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PubMed1995

The ageing spontaneously hypertensive rat as a model of the transition from stable compensated hypertrophy to heart failure.

Spontaneously hypertensive rats (SHR) of advanced age exhibit depressed myocardial contractile function and ventricular fibrosis, as stable compensated hypertrophy progresses to heart failure. Transition to heart failure in SHR aged 18-24 months was characterized by impaired left ventricular (LV) function, ventricular dilatation, and reduced ejection fraction without an increase in LV mass. Studies of papillary muscles from SHR with failing hearts (SHR-F), SHR without failure (SHR-NF), and age-matched Wistar Kyoto (WKY) rats allowed examination of changes in the mechanical properties of myocardium during the transition to heart failure. Papillary muscles of SHR-F exhibited increased fibrosis, impaired contraction, and decreased myocyte fractional area. These findings in papillary muscles were correlated with a higher concentration of hydroxyproline and increased histological evidence of fibrosis in the LV free wall. While a depression in active tension accompanied these structural alterations in papillary muscles, it was not evident when active tension was normalized to myocyte fractional area. Together, these data suggest that individual myocyte function may be preserved but that myocyte loss and replacement by extracellular matrix contribute substantially to the decrement in active tension. An absent or negative inotropic response to isoproterenol is observed in SHR-F and SHR-NF papillary muscles and may result in part from age-related alterations in beta-adrenergic receptor dynamics and a shift from alpha- to beta-myosin heavy chain (MHC) protein. During the transition to failure, ventricles of SHR exhibit a marked increase in collagen and fibronectin mRNA levels, suggesting that an increase in the expression of specific extracellular matrix genes may contribute to fibrosis, tissue stiffness, and impaired function. Transforming growth factor-beta 1 (TGF-beta 1) mRNA levels also increase in SHR-F, consistent with the concept that TGF-beta 1 plays a key regulatory role in remodelling of the extracellular matrix gene during the transition to failure. The renin-angiotensin-aldosterone system is also implicated in the transition to failure: SHR treated with the angiotensin converting enzyme inhibitor captopril starting at 12 months of age did not develop heart failure during the 18-24 month observation period. Captopril treatment that was initiated after rats were identified with evidence of failure led to a reappearance of alpha-MHC mRNA but did not improve papillary muscle function. Research opportunities include investigation of apoptosis as a mechanism of cell loss, delineation of the regulatory roles of TGF-beta 1 and the renin-angiotensin-aldosterone system in matrix accumulation, and studies of proteinase cascades that regulate matrix remodelling.

Age Factors↗
PubMed2025

Genome-Wide Association Study on Muscle Stiffness Identified Novel Locus for Predisposition to Muscle Strain Injury.

PURPOSE: We aimed to screen the entire genome for genetic variants associated with passive muscle stiffness, which has been suggested as a risk factor for muscle strain injury. METHODS: This genome-wide association study (GWAS) on passive muscle stiffness included 350 physically active young Japanese individuals. Three hamstring constituents were measured using ultrasound shear wave elastography. Skeletal muscle transcriptomes were compared across the genotypes of GWAS-identified variants in 48 healthy Japanese individuals. Association between GWAS-identified variants and history of muscle strain injury was examined in 1428 Japanese athletes. RESULTS: Two loci on chromosome 11 demonstrated a genome-wide significant association with passive muscle stiffness of the biceps femoris long head (rs12807854 T/C: P = 5.19 × 10 -10 , rs78405694 T/C: P = 2.09 × 10 -8 ; linear regression analysis adjusted for sex, age, and stretching exercise habits). Skeletal muscle RNA sequencing revealed significantly elevated expression of extracellular matrix-related genes in muscles carrying stiffness-increasing alleles of these variants. Among athletes, rs12807854 T/C was significantly associated with a history of muscle strain injury ( P = 0.0254; logistic regression analysis adjusted for age, sex, competitive level, and main sport). Carriers of the C allele, associated with increased muscle stiffness, exhibited a heightened risk of muscle strain injury (odds ratio = 1.62; 95% confidence interval = 1.06-2.47 per C allele increase). By contrast, rs78405694 did not show a significant association with muscle strain injury in this population. CONCLUSIONS: A novel locus associated with passive muscle stiffness and muscle strain injury was identified. Elucidating the detailed mechanisms linking the identified locus to passive muscle stiffness may lead to the development of new strategies to prevent muscle strain injuries.

Humans↗
PubMed1990

Enhanced deposition of predominantly type I collagen in myocardial disease.

