The effect of pressure or flow stress on right ventricular protein synthesis in the face of constant and restricted coronary perfusion.

Schreiber, Sidney S.; Rothschild, Marcus A.; Evans, Carole; Reff, Francine; Oratz, Murray

doi:10.1172/jci107899

Cited by 38 publications

(15 citation statements)

References 25 publications

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“…LVSP in guinea pigs in vivo measured with this method was considerably higher than the 36 mm Hg determined in vivo after puncturing the left ventricular cavity through the interventricular septum with a needle that was inserted transthoracically into the right ventricle (16). On the other hand, LVSP of the rat heart in vivo (table 1) is of the same order of magnitude as that measured in situ by puncturing the left ventricle subsequent to thoracotomy (4).…”

Section: Discussionmentioning

confidence: 58%

Measurement of left ventricular hemodynamic parameters in closed-chest rats under control and various pathophysiologic conditions

Zimmer¹

1983

Basic Res Cardiol

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A prototype of a recently developed mikro-tip pressure transducer catheter (3 French) was inserted into the left ventricle of closed-chest rats via the right carotid artery. In thiobutabarbital-sodium anesthesia, heart rate (409 +/- 7 beats/min), left ventricular systolic pressure (LVSP: 142 +/- 4 mm Hg) and the maximal rate of rise of left ventricular pressure (LV dP/dtmax: 6073 +/- 187 mm Hg/sec, mean values +/- SEM, n = 19) were measured. The baroreceptor reflex was intact under these experimental conditions. In closed-chest guinea pigs, all functional parameters determined were lower (heart rate: 271 +/- 11 beats/min; LVSP: 94 +/- 6 mm Hg; LV dP/dtmax: 3248 +/- 295 mm Hg/sec, mean values +/- SEM, n = 9). To test the applicability of the new catheter tip manometer, cardiac hemodynamic parameters were determined in rats under various pathophysiologic conditions: Several periods of asphyxia were followed by progressive depressions in heart rate, LVSP and LV dP/dtmax, and acute as well as chronic stimulation with catecholamines (noradrenaline and isoproterenol) and with triiodothyronine was characterized by a pronounced positive inotropic and chronotropic effect. The technique described has many potential applications in cardiovascular studies on intact small laboratory animals.

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Section: Discussionmentioning

confidence: 58%

Measurement of left ventricular hemodynamic parameters in closed-chest rats under control and various pathophysiologic conditions

Zimmer¹

1983

Basic Res Cardiol

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“…Amino acid concentrations used in the present study are saturating for protein synthesis (Smith & Sugden, 1983b). We found that left-atrial protein-synthesis rates at two aortic pressures were stimulated by 30-40% by increasing the left atrial pressure 3-4-fold ( (Hjalmarson & Isaksson, 1972a;Schreiber et al, 1975 (Hjalmarson & Isaksson, 1972a). An increase in filling pressure at a given aortic pressure increases the external work done by the heart.…”

Section: General Considerationsmentioning

confidence: 48%

“…For example, the time course of protein synthesis has been non-linear during experiments (Hjalmarson & Isaksson, 1972a), working hearts have been compared with Langendorff (1895)-perfused hearts (Morgan et al, 1980), and increases in aortic pressure proportionally increase the rates of coronary flow, which may itself stimulate protein synthesis by, for example, improving substrate delivery and opening previously constricted capillaries. The experiments of Schreiber et al (1975) have suggested a lack of effect of coronary flow on protein synthesis, provided that the rate of coronary flow is sufficient to meet the oxygen and substrate supply to the heart. Furthermore, in vivo, hearts exposed to a raised aortic pressure, but with a relatively constant stroke volume (increased pressure workload), hypertrophy by thickening their left-ventricular wall widths but keeping their chamber volumes relatively constant (concentric hypertrophy).…”

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confidence: 99%

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Stimulation of left-atrial protein-synthesis rates by increased left-atrial filling pressures in the perfused working rat heart in vitro

Smith¹,

Sugden²

1983

Biochemical Journal

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We investigated the effect of an increase in the left-atrial filling pressure on the rate of left-atrial protein synthesis in the left-side-perfused working rat heart preparation of Taegtmeyer, Hems & Krebs [(1980) Biochem. J. 186, 701-7111. An increase in filling pressure (preload) at a constant aortic pressure (afterload) increased both the intra-atrial pressure and the atrial stroke volume. The aortic pressure (afterload) was held constant. An increase in filling pressure from 5 to 20cmH20 at an aortic pressure of 70cmH2O, or an increase in filling pressure of 7.5 to 20cmH20 at an aortic pressure of 100 cmH20, significantly stimulated the rates of left-at-rial protein synthesis by 30-40%. The stimulation was observed when the rates of protein synthesis were expressed relative to either protein or RNA content. Since perfusate entering the right atrium from the coronary circulation left that atrium passively, the rate of protein synthesis in this compartment can be used as an internal control. Rates of right-atrial protein synthesis were similar to those in the left atria exposed to the lower filling pressures and were unaffected by the increases in left-atrial filling pressure. We suggest that the acute effects of increased left-atrial filling pressure on protein synthesis in that compartment may be important in the development of left-atrial hypertrophy. This condition is seen in patients who have raised pulmonary venous pressures in, for example, mitral stenosis.

