Age-related alterations of cardiac tissue microstructure and material properties in Fischer 344 rats

Nguyen, Cuong Tu; Hall, Christopher S.; Scott, Michael J.; Zhu, Qingyan; Marsh, Jon N.; Wickline, Samuel A.

doi:10.1016/s0301-5629(01)00343-x

Cited by 24 publications

(17 citation statements)

References 37 publications

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“…In contrast, a significant increase in collagen content was found on day 5 by biochemical analysis. This change probably accounts for the increase in backscatter measured on day 5, since investigators in previous studies on other tissues have reported a relationship between collagen content and backscatter (25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 71%

Effects of antiinflammatory drugs on arthritic cartilage: A high‐frequency quantitative ultrasound study in rats

Jaffre¹,

Watrin²,

Lœuille³

et al. 2003

Arthritis & Rheumatism

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Objective. To evaluate the ability of 55-MHz quantitative ultrasound (US) to detect the in vivo effects of experimental arthritis, as well as those of two antiinflammatory drugs, naproxen (NPX) and dexamethasone (DEX), on cartilage and subchondral bone.Methods. Arthritis was induced in both knees of 108 rats by intraarticular injection of zymosan (ZYM). Two groups of arthritic rats (n ‫؍‬ 36 per group) were treated daily with either NPX (10 mg/kg/day) or DEX (0.1 mg/kg/day). Using a 3-dimensional US microscope, patellae were explored in vitro on days 5, 14, and 21 after injections. US assessment included the analysis of quantitative indices of local modifications involving cartilage and bone: integrated reflection coefficient (IRC) from the cartilage surface and apparent integrated backscatter from the cartilage internal structure (cartilage matrix) (AIB cartilage ) and the cartilage-bone interface (AIB bone ).Results. ZYM induced articular surface fibrillation that resulted in a decrease in IRC at all times (P < 0.02) and in an increase in AIB bone on days 5 and 14 (P < 0.005). Fibrillation was not changed by NPX administration, while it disappeared following DEX treatment. Cartilage-bone interface alterations were prevented by DEX and partially compensated for by NPX. Cartilage matrix echogenicity decreased with time in all groups due to maturation (P < 0.05), except in DEX-treated rats.Conclusion. Quantitative 55 MHz US allowed detection of early cartilage and bone lesions due to experimental arthritis, and also allowed detection of the effects of antiinflammatory drugs. NPX seemed to have an effect on subchondral bone lesions, but not on cartilage. DEX appeared to repair articular surface and bone, but prevented animal growth and cartilage maturation.In rheumatoid arthritis (RA), synovial inflammation and pannus releasing matrix metalloproteinases, oxygen-derived free radicals, cytokines, and prostaglandins degrade articular cartilage. These mediators provoke proteoglycan (PG) synthesis inhibition, cartilage destruction, bone erosions, and ancillary progressive articular loss of function (1,2). They are also responsible for the swelling and pain in arthritic joints. Nonsteroidal antiinflammatory drugs (NSAIDs) and oral steroids reduce the RA symptoms of joint pain and swelling. However, evidence in clinics and from in vitro studies that NSAIDs and steroids can prevent the progression of chronic, destructive arthritis is both sparse and controversial (3-7). Furthermore, most in vitro studies rely on destructive techniques (e.g., histology and biochemistry), and the criteria for determining cartilage degradation remain qualitative.There is increasing interest in the use of ultrasonography in rheumatology, since ultrasound (US) is noninvasive, safe, more accurate than clinical evaluation of synovitis and cartilage thickness in small joints, and can be used repeatedly in RA patients (8). Recent research suggests that high-frequency US may also serve ex vivo as a useful means for the investigation of cartilage ma...