The myocardium consists of a muscle fibre array surrounded and interspersed by a network of connective tissue, principally collagen, which maintains the functional integrity of the heart. Changes in collagen composition may therefore contribute to altered ventricular function. Collagen composition was examined in cardiac tissue from 15 patients undergoing orthotopic cardiac transplantation. Of these, 10 had severely impaired left ventricular function due to coronary artery disease. The remaining five had dilated cardiomyopathy. Normal heart tissue was taken at autopsy from 25 patients who died of causes unrelated to cardiovascular disease. Left ventricular collagen concentration, estimated from hydroxyproline levels, increased from 48.6 +/- 4.1 mg/g dry weight of tissue in the control group to 95.3 +/- 9.7 mg/g (P less than 0.01) in patients with dilated cardiomyopathy and to 63.5 +/- 9.8 mg/g in the coronary artery disease group. This increase was attributable to an increase in absolute concentrations of both type I and III collagen, determined by separation of cyanogen bromide peptides by sodium dodecyl sulphate polyacrylamide gel electrophoresis. However, there was a significant decrease in the proportion of type III collagen (compared with type I plus III) from 41.8 +/- 1.1% in controls, to 34.6 +/- 1.5% (P less than 0.01) in the coronary artery disease group and 35.8 +/- 2.8% (P less than 0.05) in the dilated cardiomyopathy group. These results suggest that excessive collagen production, with a preponderance of type I, occurs in these forms of myocardial disease, indicative of a remodelling of the collagen matrix, which, by increasing passive myocardial stiffness may contribute to impaired heart function seen in these groups of patients.

Adult↗
PubMed2002

Growth hormone influences the content and composition of collagen in the aorta from old rats.

Collagen and elastin are major components of the aortic extracellular matrix and crucial in determining the stiffness of the aorta. We recently showed that growth hormone (GH) changes the mechanical properties, content and composition of aortic collagen from young rats. In the present study, the effect of GH on aorta from old rats was investigated. Old female rats (18(1/2)-20(1/2) months) were injected with either GH (5 mg/kg per day; n=15) or vehicle (n=14) for 80 days. Mechanical and biochemical properties of the thoracic aorta were investigated. Long-term GH injections increased the body weight of female rats by 47% accompanied by a threefold increase in serum IGF-I. The diameter of the aorta was increased by 5%, resulting in a 10% increase in the cross-section of the aortic lumen. Growth hormone increased the content of collagen per sample by 6% and increased the amount of type I collagen relative to type III collagen. No changes in the mechanical properties or elastin content per sample were found. In conclusion, GH induced a substantial growth of old rats. However, although the diameter and the collagen content were increased, the mechanical properties of the aorta were preserved in the GH-injected rats.

Aging↗
PubMedDate not supplied

Mechanical and structural characteristics of the new BONE-LOK cortical-cancellous internal fixation device.

The purpose of this study was to evaluate the structural and mechanical characteristics of a new and unique titanium cortical-cancellous helical compression anchor with BONE-LOK (Triage Medical, Inc., Irvine, CA) technology for compressive internal fixation of fractures and osteotomies. This device provides fixation through the use of a distal helical anchor and a proximal retentive collar that are united by an axially movable pin (U.S. and international patents issued and pending). The helical compression anchor (2.7-mm diameter) was compared with 3.0-mm diameter titanium cancellous screws (Synthes, Paoli, PA) for pullout strength and compression in 7# and 12# synthetic rigid polyurethane foam (simulated bone matrix), and for 3-point bending stiffness. The following results (mean +/- standard deviation) were obtained: foam block pullout strength in 12# foam: 2.7-mm helical compression anchor 70 +/- 2.0 N and 3.0-mm titanium cancellous screws 37 +/- 11 N; in 7# foam: 2.7-mm helical compression anchor 33 +/- 3 N and 3.0-mm titanium cancellous screws 31 +/- 12 N. Three-point bending stiffness, 2.7-mm helical compression anchor 988 +/- 68 N/mm and 3.0-mm titanium cancellous screws 845 +/- 88 N/mm. Compression strength testing in 12# foam: 2.7-mm helical compression anchor 70.8 +/- 4.8 N and 3.0-mm titanium cancellous screws 23.0 +/- 3.1 N, in 7# foam: 2.7-mm helical compression anchor 42.6 +/- 3.2 N and 3.0-mm titanium cancellous screws 10.4 +/- 0.9 N. Results showed greater pullout strength, 3-point bending stiffness, and compression strength for the 2.7-mm helical compression anchor as compared with the 3.0-mm titanium cancellous screws in these testing models. This difference represents a distinct advantage in the new device that warrants further in vivo testing.