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“…Although the pressure overload is a dominant feature of this model, other features include a volume overload by increasing intra-left ventricular balloon volume and an elevated coronary perfusion pressure that is due to constant coronary flow throughout the intra-left ventricular balloon inflation. Strict and independent control of pressure overload, volume overload, and coronary perfusion 16 would provide us with more accurate information regarding the effects of hemodynamic overload on the MAP kinase pathway. Although the phenomenon during the balloon inflation was primarily due to the hemodynamic overload, there is a possibility of unexpected myocardial injury.…”

Section: Left Ventricular Hemodynamic Overload In a Buffer-perfused Rmentioning

confidence: 99%

Hemodynamic Overload–Induced Activation of Myocardial Mitogen-Activated Protein Kinases In Vivo

Aoyagi

Izumo

2001

Hypertension

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Abstract-Mitogen-activated protein (MAP) kinases have been shown to be activated by various growth factors in cultured or isolated cardiomyocytes. However, little is known about the regulation of MAP kinases in vivo, especially in clinically important conditions, such as hypertension and senescence. In this study, we assessed mechanical overload-induced activation of myocardial MAP kinases in beating hearts from hypertensive or senescent rats. Key Words: protein kinases Ⅲ hypertrophy Ⅲ aging Ⅲ rats, inbred spontaneously hypertensive Ⅲ hemodynamics M itogen-activated protein (MAP) kinases, 1-3 especially the first identified extracellular signal-regulated kinases (ERKs) of molecular sizes 42 and 44 kDa, seem to be involved in cell growth processes, such as proliferation and hypertrophy. 4 The ERKs are known to phosphorylate MAP kinase-activated protein kinase-1/90-kDa ribosomal S6 kinase and to regulate its activity. 5,6 Most studies involving MAP kinase activation were performed by using growth factor-stimulated cells in culture. Mechanical stretch of cardiomyocytes, which causes cellular hypertrophy, was shown to activate MAP kinases. 7,8 In these in vitro conditions, most MAP kinase substrates can be phosphorylated by most MAP kinases, resulting in the confusion in physiological significance of each pathway reported in vitro. In contrast, little is known about the in vivo regulation of MAP kinase activity in response to mechanical stimulation.In cardiac and skeletal muscle, mechanical load plays a critical role in determining muscle mass and its phenotype. However, myocardial response to mechanical load is significantly different in different animal models. For example, we have previously shown that senescent rat myocardium failed to induce immediate-early genes in response to pressure overload. 9 The senescent heart has a marked decrease in hypertrophic capacity in response to either pressure or volume overload. 10,11 On the other hand, young spontaneously hypertensive rats (SHR) are known to develop enhanced left ventricular hypertrophy, which is disproportional to the degree of hypertension. 12 Because MAP kinases have been shown to play critical roles in the regulation of immediateearly genes and cell growth, we hypothesized that the myocardial MAP kinase activity may be altered in SHR and aged rats. In vivo assessment is necessary to evaluate the physiological roles of the MAP kinase cascade in many clinically important situations, including hypertensive hypertrophy and senescence. Alterations in the protein level of MAP kinase may contribute to changes in hypertrophic response in these animals.In the present study, we determined the activation of myocardial tissue MAP kinase by left ventricular hemodynamic overload. We assessed MAP kinase activity and its response to hemodynamic overload in 4-and 20-week-old SHR to assess myocardial MAP kinase activation in an early phase and in an established phase of pressure-overload

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The effect of pressure or flow stress on right ventricular protein synthesis in the face of constant and restricted coronary perfusion.

Cited by 38 publications

References 25 publications

Measurement of left ventricular hemodynamic parameters in closed-chest rats under control and various pathophysiologic conditions

Measurement of left ventricular hemodynamic parameters in closed-chest rats under control and various pathophysiologic conditions

Stimulation of left-atrial protein-synthesis rates by increased left-atrial filling pressures in the perfused working rat heart in vitro

Hemodynamic Overload–Induced Activation of Myocardial Mitogen-Activated Protein Kinases In Vivo

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