Cellular and molecular mechanisms of systolic and diastolic dysfunction in an avian model of dilated cardiomyopathy

Wu, Yingliang

doi:10.1016/j.yjmcc.2004.04.010

Cited by 29 publications

(33 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Limited information exists on the role of the cellular Frank-Starling response in bird hearts. Based on work from whole bird hearts and histological sections (Wu et al, 2004), pressure-volume relationships and SLs at end-diastolic and endsystolic volumes in birds are closer to values in mammals than amphibians or fish. Reports exist of increased cardiac output based solely on changes in heart rate in ducks (fourfold) (Grubb, 1982) and pigeons (sixfold) (Peters et al, 2005).…”

Section: Reptiles and Birdsmentioning

confidence: 90%

The Frank–Starling mechanism in vertebrate cardiac myocytes

Shiels

White

2008

Journal of Experimental Biology

157

107

View full text Add to dashboard Cite

SUMMARY The Frank–Starling law of the heart applies to all classes of vertebrates. It describes how stretch of cardiac muscle, up to an optimum length, increases contractility thereby linking cardiac ejection to cardiac filling. The cellular mechanisms underlying the Frank–Starling response include an increase in myofilament sensitivity for Ca2+, decreased myofilament lattice spacing and increased thin filament cooperativity. Stretching of mammalian, amphibian and fish cardiac myocytes reveal that the functional peak of the sarcomere length (SL)–tension relationship occurs at longer SL in the non-mammalian classes. These findings correlate with in vivo cardiac function as non-mammalian vertebrates, such as fish,vary stroke volume to a relatively larger extent than mammals. Thus, it seems the length-dependent properties of individual myocytes are modified to accommodate differences in organ function, and the high extensibility of certain hearts is matched by the extensibility of their myocytes. Reasons for the differences between classes are still to be elucidated, however, the structure of mammalian ventricular myocytes, with larger widths and higher levels of passive stiffness than those from other vertebrate classes may be implicated.

show abstract

Section: Reptiles and Birdsmentioning

confidence: 90%

The Frank–Starling mechanism in vertebrate cardiac myocytes

Shiels

White

2008

Journal of Experimental Biology

157

107

View full text Add to dashboard Cite

show abstract

“…Also addition of Fz may have led to direct toxicity or mechanical insults such as; chronic volume overload in mitral valvular regurgitation with myocyte failure and cytoskeletal uncoupling of the chambers leading to dilation (Goldstein et al, 1998). The differences observed between LVIDd and LVISd for poults fed Fz-containing diets and those in the control group are similar to that of Wu et al (2004), which reported increased left ventricular dimension for poults fed Fz-containing diets. More so, a review by Vlahovic and Popovic (1999), reported impaired left ventricular diastolic function to be one of the abnormalities associated with cardiac diseases accompanied by changes in filling patterns in humans, from delayed relaxation, through pseudo-normalization and, finally, to restrictive filling.…”

Section: Discussionmentioning

confidence: 58%

“…The in vivo contractile performance of the heart of each poult was estimated according to Wu et al (2004) using the equation:…”

Section: Shortening Fractionmentioning

confidence: 99%

“…On the other hand, electrocardiogram is expensive and can only be efficiently used for older birds often past the age that they are most susceptible to DCM. Though Echocardiography (ECHO) has previously been used as a diagnostic tool in birds at or around 4 weeks-of-age, it remains unclear which ECHO parameters are most efficient for the identification of DCM-affected birds from 0 to 4 weeks-of-age (Wu et al, 2004). To be useful, ECHO requires the establishment of baseline parameters that can be referenced in the diagnosis of the incidence and severity of DCM.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

AN ASSESSMENT OF ECHOCARDIOGRAPHY AS A DIAGNOSTIC TOOL FOR DILATED CARDIOMYOPATHY IN TURKEY (<i>MELEAGRIS GALLOPAVO</i>)

