Morphometry and ultrastructure of heart hypertrophy induced by chronic volume overload (aorto-caval fistula in the rat)

Hatt, P. Y.

doi:10.1016/0022-2828(79)90390-0

Cited by 66 publications

(34 citation statements)

References 14 publications

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“…This finding is at variance with previous observations (5-7) obtained in fetal lambs with cardiopulmonary shunt, in which higher concentrations of cGMP were detected in lung tissue. In the condition of chronic high pulmonary blood flow (also known as models of volume-overload heart failure) (25), increased cGMP in the lung tissue can be caused by activation of heme oxygenase-1 (30). However, in the present study cGMP was measured in the PA rather than lung tissue, thereby reflecting changes of cGMP in the vascular wall.…”

Section: Discussionmentioning

confidence: 67%

Functional adaptation and remodeling of pulmonary artery in flow-induced pulmonary hypertension

Lam¹,

Peterson²,

Croatt³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Patients with left-to-right shunt congenital heart disease may develop pulmonary hypertension. Perioperative mortality of these patients is high due to abnormal vasoreactivity of the pulmonary artery (PA). We studied the changes in the PA induced by high pulmonary blood flow in rats with aortocaval fistula. Eight weeks after surgery, morphological changes of the PA were studied and vasomotor function was assessed by isometric force recording. Expression of endothelial nitric oxide (NO) synthase (eNOS), VEGF, and cyclooxygenase-2 (COX-2) proteins and levels of cGMP in the PA were analyzed. Rats with high pulmonary blood flow developed pulmonary hypertension, medial thickening, and increasing of internal elastic lamina and basement membrane in the PA. When compared with sham-operated animals, rats with fistula had significantly increased contractions in the PA, whereas relaxations to acetylcholine and NO donor were reduced. Concentrations of cGMP were reduced in the PA of rats with pulmonary hypertension (18.4 Ϯ 3.3 vs. 9.4 Ϯ 1.7 pmol/mg protein; P ϭ 0.04). The altered vasomotor function was normalized by treatment with indomethacin. The PA of rats with fistula expressed higher levels of eNOS, phosphorylated eNOS, and COX-2. Sustained high PA blood flow in rats causes pulmonary hypertension that is morphologically and functionally identical with patients with flow-induced pulmonary hypertension. Abnormal vasomotor function of the PA in these animals appears to be mediated by reduced availability and the biological effect of endogenous NO and the high production of vasoconstrictor prostanoids. Increased eNOS and phosphorylated eNOS are most likely the adaptive changes in response to an increase in PA pressure secondary to high blood flow. guanosine 3Ј,5Ј-cyclic monophosphate; cyclooxygenase-2; endothelium; endothelial nitric oxide synthase PULMONARY HYPERTENSION, secondary to increased pulmonary blood flow, may develop in patients with left-to-right shunt congenital heart defects or systemic arteriovenous shunt, such as arteriovenous access for hemodialysis (21,26,37,53). The characteristic vascular changes include intimal hyperplasia/ fibrosis, medial hypertrophy, extensive extracellular matrix modulation, and, in more severe cases, the formation of plexiform lesion (21). These changes lead to decreased compliance of pulmonary vasculature and changes in vasoreactivity of pulmonary arteries (PAs) (34). Patients with flow-induced pulmonary hypertension have significantly higher perioperative mortality and a lower long-term survival after a cardiac operation (3,24,44). During and after an operation, these patients often exhibit fatal pulmonary vasoconstriction (2, 45). Patients with flow-induced pulmonary hypertension also showed significantly impaired endothelium-dependent relaxation in the PAs, whereas endothelium-independent relaxation is relatively preserved (10,17,29).The underlying pathogenesis of flow-induced pulmonary hypertension remains poorly understood (4). The patients with left-to-right congenital heart...

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Section: Discussionmentioning

confidence: 67%

Functional adaptation and remodeling of pulmonary artery in flow-induced pulmonary hypertension

Lam¹,

Peterson²,

Croatt³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Ryan et al described remodeling process induced by bradykinin (Ryan et al, 2007). Study of Hatt et al (1979) is closest to our morphological approach. Hatt et al measured cells in failing hearts and our study generally corresponds with their findings.…”

Section: Discussionmentioning

confidence: 94%

“…Diminished systemic perfusion leads to redistribution of cardiac output and neurohumoral activation. When compensatory mechanisms become inadequate, overt heart failure (HF) develops (Hood et al, 1968) in a way similar to other models of LV hypertrophy-HF transition (Hatt et al, 1979;Legault et al, 1990;Ruzicka et al, 1993;Ryan et al, 2007).…”

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confidence: 96%

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Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

Beneš

Melenovský

Škaroupková

et al. 2010

The Anatomical Record

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Chronic volume overload leads to cardiac hypertrophy and later to heart failure (HF), which are both associated with increased risk of cardiac arrhythmias. The goal of this study was to describe changes in myocardial morphology and to characterize arrhythmogenic substrate in rat model of developing HF due to volume overload. An arteriovenous fistula (AVF) was created in male Wistar rats between the inferior vena cava and abdominal aorta using needle technique. Myocardial morphology, tissue fibrosis, and connexin43 distribution, localization and phosphorylation were examined using confocal microscopy and Western blotting in the stage of compensated hypertrophy (11 weeks), and decompensated HF (21 weeks). Heart to body weight (BW) ratio was 89% and 133% higher in AVF rats at 11 and 21 weeks, respectively. At 21 weeks but not 11 weeks, AVF rats had pulmonary congestion (increased lung to BW ratio) indicating presence of decompensated HF. The myocytes in left ventricular midmyocardium were significantly thicker (þ8% and þ45%) and longer (þ88% and þ97%). Despite extensive hypertrophy, there was no excessive fibrosis in the AVF ventricles. Distribution and localization of connexin43 were similar between groups, but its phosphorylation was significantly lower in AVF hearts at 21st week, but not 11th week, suggesting that HF,

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“…This growth response has been found to occur as early as 8 d after constriction of the abdominal aorta ( 19). Longer time intervals up to 2 mo after the imposition of an increased work load have not produced a greater magnitude of cardiac hypertrophy (9,20,21). This is confirmed by the results obtained in the present study in which a 76% ventricular hypertrophy was attained 6 mo after pulmonary artery banding.…”

Section: Discussionmentioning

confidence: 99%

Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

Olivetti¹,

Ricci²,

Anversa³

1987

J. Clin. Invest.

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In contrast to observations made in the human heart, hyperplasia of myocyte nuclei has never been demonstrated in experimental cardiac hypertrophy. To test the hypothesis that the duration of the mechanical load more than the magnitude of ventricular hypertrophy may be the inciting stimulus for myocyte nuclei hyperplasia, constriction of the pulmonary artery was produced in rats and the hearts were examined 6 mo later. A 76% increase in right ventricular weight was measured. This hypertrophic response was accompanied by a 41% increase in the total number of myocyte nuclei in the ventricle. Furthermore, average myocyte cell volume per nucleus increased by 28%. No changes in weight, myocyte size, and nuclear number were observed in the left ventricle. In conclusion, myocyte nuclear hyperplasia and cellular hypertrophy both participate to the adaptive response of the right ventricular myocardium in long-standing pressure overload cardiac hypertrophy.

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Morphometry and ultrastructure of heart hypertrophy induced by chronic volume overload (aorto-caval fistula in the rat)

Cited by 66 publications

References 14 publications

Functional adaptation and remodeling of pulmonary artery in flow-induced pulmonary hypertension

Functional adaptation and remodeling of pulmonary artery in flow-induced pulmonary hypertension

Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

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