Bone Screws↗
PubMed1990

Cracks emanating from circular voids or elastic inclusions in PMMA near a bone-implant interface.

Mechanical fracture is believed to be a primary reason for loss of fixation at the bone-cement-implant interface. In addition to the expected cracks at the bone-cement interface, cracks are also observed to be formed at voids and inclusions within the cement. An analytical solution is presented for cracks emanating from circular voids or elastic inclusions under uniaxial tension using the solution for a single dislocation as a Green's function. Stress intensity factors are calculated for arbitrary orientations of the cracks, and for varying relative stiffnesses of the inclusion and the matrix, to determine the most favorable combination of parameters for crack growth.

Biomechanical Phenomena↗
PubMed2001

Pulse pressure, aortic reactivity, and endothelium dysfunction in old hypertensive rats.

The reactivity of old hypertensive rat aortas has not been investigated in relation to each phenotype of the blood pressure curve, mean arterial pressure (MAP), and pulse pressure (PP). Aortic reactivities from 3- to 78-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were studied with the use of organ chambers and invasive blood pressure, carotid diameter, and histomorphometry. MAP and PP were elevated in SHR, but at 78 weeks, a selective increase of PP without further MAP increase was observed for the same carotid diameter as WKY. Aortic relaxation in response to carbamylcholine decreased similarly with age in both strains. With (+) or without (-) endothelium (E), maximal developed tension (MDT) under KCl increased linearly with age in SHR, proportionally to wall thickness and MAP increase. Under norepinephrine (NE), MDT of E(-) aortas from SHR and controls increased with age and reached plateaus at 12 weeks, whereas MDT of E(+) aortas from SHR increased linearly with age. Because the NE-induced MDT was higher for E(-) than E(+), the difference estimated endothelial function. This difference reached plateaus from 12 to 78 weeks in WKY but was abolished beyond 12 weeks in SHR, a finding also observed under NO-synthase inhibition. In old hypertensive rats, (1) increased KCl reactivity is endothelium independent but influenced by the MAP-dependent aortic hypertrophy with resulting increased vascular smooth muscle reactivity, whereas (2) increased NE reactivity is endothelium dependent in association with increased PP, altered endothelial function, and extracellular matrix, with resulting enhanced intrinsic arterial stiffness.

Aging↗
PubMed1998

Inhibitory effect of tranilast on hypertrophic collagen production in the spontaneously hypertensive rat heart.

Tranilast, N-(3,4-dimethoxycinnamoyl) anthranilic acid, a widely used antiallergy drug in Japan, has been shown to inhibit transforming growth factor-beta1 release from fibroblasts and reduce collagen synthesis in keloid cells. In the present study, we have investigated the effect of this drug on cardiac hypertrophy in spontaneously hypertensive rats (SHR), with a focus on the cardiac collagen matrix, which is associated with myocardial stiffness. Twenty-four-week-old SHRs and Wistar Kyoto rats (WKYs) were administered tranilast (300 mg/kg) orally once a day for 4 weeks. This treatment significantly suppressed increases in left ventricular collagen concentration (P < 0.05) and the left ventricular weight/body weights ratios (P < 0.05) in SHRs, and tranilast was ineffective on collagen concentration and ventricular weight/body weights ratios in WKYs. Tranilast did not affect systolic or diastolic blood pressure, end-diastolic left ventricular pressure and heart rate in both SHRs and WKYs, and the agent did not change positive dp/dt or cardiac output in SHRs. The pressure-volume relationship curve was shifted to the left by the drug; the slope (k) of the logarithm of the pressure-volume relationship curve was significantly increased (P < 0.05) in SHRs. It is concluded that the suppression of increases in cardiac collagen and left ventricular mass by tranilast results in a corresponding prevention of cardiac stiffness as studied in the SHR.

Animals↗
PubMed2005

Serum tissue inhibitors of metalloproteinases 1 (TIMP-1) and carotid atherosclerosis and aortic arterial stiffness.

