Hypertrophy, Hyperplasia and Structural Dilatation of the Human Heart

Aj, Linzbach

doi:10.1159/000399507

Cited by 59 publications

(19 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Cardiomyocyte adherence to the basement membrane provides a means by which to maintain ventricular size and shape and to transduce the contractile force. Accordingly, reduced cardiomyocyte adhesion may be a mechanism contributing to wall thinning and ventricular dilatation (28,34). However, this is the first study to show estrogen alters integrin expression in the heart.…”

Section: Discussionmentioning

confidence: 78%

Estrogenic modulation of inflammation-related genes in male rats following volume overload

McLarty

Meléndez

Levick

et al. 2012

Physiological Genomics

View full text Add to dashboard Cite

Our laboratory has previously reported significant increases of the proinflammatory cytokine TNF-␣ in male hearts secondary to sustained volume overload. These elevated levels of TNF-␣ are accompanied by left ventricular (LV) dilatation and cardiac dysfunction. In contrast, estrogen has been shown to protect against this adverse cardiac remodeling in both female and male rats. The purpose of this study was to determine whether estrogen has an effect on inflammation-related genes that contribute to this estrogen-mediated cardioprotection. Myocardial volume overload was induced by aortocaval fistula in 8 wk old male Sprague-Dawley rats (n ϭ 30), and genes of interest were identified using an inflammatory PCR array in Sham, Fistula, and Fistula ϩ Estrogen-treated (0.02 mg/kg per day beginning 2 wk prior to fistula) groups. A total of 55 inflammatory genes were modified (Ն2-fold change) at 3 days postfistula. The number of inflammatory gene was reduced to 21 genes by estrogen treatment, whereas 13 genes were comparably modulated in both fistula groups. The most notable were TNF-␣, which was downregulated by estrogen, and the TNF-␣ receptors, which were differentially regulated by estrogen. Specific genes related to arachidonic acid metabolism were downregulated by estrogen, including cyclooxygenase-1 and -2. Finally, gene expression for the ␤1-integrin cell adhesion subunit was significantly upregulated in the LV of estrogen-treated animals. Protein levels reflected the changes observed at the gene level. These data suggest that estrogen provides its cardioprotective effects, at least in part, via genomic modulation of numerous inflammation-related genes. aortocaval fistula; tumor necrosis factor-␣; tumor necrosis factor-␣ receptors; prostaglandin; ␤1-integrin THE ABDOMINAL AORTOCAVAL FISTULA model of volume overload is an excellent approach in which to study sex differences in heart failure. In this model, males undergo collagen degradation and develop significant left ventricular (LV) wall thinning, ventricular dilatation, and increased myocardial compliance (5,9,10

show abstract

Section: Discussionmentioning

confidence: 78%

Estrogenic modulation of inflammation-related genes in male rats following volume overload

McLarty

Meléndez

Levick

et al. 2012

Physiological Genomics

View full text Add to dashboard Cite

show abstract

“…These results agree with the findings of other investigators. By counting the number ofmyocytes across the wall and cross-sectional area ofmyocytes, Linzbach et al (9) showed that ventricular dilatation due to chronic volume overload could not be explained by myocyte stretch but rather by a sliding displacement or slippage of heart layers leading to a decrease in the number of muscle layers in the ventricular wall. Spotnitz et al (10) also reported a strong correlation between changes in wall thickness and changes in transmural cell number but not cell density when studying rat hearts postmortem, passively distended with varying left ventricular volume.…”

Section: Discussionmentioning

confidence: 99%

“…First, necrotic myocytes may rupture or tear, leaving fewer intact myocytes across the wall resulting in wall thinning and cavity dilatation (5,7). Another possibility is that necrotic myocytes are stretched so that cell lengthening and thinning account for the infarct wall thinning (8,9). A final possibility is that wall thinning is due to a geometric rearrangement or a slippage of necrotic myocyte bundles resulting in fewer myocytes across the wall with little or no change in myocyte dimensions (9-1 1).…”

Section: Introductionmentioning

confidence: 99%

Steroid administration after myocardial infarction promotes early infarct expansion. A study in the rat.

