and dp/dt max, p < 0.05), with no diastolic impairment. This study demonstrates that DMVA can provide synchronized partial assist, resulting in a decrease in the workload of the native heart, thus having a potential application for heart failure patients.     

Dysregulation of matrix metalloproteinases and their tissue inhibitors is related to abnormality of left ventricular geometry and function in streptozotocin-induced diabetic minipigs

This study aimed to characterize matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in relation to changes in left ventricle (LV) geometry and function in a porcine model with streptozotocin (STZ)-induced diabetes. In 15 Chinese Guizhou minipigs with STZ-induced diabetes (diabetic group) and 15 age-matched normal controls (control group), Doppler tissue imaging was performed at 6 months of diabetes. Serum MMP-2, -9, TIMP-1, -4 and B-type natriuretic peptide (BNP) were determined. Expression of MMPs, TIMPs, urokinase type-plasminogen activator (uPA), its receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1) in aortic intima and LV myocardium was evaluated, with gelatinolytic activities of tissue MMP-2, -9 accessed by zymography. Left ventricle end-diastolic septum thickness (P < 0.05) and mass (P < 0.05) were increased, whereas peak systolic mitral annulus velocity (Sm, P < 0.001), LV systolic (P = 0.01) and diastolic strain (P < 0.001) were significantly decreased in diabetic group than in controls. Diabetic group showed higher expression of TIMP-1, -4 in aortic intima and LV myocardium (P < 0.01 or P < 0.05), with increased collagen content and elevated serum BNP level (P = 0.004) and lower gelatinolytic activities of tissue MMP-2, -9 (all P < 0.05). Semi-quantitative RT-PCR of those diabetic tissues revealed elevated mRNA levels of major TIMPs, uPA, uPAR and PAI-1. Reduction of serum MMP-2 and -9 levels was observed in diabetic group vs. control group (both P < 0.05). This study features elevated levels of TIMP-1, -4, uPA, uPAR and PAI-1, and decreased activities of MMP-2, -9 in aorta and myocardium in STZ-induced diabetic minipigs, indicating that MMP-TIMP dysregulation is associated with LV hypertrophy, cardiac dysfunction and increased cardiovascular fibrosis in diabetes.     

Cardiovascular ultrasound: applications for the assessment of cardiac function

Congestive heart failure(CHF) is usually associated with impaired left ventricular(LV) systolic function, and thus, the measurement of systolic function is an essential component of the evaluation of any patients with known or suspected cardiac disease. Among many parameters, most frequently used are LV percent fractional shortening and ejection fraction(EF), which can be easily measured from an M-mode echocardiogram. However, these M-mode measurements may be inaccurate in patients with asymmetrical LV due to myocardial infarction, right ventricular overload or sigmoid septum. Especially in such cases, EF should be measured using two-dimensional echocardiography. Usually, LV volumes and EF are calculated using the disc-summation method through the manual tracing of apical two-chamber and four-chamber echocardiograms. On the other hand, it has been recognized that congestive heart failure may arise in the absence of any systolic dysfunction and CHF due to systolic dysfunction never occurs in the absence of concomitant diastolic dysfunction. Although the analysis of pulsed-Doppler transmitral flow velocity has been most widely used for the noninvasive assessment of LV diastolic function, an increase in left atrial pressure during CHF can pseudonormalize an abnormal flow pattern and mask LV diastolic dysfunction. Recently, we proposed a new index for assessing LV diastolic function, flow propagation velocity, which can be measured with color M-mode Doppler echocardiography and baseline-shift technique. Recent studies have shown that the flow propagation velocity is a unique noninvasive parameter of LV diastolic function which can accurately detect the diastolic impairment in patients with different types of cardiac diseases with various loading conditions.     