BACKGROUND: The results of experimental studies have suggested that matrix metalloproteinases (MMPs) and their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs), are involved in vascular remodeling. In a population-based study, we report the relationships of serum TIMP-1 with carotid intima-media thickness, carotid plaques and aortic arterial stiffness. METHODS: Free health examinations were performed on 238 men free of coronary heart diseases (aged 56.5 +/- 10.4 years, 57.1% were hypertensive). Carotid-femoral pulse-wave velocity (PWV) was used to assess aortic stiffness. Carotid ultrasound examination included measurements (at sites free of plaques) of intima-media thickness (IMT) at the common carotid arteries (CCA) and assessment of atherosclerotic plaques in the extracranial carotid arteries. RESULTS: The percentage of subjects with plaques was lower in subjects with low TIMP-1 values (P for trend = 0.0001). In multivariate analysis adjusted for age, body mass index, smoking habits, total cholesterol, triglycerides, C-reactive protein, heart rate, diabetes and systolic blood pressure, the odds ratio of carotid plaques in subjects with high values of TIMP-1 (tertile 3) compared to those with low values (tertile 1) was 2.89 (95% confidence interval 1.12-7.47, P < 0.01). TIMP-1 was positively associated with CCA-IMT and PWV in univariate analysis. However, the associations disappeared once age and systolic blood pressure were taken into account in the multivariate analysis. CONCLUSION: This study shows that there is a differential association of TIMP-1 with PWV, CCA-IMT and carotid plaques. Our results suggest that TIMP-1 might be involved in plaque formation.

Aged↗
PubMed1998

Collagen subtypes and matrix metalloproteinase in idiopathic restrictive cardiomyopathy.

BACKGROUND: Idiopathic restrictive cardiomyopathy is a rare disease characterized by diastolic dysfunction, and the pathogenesis of the stiff heart remains unclear. The purpose of this study was to analyze the subpopulation of collagen fibers and determine the expression of matrix metalloproteinase in restrictive cardiomyopathy. METHODS AND RESULTS: In endomyocardial biopsy specimens obtained from seven patients with restrictive cardiomyopathy, collagen fiber types I, III, and IV, and matrix metalloproteinase- and two were observed by light and electron microscopy, using monoclonal antibodies. Type I collagen was less prominent in the interstitium, whereas the immunoreactivity for type III collagen was marked. The immunoreactivity against matrix metalloproteinase-1 was observed along with types I and III collagen fibers and in the cytoplasm of some fibrocytes/fibroblasts. The matrix metalloproteinase-1 tended to increase when the reactivity against types I and III collagen was prominent. Both type IV collagen and matrix metalloproteinase-2 were observed along arterial walls and the basement membrane of cardiocytes. CONCLUSIONS: Increased type III collagen may play an important role as the cause of left ventricular stiffness in restrictive cardiomyopathy. The matrix metalloproteinase appeared to be involved in a cascade of collagen synthesis and the remodeling of the heart in patients with restrictive cardiomyopathy.

Adult↗
PubMed2000

Factors regulating bone maturity and strength in poultry.

Adolescent meat-type poultry and cage layers exhibit a high incidence of bone problems that include bone weakness, deformity, breakage, and infection and osteoporosis-related mortalities. These problems include economic and welfare issues. To improve bone quality in poultry, it is essential to understand the physiological basis of bone maturity and strength in poultry. A complex array of factors that include structural, architectural, compositional, physiological, and nutritional factors interactively determine bone quality and strength. Bone is approximately 70% mineral, 20% organic, and 10% water. Collagen is the major organic matrix that confers tensile strength to the bone, whereas hydroxyapatite provides compressional strength. In recent years, the roles of different collagen crosslinks have been shown to be important in the increase of bone mechanical strength. Similarly, age-related glyco-oxidative modifications of collagen have been shown to increase the stiffness of collagen. These posttranslational modifications of matrix can affect bone quality as it would be affected by the changes in the mineralization process. Our studies show that the growth in the tibia continued until 25 wk of age, which correlated with the increase in the content of hydroxylysylpridinoline (HP) and lysylpyridinoline (LP), the collagen crosslinks. The tibia from 5-wk-old chicks were strong but brittle because of low collagen crosslinks and high mineral content. Bone maturity may relate to its crosslink content. Compared to crosslink content, bone density and ash content showed moderate increases during growth. The bones from younger turkeys were more susceptible to corticosteroid-induced stunting of growth, which also resulted in decreased bone strength. This review discusses how different factors can compromise bone strength by reducing growth, altering shape, affecting mineralization, and affecting collagen crosslinking.

Aging↗
PubMed1996

Fibrous matrix of ventricular myocardium in tricuspid atresia compared with normal heart. A quantitative analysis.