Mannisi¹,

Weisman²,

Bush³

et al. 1987

J. Clin. Invest.

View full text Add to dashboard Cite

(4), a second possibility is that steroids lead to a prolonged phase during which "soft" necrotic myocardium thins and dilates. The third possibility is that steroids act solely by promoting the early expansion of freshly necrotic myocardium before collagen deposition begins. Infarct expansion, the thinning and dilatation of freshly infarcted myocardium that begins within the first few hours after transmural infarction,

show abstract

“…For example, in rats ventricular cellular hypertrophy is associated with a decrease in DNA concentration (Vliegen et al, 1990). By contrast, concomitant increases in both DNA content and ventricular size are indicative of hyperplastic cellular and subcellular 'growth' (Grimm et al, 1970;Linzbach, 1976;Herget et al, 1997;Leeuwenburgh et al, 2008). Hyperplastic growth of the myocardium occurs during normal embryonic and fetal vertebrate development and continues for a short, but indefinite period after hatching or parturition (Li et al, J. Eme and others Mean number of apnoeas Sham Table 2.…”

Section: Removing Crocodilian R-l Cardiac Shunt Causes Ventricular Enmentioning

confidence: 99%

Surgical removal of right-to-left cardiac shunt in the American alligator(Alligator mississippiensis) causes ventricular enlargement but does not alter apnoea or metabolism during diving

Eme

Gwalthney

Blank

et al. 2009

Journal of Experimental Biology

View full text Add to dashboard Cite

All crocodilians have complete anatomical separation between the right and left ventricles, which is similar to birds and mammals and unlike all other non-avian reptiles. However, the crocodilian heart retains two systemic aortae (left aorta and right aortic arch), a feature that is common to all non-avian reptiles. In crocodilians, the left aorta (LAo) emerges from the right ventricle (RV) alongside the pulmonary artery (PA), and the right aortic arch (RAo) emerges from the left ventricle (LV) (Webb, 1979). This anatomical arrangement results in the capacity for a 'right-to-left' (R-L) cardiac shunt, a 'pulmonary bypass' cardiac shunt, in which a fraction of systemic venous blood recirculates into the systemic arterial circulation (Hicks, 1998).The crocodilian RAo and LAo communicate at two distinct points. As the aortae emerge from the heart, they run side-by-side, sharing a common wall for several centimetres. Near the base of this common wall and just downstream of the aortic valves, there is a small opening called the foramen of Panizza (FoP) (Panizza, 1833), which is of variable calibre and allows for potential blood flow between the RAo and LAo (Grigg and Johansen, 1987;Axelsson et al., 1996;Axelsson and Franklin, 2001). The second point of communication between the aortae is an arterial anastomosis in the abdominal cavity, caudal to the liver. Beyond this anastomosis, the RAo continues as the dorsal aortal, and the LAo becomes the coeliac artery, which gives rise to smaller arteries that supply most of the blood flow to the gastrointestinal tract. Consequently, the LAo is the primary source of blood for the splanchnic circulation, although blood from the RAo can also enter the splanchnic bed via the anastomosis (Axelsson et al., 1991).R-L cardiac shunt has been hypothesised to be important in various activities and physiological functions (Hicks, 1998;Hicks, 2002). For semi-aquatic reptiles like crocodilians, generation of a R-L cardiac shunt has often been observed during breath-holds associated with diving (White, 1969;Grigg and Johansen, 1987;Hicks and Wang, 1996). The reduction in pulmonary blood flow during apnoea has been hypothesised to conserve lung O 2 stores and sequester CO 2 away from the lung, possibly extending aerobic dive times (White, 1978;White, 1985;Grigg and Johansen, 1987). The development of a R-L cardiac shunt also results in arterial desaturation through admixture of venous blood, and the resulting systemic hypoxemia can trigger tissue hypometabolism, which could contribute to the prolongation of aerobic dives (Hicks and Wang, 1999;Platzack and Hicks, 2001).Crocodilians provide an opportunity to investigate experimentally the proximate functions of reptilian cardiac shunting. Their cardiac anatomy lends itself to surgical modification that prevents R-L cardiac shunt while maintaining the integrity of the ventricular chambers, a procedure that is not possible in other reptiles. The purpose of the present study was to test the hypotheses that removal of shunt (occlusion of LAo) woul...

show abstract

Hypertrophy, Hyperplasia and Structural Dilatation of the Human Heart

Cited by 59 publications

References 0 publications

Estrogenic modulation of inflammation-related genes in male rats following volume overload

Estrogenic modulation of inflammation-related genes in male rats following volume overload

Steroid administration after myocardial infarction promotes early infarct expansion. A study in the rat.

Surgical removal of right-to-left cardiac shunt in the American alligator(Alligator mississippiensis) causes ventricular enlargement but does not alter apnoea or metabolism during diving

Contact Info

Product

Resources

About