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Section: Discussionmentioning

confidence: 71%

Effects of antiinflammatory drugs on arthritic cartilage: A high‐frequency quantitative ultrasound study in rats

Jaffre¹,

Watrin²,

Lœuille³

et al. 2003

Arthritis & Rheumatism

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“…The cardiac aging process is accompanied by increased myocardial stiffness [24] . Therefore, we used picric acidSirius red staining to study the alteration of collagen deposition.…”

Section: Avt Decreased the Collagen Content In The Aging Rat Heartsmentioning

confidence: 99%

Atorvastatin May Delay Cardiac Aging by Upregulating Peroxisome Proliferator-Activated Receptors in Rats

Han

Liu

et al. 2012

Pharmacology

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Aims: To investigate the effect of atorvastatin on cardiac aging in rats. Materials: Ninety 20-month-old Wistar rats were administered oral atorvastatin (AVT; 10 or 1 mg·kg^-1·day^-1) or saline for 4 months. At the end of the experiment, age-related changes in hearts were measured. Results: Compared with young rats, obvious increases were found in the aging rats in left ventricle thickness, diameter of cardiocytes, collagen deposition, the ratio of type I/type III collagen, β-galactosidase and malondialdehyde (MDA), and obvious decreases were found in superoxide dismutase (SOD), catalase (CAT) and nitric oxide synthase (NOS). The treatment with AVT led to significant decreases in the thickness of the left ventricle, diameter of cardiocytes, collagen deposition, I/III collagen ratio, MDA, β-galactosidase and increases in the activity of SOD, CAT and NOS. Some aging-related inflammatory cytokines like interleukin (IL)-1β, tumour necrosis factor (TNF)-α and matrix metalloproteinase (MMP)-9 were found to be overexpressed in the aging rats. AVT treatment could inhibit the expression of IL-1β, TNF-α and MMP-9 on both the mRNA and protein levels, and increase the expression of peroxisome proliferator-activated receptors (PPAR-α/β/δ/γ). Pretreatment with PPAR inhibitors attenuated the inhibitory effect of AVT on the expression of inflammatory cytokines. Conclusion: AVT may retard the cardiac aging process by upregulating PPARs.

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“…In addition, LV function and structural changes can also affect mechanical load and wall stress. Age-related changes in mechanical properties of myocardial and vascular tissue have been characterized experimentally (Nguyen et al 2001;Cheitlin 2003), and collagen turnover in response to changes in wall stress has been demonstrated in adult myocardium (Miller and Tyagi 2002). End-diastolic wall strain is normalized in hypertrophic remodeling (Emery and Omens 1997).…”

Section: Introductionmentioning

confidence: 99%

Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms

Lin

Lopez

Jin³

et al. 2008

Experimental Gerontology

101

109

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Age-related skeletal muscle sarcopenia has been extensively studied and smooth muscle sarcopenia has been recently described, but age-related cardiac sarcopenia has not been previously examined. Therefore, we evaluated adult (7.5±0.5 months; n=27) and senescent (31.8±0.4 months; n=26) C57BL/6J mice for cardiac sarcopenia using physiological, histological, and biochemical assessments. Mice do not develop hypertension, even into senescence, which allowed us to decouple vascular effects and monitor cardiac-dependent variables. We then developed a mathematical model to describe the relationship between age-related changes in cardiac muscle structure and function. Our results showed that, compared to adult mice, senescent mice demonstrated increased left ventricular (LV) end diastolic dimension, decreased wall thickness, and decreased ejection fraction, indicating dilation and reduced contractile performance. Myocyte numbers decreased, and interstitial fibrosis was punctate but doubled in the senescent mice, indicating reparative fibrosis. Electrocardiogram analysis showed that PR interval and QRS interval increased and R amplitude decreased in the senescent mice, indicating prolonged conduction times consistent with increased fibrosis. Intracellular lipid accumulation was accompanied by a decrease in glycogen stores in the senescent mice. Mathematical simulation indicated that changes in LV dimension, collagen deposition, wall stress, and wall stiffness precede LV dysfunction. We conclude that age-related cardiac sarcopenia occurs in mice and that LV remodeling due to increased end diastolic pressure could be an underlying mechanism for age-related LV dysfunction.

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Age-related alterations of cardiac tissue microstructure and material properties in Fischer 344 rats

Cited by 24 publications

References 37 publications

Effects of antiinflammatory drugs on arthritic cartilage: A high‐frequency quantitative ultrasound study in rats

Effects of antiinflammatory drugs on arthritic cartilage: A high‐frequency quantitative ultrasound study in rats

Atorvastatin May Delay Cardiac Aging by Upregulating Peroxisome Proliferator-Activated Receptors in Rats

Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms

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