BACKGROUND: The collagen matrix is a small component of the myocardium, but it provides a supportive framework. An increase in collagen in the pressure-overloaded ventricle is known to cause myocardial stiffness. However, little is known about the collagen matrix in the volume-overloaded ventricle, particularly in relation to congenital heart disease. METHODS AND RESULTS: We examined a total of 53 hearts with tricuspid atresia and 58 normal hearts matched for age. Using a microscopic-morphometric method, we analyzed the percentage per field area occupied by interstitial fibrous tissue in four sites in the ventricular mass for each specimen. A comparison of sampling sites showed no significant variations between normal and malformed hearts. Results from a homogeneity of regression co-efficients analysis suggested that the two groups shared the same basic relation of proportion of fibrosis with age. The use of ANCOVA, however, revealed a clear separation between the extents of fibrous tissue in the two groups of hearts. CONCLUSIONS: The myocardium of hearts with tricuspid atresia is consistently more fibrotic than normal heart and is probably an inherent part of the malformation. This difference could explain, at least in part, the clinical observation that the left ventricle is frequently abnormal, even at an early age.

Adolescent↗
PubMed1993

Fibronectin-like immunoreactivity of the basilar membrane of young and aged rats.

Dysfunction of cochlear mechanics has been hypothesized to be a source of age-related hearing loss and the basilar membrane mass and stiffness contribute to normal cochlear mechanics. Fibronectin, a large, extracellular matrix protein and a major component of the basilar membrane, may contribute to both the mass and stiffness of the membrane. Mesothelial cells underlying the basilar membrane may produce the fibronectin and also contribute to the mass of the membrane. Changes in either the fibronectin or the mesothelial cells might, therefore, have an effect on cochlear mechanics. In order to assess basilar membrane changes in aged animals, young adult (2-4 months) and aged (24-26 months) Sprague-Dawley rats were evaluated for the presence of fibronectin-like protein and mesothelial cells. The basilar membrane in the young animals had strong fibronectin-like immunoreactivity throughout its length. The old animals, on the other hand, showed normal fibronectin immunoreactivity in the basilar membrane of the basal turn, but little or no reactivity in the apical cochlear turn. The number of mesothelial cells was reduced throughout the length of the membrane in aged animals, with the greatest loss in the basal turn (60% fewer cells). These two degenerative changes, which appear to be independent of each other, may contribute to the observed threshold shifts in aged cochleas.

Aging↗
PubMed1984

The healing of segmental bone defects induced by demineralized bone matrix. A radiographic and biomechanical study.

UNLABELLED: We studied the effect of demineralized bone matrix on the repair of large femoral diaphyseal defects in a rat model by clinical, radiographic, and biomechanical methods. A standard procedure was first developed to create segmental defects that did not heal and in which non-union developed consistently. The effect of demineralized bone matrix on repair was then assessed by physical examination, serial radiographs, and biomechanical studies to determine deformation to failure, stiffness, torsional strength, and energy absorption. By twelve weeks, the defects that had been treated with demineralized bone matrix showed satisfactory repair and remodeling in most animals based on clinical and radiographic evaluation. The biomechanical studies demonstrated that the bone induced by demineralized bone matrix had an energy-absorption capacity and stiffness equal to those of intact rat femoral bone. The bone induced by demineralized bone matrix achieved 35 per cent of the torsional strength of normal bone and an increased capacity to deform under load. These biomechanical properties are similar to those observed in the early stages of normal fracture repair. CLINICAL RELEVANCE: An effective, readily available alternative to autologous bone-graft material would have a variety of clinical uses in orthopaedic surgery, such as augmenting fusions, aiding in the repair of high-risk fractures, and filling or bridging bone defects. Demineralized bone matrix may provide an important tool for these purposes by inducing bone that has the mechanical properties of fracture callus. This would reduce the morbidity associated with harvesting autologous bone and have an advantage over allografts or synthetic biomaterials that require incorporation by the host before they can support mechanical loads.

Animals↗
PubMed2005

Aging is associated with increased matrix metalloproteinase-2 activity in the human aorta.