Ali¹

2012

American Journal of Animal and Veterinary Sciences

View full text Add to dashboard Cite

Our understanding of the etiology of Dilated Cardiomyopathy (DCM), which affects about 5% of turkeys, is limited. This limitation may be due to the lack of an easy-to-use diagnostic tool with well-defined parameters and does not involve necropsy. This lack of a widely tested non-necropsy method makes it difficult for a largescale study of the genetic factors that underlie DCM. Here, we Evaluated Echocardiography (ECHO) for its ease and reliability for identifying DCM-affected turkeys from hatch to four weeks-of-age. The parameters evaluated included Left Ventricular Internal-Diastolic (LVIDd), Internal-Systolic Dimension (LVISd), Interventricular Septum End-Diastolic (IVSEd), Interventricular Septum End-Systolic (IVSEs), Left Ventricular Wall End-Systolic (LVWEs) and Left Ventricular Wall End-Diastolic (LVWEd). To induce DCM, feed containing 700 ppm of Furazolidone (Fz) was fed to turkey poults from one to 28 days-of-age. The LVIDd and LVISd were the most consistent indicators of DCM. Both parameters revealed differences between control and treatment poults of between 25 and 326% at the 4 ages at which ECHO measurements were taken. The average difference in LVIDd between control and poults fed Fz-containing diets ranged from 25% in one week-old to 80% in 4-week-old poults. At similar ages, average differences between control and poults fed Fz-containing diets in LVISd were 74 and 326% respectively. Necropsy of poults that survived to the end of the 4-week Fz-treatment confirmed these ECHO measurements in treatment and normal poults. Our data suggest that using LVIDd and LVISd as parameters make ECHO a reliable tool for identifying DCM in turkeys.

show abstract

“…The reason for cardiac fibrosis remains to be determined, but lymphedema may be one important factor that is closely related to myocardial fibrosis (Laine and Allen, 1991;Stolyarov et al, 2002;Kong et al, 2006). Cardiac fibrosis makes the heart ''harder'' and has a negative influence on systole and diastole of the heart (Wu et al, 2004). Little is known about the effect of fibrosis on the cardiac lymphatics.…”

Section: Discussion Cardiac Lymphatic Fibrosis In the Hypertensive Heartmentioning

confidence: 99%

Ultrastructure Changes of Cardiac Lymphatics During Cardiac Fibrosis in Hypertensive Rats

Shimada

Zhang

et al. 2009

The Anatomical Record

View full text Add to dashboard Cite

Hypertension is one of the most common diseases that induce a series of pathological changes in different organs of the human body, especially in the heart. There is a wealth of evidence about blood vessels in hypertensive myocardium, but little is known about structural changes in the cardiac lymphatic system. To clarify the changes in structure of the cardiac lymphatic system during hypertension, we developed a hypertension animal model with Dahl S rats and we used Dahl R rats as the control group. We examined the expression of collagen fibers, atrial natriuretic peptide, connexin43, and LYVE-1 in the rat heart by immunohistochemistry. The ultrastructure of the cardiac lymphatics was detected by transmission electron microscopy and scanning electron microscopy. We demonstrated extensive lymphatic fibrosis in the hearts of the Dahl S hypertension group, characterized by increased thin collagen fibrils that connected with the lymphatics directly. Ultrastructural changes in the cardiac lymphatic endothelium such as an increase of vesicles and occurrence of vacuoles, active exocytosis, and cytoplasmic processes, restored the draining of tissue fluid. Our study suggests that during hypertension, the changes in structure of the cardiac lymphatics may be one important factor involved in cardiac fibrosis. Therefore, the lymphatics may be a possible target for reducing fibrosis in the treatment of hypertension.

show abstract

Cellular and molecular mechanisms of systolic and diastolic dysfunction in an avian model of dilated cardiomyopathy

Cited by 29 publications

References 30 publications

The Frank–Starling mechanism in vertebrate cardiac myocytes

The Frank–Starling mechanism in vertebrate cardiac myocytes

AN ASSESSMENT OF ECHOCARDIOGRAPHY AS A DIAGNOSTIC TOOL FOR DILATED CARDIOMYOPATHY IN TURKEY (<i>MELEAGRIS GALLOPAVO</i>)

Ultrastructure Changes of Cardiac Lymphatics During Cardiac Fibrosis in Hypertensive Rats

Contact Info

Product

Resources

About