Cardiac compliance and dimensions in carbon monoxide-induced cardiomegaly

Penney, David G.; Barthel, Bernd; Skoney, Joseph A.

doi:10.1093/cvr/18.5.270

Cited by 24 publications

(9 citation statements)

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“…Several studies have revealed detrimental effects of HO-derived by-products. For example, chronic CO inhalation at a dose mimicking levels normally registered with tobacco smoking (500 parts per million) worsens post-MI LV remodeling (37,42). In addition, CO inhibits oxygen binding to myoglobin (19), and CO inhibits other hemoproteins, including cytochrome c (43,45,46) and endothelial nitric oxide synthase.…”

Section: Discussionmentioning

confidence: 99%

Preemptive heme oxygenase-1 gene delivery reveals reduced mortality and preservation of left ventricular function 1 yr after acute myocardial infarction

Liu

Simpson²,

Brunt³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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-We reported previously that predelivery of heme oxygenase-1 (HO-1) gene to the heart by adenoassociated virus-2 (AAV-2) markedly reduces ischemia and reperfusion (I/R)-induced myocardial injury. However, the effect of preemptive HO-1 gene delivery on long-term survival and prevention of postinfarction heart failure has not been determined. We assessed the effect of HO-1 gene delivery on long-term survival, myocardial function, and left ventricular (LV) remodeling 1 yr after myocardial infarction (MI) using echocardiographic imaging, pressure-volume (PV) analysis, and histomorphometric approaches. Two groups of Lewis rats were injected with 2 ϫ 10 11 particles of AAV-LacZ (control) or AAV-human HO-1 (hHO-1) in the anterior-posterior apical region of the LV wall. Six weeks after gene transfer, animals were subjected to 30 min of ischemia by ligation of the left anterior descending artery followed by reperfusion. Echocardiographic measurements and PV analysis of LV function were obtained at 2 wk and 12 mo after I/R. One year after acute MI, mortality was markedly reduced in the HO-1-treated animals compared with the LacZ-treated animals. PV analysis demonstrated significantly enhanced LV developed pressure, elevated maximal dP/dt, and lower end-diastolic volume in the HO-1 animals compared with the LacZ animals. Echocardiography showed a larger apical anterior-to-posterior wall ratio in HO-1 animals compared with LacZ animals. Morphometric analysis revealed extensive myocardial scarring and fibrosis in the infarcted LV area of LacZ animals, which was reduced by 62% in HO-1 animals. These results suggest that preemptive HO-1 gene delivery may be useful as a therapeutic strategy to reduce post-MI LV remodeling and heart failure.

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Section: Discussionmentioning

confidence: 99%

Preemptive heme oxygenase-1 gene delivery reveals reduced mortality and preservation of left ventricular function 1 yr after acute myocardial infarction

Liu

Simpson²,

Brunt³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…1 mg. A relative mass determination of each region was carried out using multiple exponential regression equations, relating heart weight and body weight of normal rats obtained previously. l 2 The stored NMR imaging data were analyzed on a cathode ray screen using Siemens software for distance measurements. The slices were coded so that the individual (Bambach) making the measurements was unaware of the previous treatment.…”

Section: Discussionmentioning

confidence: 99%

In situ assessment of the rat heart during chronic carbon monoxide exposure using nuclear magnetic resonance imaging

Bambach

Penney

Negendank

1991

J of Applied Toxicology

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Ventricular hypertrophy induced in male Sprague-Dawley rats by inhalation of 500 ppm carbon monoxide (40% carboxyhemoglobin level) for 0-62 days was assessed by contiguous 2-mm thick axial cardiac cross-sections, using 32 accumulated averages of ungated fast-scan gradient-recalled nuclear magnetic resonance (NMR) images. Following final imaging, the rats were sacrificed and the hematocrit and heart mass were determined. The mean outside diameter of the left ventricle plus interventricular septum (LV + S) showed a strong correlation (r = 0.73, P less than 0.01) with the duration of CO exposure, while the correlation coefficients for the LV + S lumen diameter and wall thickness were marginally significant. The mean pleural space diameter also increased significantly (r = 0.64, P less than 0.05) with the duration of CO exposure. The ratio of the LV + S wall thickness and the lumen radius was 0.53 in the rats exposed to CO for 0-8 days; this value did not change with longer CO exposure. The LV + S outside and lumen diameter showed significant correlations to the hematocrit (r = 0.72, p less than 0.05 and r = 0.66, P less than 0.05, respectively), and the LV + S outside diameter correlated with the increase in the LV + S mass (r = 0.72, P less than 0.05). The results achieved with NMR imaging are consistent with past morphometric studies of CO-induced ventricular hypertrophy, where heart dimensions were determined in relaxed frozen tissue, and corroborate the eccentric nature of CO-induced ventricular hypertrophy.