基质金属蛋白酶及其组织抑制因子在左心室机械辅助减负荷模型中的表达

目的 研究基质金属蛋白酶(MMP)及其组织抑制因子(TIMP)在左心室机械辅助减负荷模型中的表达,探讨左心室减负荷后心肌逆向重构的分子机制.方法 结扎Lewis大鼠冠状动脉左前降支诱导心力衰竭,4周后将14只心力衰竭大鼠随机分为心力衰竭组(n=7)与移植组(n=7).将供体移植组心力衰竭大鼠的心脏及右肺移植到受体正常Lewis大鼠的腹部,通过供体的升主动脉与受体的降主动脉吻合.7只正常Lewis大鼠作为正常组.结扎左前降支4周后心脏超声测量3组大鼠心室直径和心肌梗死范围.移植2周后,称取各组大鼠心脏、左心室质量;显微镜观测左心室心肌细胞直径与心肌纤维化程度;采用实时荧光定量PCR检测MMP-1、MMP-9、TIMP-1的mRNA表达及计算MMP-1mRNA/TIMP-1 mRNA的比值.结果 结扎左前降支4周后,心力衰竭组及移植组舒张末直径(LVEDD)较正常组升高、左心室短轴缩短率(LVFS)较正常组下降,而此两组间LVEDD、LVFS及心肌梗死范围比较差异无统计学意义,两组的心力衰竭严重程度差异也无统计学意义.心力衰竭组心脏、左心室质量和左心室心肌细胞直径大于移植组与正常组;移植组心脏、左心室质量、左心室心肌细胞直径接近正常组.心肌纤维化的程度移植组＞心力衰竭组＞正常组[(7.90±2.32)％比(4.20±1.84)％比(1.54±0.31)％,均P＜0.05].心力衰竭组和移植组MMP-1、MMP-9mRNA表达均高于正常组(1.89±0.23、1.32±0.16比0.41±0.01,2.03±0.15、1.50±0.13比0.46+0.01,均P＜0.05),但心力衰竭组与移植组比较差异无统计学意义.心力衰竭组TIMP-1mRNA表达低于正常组与移植组(0.72±0.18比1.21±0.02、1.68±0.21,均P＜0.05);正常组与移植组比较差异无统计学意义.心力衰竭组MMP-1 mRNA/TIMP-1mRNA比值较正常组及移植组明显增高(2.03±0.15比0.30±0.01、0.81±0.11,均P＜0.05);正常组与移植组差异则无统计学意义.结论 左心室减负荷后,心肌逆向重塑的过程伴随着心肌细胞MMP及TIMP水平的改变.     

Ethanol extract from Epimedium brevicornum attenuates left ventricular dysfunction and cardiac remodeling through down-regulating matrix metalloproteinase-2 and -9 activity and myocardial apoptosis in rats with congestive heart failure

Epimedium, a traditional Chinese herb, has been used for the remedy of coronary heart disease, impotence and osteoporosis in traditional oriental medicine. However, despite extensive pharmacological studies, the molecular mechanism of the anti-heart failure effect of epimedium is little known. In the present study, we investigated the pharmacological action mechanism of ethanol extract of epimedium (EPI-ext) on isoproterenol-induced congestive heart failure (CHF) in rats. Isoproterenol administration resulted in severe heart failure, as shown by the increased levels of left ventricular (LV) weight index and heart rate, as well as LV end diastolic pressure, and by the decreased levels of LV systolic pressure, maximal rate of LV pressure rise, and maximal rate of LV pressure decline. EPI-ext dose-dependently reversed the changes of these cardiac morphometric and hemodynamic parameters. In addition, EPI-ext significantly inhibited the serum levels of tumor necrosis factor alpha, norepinephrine, angiotensin II and brain natriuretic peptide in rats with CHF and improved the histological changes including cadiocyte hypertrophy, cadiocyte degeneration, inflammatory infiltration, and cardiac desmoplasia. Furthermore, the expression and activities of matrix metalloproteinase-2 and -9, which regulate collagen production, were also blocked by EPI-ext. Moreover, myocardial apoptosis was remarkably attenuated by EPI-ext through the regulating Bcl-2/Bax axle. In conclusion, EPI-ext ameliorates LV dysfunction and cardiac remodeling through down-regulating matrix metalloproteinase-2 and -9 activity and myocardial apoptosis in rats with CHF.     

The effects of asymmetric ventricular filling on left–right ventricular interaction in the normal rat heart

Heart failure is characterised by ventricular dysfunction and with the potential for changes to ventricular volumes constraining the mechanical performance of the heart. The contribution of this interaction from geometric changes rather than fibrosis or metabolic changes is unclear. Using the constant pressure Langendorff-perfused rat heart, the volume interaction between left ventricle (LV) and right ventricle (RV) was investigated. RV diastolic stiffness (P?<?0.001) and developed pressure (P?<?0.001) were significantly lower than LV. When the RV was fixed at the end-diastolic volume (EDV) or EDV?+?50?%, both LV systolic and diastolic performance were unaffected with increasing LV balloon volume. However, at fixed LV volume, RV systolic performance was significantly decreased when LV volume increased to EDV?+?50?% when RV volume was increased incrementally between 50 and 300?μl (P?<?0.001). Systolic interaction in RV was noted as declining RV peak systolic load with increasing LV systolic pressure (P?<?0.05) and diastolic interaction was noted for RV when LV volume was increased from EDV to EDV?+?50?% (P?<?0.05). RV diastolic wall stress was increased with increasing LV balloon volume (P?<?0.05), but LV wall stress was unaltered at fixed RV balloon volume. Taken together, increasing LV volume above EDV decreased systolic performance and triggered ventricular constraint in the RV but the RV itself had no effect on the performance of the LV. These results are consistent with overload of the LV impairing pulmonary perfusion by direct ventricular interaction with potential alteration to ventilation–perfusion characteristics within the lung.