BACKGROUND: Aging is a major risk factor for the development of arterial stiffness and vascular disease, and it is related to the upregulation of matrix metalloproteinase-2 (MMP-2) in the aorta of rats and nonhuman primates. This study aimed to determine whether MMP activity in the human vasculature changes with aging. We also assessed regional differences in MMP activity at two locations in the arterial tree, the aorta and the internal mammary artery (IMA). METHODS: Both MMP-2 and MMP-9 activity in the human aorta and IMA were determined by gelatin zymography and were localized within the tissue using in situ zymography. Tissue inhibitor of metalloproteinase-2 (TIMP-2) levels was determined by Western blot. RESULTS: Active MMP-2 (but not pro-MMP-2, pro-MMP-9, or active MMP-9) was positively correlated with age in the human aorta (r = 0.65; P < .001) but not in the IMA. Active MMP-2 and TIMP-2 (but not pro-MMP-2 or pro- or active MMP-9) levels are higher in the aorta than in the IMA (P < .001; P < .05). In the aorta, MMP activity is highest in the intima and is also detectable in the media and adventitia. To a lesser extent, MMP activity is present in all layers of the IMA. CONCLUSIONS: This study demonstrates that age-related MMP-2 upregulation occurs in the human aorta but not in the IMA.

Aged↗
PubMed1994

A microstructural model for the elastic response of articular cartilage.

A model of articular cartilage is developed in which the continuum stiffness tensor is related to the tissue's microstructure. The model consists of bilinear elastic fibers embedded in an elastic matrix. Homogenization techniques are used to relate this level of organization to the macroscopic response of the tissue. The model includes the effects of spatial orientation of fibers, pre-stress in the fibers and matrix resulting from matrix swelling, slipping at the interface between the fibers and the matrix, fiber buckling in compression, and deformation-induced fiber reorientation. The model predicts increased axial stiffness with increasing stretch due to fiber reorientation, reduced axial and shear stiffness with slipping between fiber and matrix and a sensitivity of the tissue response to the swelling pressure in the matrix, the matrix modulus and the bonding of the fiber matrix interface.

Algorithms↗
PubMed2005

h2-Calponin is regulated by mechanical tension and modifies the function of actin cytoskeleton.

Calponin is an extensively studied actin-binding protein, but its function is not well understood. Among three isoforms of calponin, h2-calponin is found in both smooth muscle and non-muscle cells. The present study demonstrates that epidermal keratinocytes and fibroblast cells express significant amounts of h2-calponin. The expression of h2-calponin is cell anchorage-dependent. The levels of h2-calponin decrease when cells are rounded up and remain low when cells are prevented from adherence to a culture dish. h2-calponin expression resumes after the floating cells are allowed to form a monolayer in plastic dish. Cell cultures on polyacrylamide gels of different stiffness demonstrated that h2-calponin expression is affected by the mechanical properties of the culture matrix. When cells are cultured on soft gel that applies less traction force to the cell and, therefore, lower mechanical tension in the cytoskeleton, the level of h2-calponin is significantly lower than that in cells cultured on hard gel or rigid plastic dish. Force-expression of h2-calponin enhanced the resistance of the actin filaments to cytochalasin B treatment. Keratinocyte differentiation is accompanied by a mechanical tension-related up-regulation of h2-calponin. Lowering the tension of actin cytoskeleton by inhibiting non-muscle myosin II ATPase decreased h2-calponin expression. In contrast to the mechanical tension regulation of endogenous h2-calponin, the expression of h2-calponin using a cytomegalovirus promotor was independent of the stiffness of culture matrix. The results suggest that h2-calponin represents a novel manifestation of mechanical tension responsive gene regulation that may modify cytoskeleton function.

Actins↗
PubMed1994

Contribution of collagen matrix to passive left ventricular mechanics in isolated rat hearts.

Although it makes up only 2-6% of left ventricular dry weight, collagen is thought to be the major structural protein determining passive ventricular stiffness. However, the relationship between structure of the extracellular matrix and passive mechanics is not understood. Hence, to deplete the collagen matrix, 16 rat hearts were perfused with bacterial collagenase for 60 min. Quantitative morphology using picrosirius red revealed a 36% decrease in collagen area fraction predominantly in the medium-sized fibers. Scanning electron microscopy revealed damage to the endomysial struts. Passive pressure-volume curves showed increases in left ventricular volume at all pressures (from 0.203 +/- 0.061 to 0.265 +/- 0.061 ml at 5 mmHg, P < 0.0001). Strain during loading, calculated from lengths obtained from a triplet of piezoelectric crystals, was unchanged with collagen depletion. However, remodeling strain computed from the collagenase-treated state referred to the Krebs solution-treated state at the same ventricular pressure showed both circumferential (0.145 +/- 0.166 to 0.170 +/- 0.158) and longitudinal (0.070 +/- 0.120 to 0.068 +/- 0.069) stretching. Sarcomere lengths increased at all depths (5.2% at midwall). Thus alterations in the extracellular matrix lead to increased ventricular volume and sarcomere lengths without altering ventricular compliance.

Animals↗