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“…Particularly, we demonstrated that under exposure to several concentrations of CO, hypertrophy begins to occur, but, at 530 ppm CO exposure, hypertrophy is significant after 1-wk exposure and is maintained throughout CO exposure to a similar value (25%). Moreover, CO exposure led to hypertrophy by volume overload (21). Cardiomegaly developed in both ventricles and atria with the addition of new myocardial constituents (19) and involved an increase in lumen dimensions with some primarily small increase in wall thickness of the ventricles (i.e., eccentric hypertrophy) (21).…”

Section: Does This Increase In 4-ap-sensitive Currents Have Functionamentioning

confidence: 99%

“…Moreover, CO exposure led to hypertrophy by volume overload (21). Cardiomegaly developed in both ventricles and atria with the addition of new myocardial constituents (19) and involved an increase in lumen dimensions with some primarily small increase in wall thickness of the ventricles (i.e., eccentric hypertrophy) (21).…”

Section: Does This Increase In 4-ap-sensitive Currents Have Functionamentioning

confidence: 99%

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

Barbé

Dubuis²,

Rochetaing

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes. Am J Physiol Heart Circ Physiol 282: H2031-H2038, 2002. First published January 24, 2002 10.1152/ajpheart.00807.2001.-A physiological role of carbon monoxide has been suggested for coronary myocytes; however, direct evidence is lacking. The objective of this study was to test the effect of chronic carbon monoxide exposure on the K ϩ currents of the coronary myocytes. The effect of 3-wk chronic exposure to carbon monoxide was assessed on K ϩ currents in isolated rat left coronary myocytes by the use of the patch-clamp technique in the whole cell configuration. Moreover, membrane potential studies were performed on coronary artery rings using intracellular microelectrodes, and coronary blood flow in isolated heart preparation was recorded. Carbon monoxide did not change the amplitude of global whole cell K ϩ current, but it did increase the component sensitive to 1 mM 4-aminopyridine. Carbon monoxide exposure hyperpolarized coronary artery segments by ϳ10 mV and, therefore, increased their sensitivity to 4-aminopyridine. This effect was associated with an enhancement of coronary blood flow. We conclude that chronic carbon monoxide increases a 4-aminopyridinesensitive current in isolated coronary myocytes. This mechanism could, in part, contribute to hyperpolarization and to increased coronary blood flow observed with carbon monoxide.voltage-gated K ϩ channels; membrane currents; vasodilation; 4-aminopyridine CARBON MONOXIDE (CO) is an endogenously generated gas that regulates vascular tone. Several lines of investigation provide evidence that CO is a vasodilator acting directly on vascular smooth muscle cells (VSMCs) (27) and that it inhibits smooth muscle cell proliferation (17). In coronary circulation, acute and chronic exogenous CO exposure induced an increase in coronary blood flow (1, 16). Several mechanisms have been suggested to explain this effect, including a direct effect of CO on coronary artery cells (8). Indeed, acute CO induced in vitro an endothelium-independent relaxation of the preconstricted coronary artery (8,14). Nevertheless, the cellular mechanism by which acute or chronic CO increases in coronary blood flow is unknown.Plasma membranes of coronary VSMCs show a dense expression of voltage-gated K ϩ (K V ) channels and high-conductance Ca 2ϩ -activated K ϩ (BK Ca ) channels. Moreover, the expression levels of these two-gene families are altered in some chronic cardiovascular pathologies, such as arterial hypertension (3). CO can influence the open-state probability of BK Ca channels in VSMC membranes (27), and it can activate K V channels in jujenal circular smooth muscle cells (6), thereby regulating the level of resting membrane potential (E m ) and contractile force in VSMCs. In the VSMCs of arterial circulation, the hyperpolarizing effect of K V and BK Ca channels contributes to the regulation of vascular tone and blood pressure by limiting voltage-dependent Ca 2ϩ influx through dihydropy...

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Cardiac compliance and dimensions in carbon monoxide-induced cardiomegaly

Cited by 24 publications

References 0 publications

Preemptive heme oxygenase-1 gene delivery reveals reduced mortality and preservation of left ventricular function 1 yr after acute myocardial infarction

Preemptive heme oxygenase-1 gene delivery reveals reduced mortality and preservation of left ventricular function 1 yr after acute myocardial infarction

In situ assessment of the rat heart during chronic carbon monoxide exposure using nuclear magnetic resonance imaging

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

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