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At least 181 records · Page 10Linked to original sources
PubMed1998

Myocardial beta-adrenergic reactivity in volume overload-induced cardiac hypertrophy in the rat.

The purpose of this study was to evaluate the changes in myocardial beta-adrenergic reactivity in animals undergoing a 4 week cardiac volume overload. Aortocaval shunt (ACS) or sham operation (sham) were performed in male Wistar rats, and 4 weeks later, isoproterenol dose-effects (chronotropic, inotropic and lusitropic properties) were studied after pithing. Noradrenaline (NA) and adrenaline (A) concentrations and NA turn-over index were evaluated in plasma and heart ventricles, while beta-adrenoceptor characteristics in ventricle homogenates and slices with [125I]iodocyanopindolol, and the beta(1)/beta(2)-adrenoceptor ratio were estimated. Four weeks of cardiac volume overload resulted in a 55% increase in ventricle weight/body weight ratio (from 2.5 +/- 0.1 to 3.9 +/- 0.1 mg/g in sham and ACS rats, respectively) and a 20% increase in protein contents (from 11.3 +/- 0.7 to 13.8 +/- 1.1 mg/100 mg ventricles in sham and ACS rats, respectively). Furthermore, NA and A concentrations and NA turn-over index were increased in ACS rats (14, 40 and 80% versus sham, respectively). A shift to the right of the responses in heart rate, left ventricular systolic pressure, +dP/dtmax and -dP/dtmax responses following increasing doses of isoproterenol was observed, without change in the dose inducing maximum effect. Total beta-adrenoceptor characteristics and beta(1)/beta(2) ratio were unchanged. However, beta(1)-adrenoceptor density increased in epicardium while decreasing in endocardium of left ventricle from ACS rats. Rightward shift at lower doses of isoproterenol-induced cardiac responses in volume-overloaded rats are not likely due to overall beta-adrenoceptor density changes.

Adrenergic beta-Agonists↗
PubMed1995

Comparison of transtracheal and extravascular Doppler determinations of stroke volume and cardiac output at various states of volume loading in piglets.

OBJECTIVE: To assess the applicability of a new technology in neonates. Transtracheal Doppler and extravascular Doppler determinations of stroke volume and cardiac output were compared with thermodilution measurements at various states of volume loading in an animal model. DESIGN: Prospective, descriptive study. SETTING: Animal research laboratory at a university medical center. SUBJECTS: Fourteen newly weaned piglets, weighing 2.8 to 6.5 kg. INTERVENTIONS: Doppler probes were placed on the endotracheal tube tip (transtracheal Doppler) and directly on the aortic adventitia (extravascular Doppler). A 4-Fr thermodilution catheter was inserted in the pulmonary artery. Stroke volume and cardiac output determinations were recorded at baseline, after a 15-mL/kg volume load and after successive 15-mL/kg blood withdrawals to exsanguination or a systolic blood pressure of < 20 mm Hg. MEASUREMENTS AND MAIN RESULTS: Transtracheal and extravascular Doppler measurements of cardiac output were not significantly different from thermodilution at any physiologic state. These techniques were able to measure stroke volumes and cardiac outputs at the low levels seen in severe hemorrhagic shock. CONCLUSIONS: Transtracheal Doppler and extravascular Doppler measurements of cardiac output compare favorably with thermodilution. These methods effectively followed trends from alterations in intravascular volume, even at very high heart rates and small stroke volumes. Transtracheal Doppler and extravascular Doppler should yield useful information in critically ill neonatal patients, where data regarding stroke volume and cardiac output may be useful in clinical management.

Animals↗
PubMed1994

The renin-angiotensin system and volume overload-induced changes in cardiac collagen and elastin.

BACKGROUND: Besides cardiac load, the renin-angiotensin system (RAS) and aldosterone may regulate collagen accumulation during maturation or hypertrophic growth. The effect of cardiac volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed. METHODS AND RESULTS: In the present study we assessed (1) the effects of 4 to 10 weeks of volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress volume overload-induced changes in cardiac collagen and elastin. Cardiac volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan prevented the relative decreases in LV collagen content and concentration induced by a shunt. Losartan also reversed the decrease in LV collagen content by aortocaval shunt. Neither blocker significantly affected the enhanced RV collagen accumulation during the initial weeks of shunt, but both blockers further potentiated RV collagen accumulation during chronic volume overload. Aortocaval shunt for 4 weeks but not 10 weeks enhanced LV and RV elastin accumulation. This initial increase in LV and RV elastin content was blocked by both enalapril and losartan. CONCLUSIONS: Cardiac volume overload, even when accompanied by increased plasma renin activity, decreases LV collagen accumulation, suggesting that in contrast to the stimulatory effect of systolic wall stress, increased diastolic wall stress inhibits collagen accumulation. In support of this concept, enalapril and losartan decreased LV preload and maintained LV collagen accumulation. In contrast to LV collagen, RV collagen accumulation was potentiated during the initial weeks of volume overload, possibly related to acute RV pressure overload shortly after aortocaval shunt and its decrease with chronic shunt. Enalapril and losartan had minimal effect on the enhanced RV collagen during the initial weeks of aortocaval shunt but potentiated RV collagen during chronic shunt, possibly by decreasing RV diastolic pressures. Altogether, these data suggest that during cardiac volume overload, the RAS affects cardiac collagen primarily by its hemodynamic effects. The RAS, however, may potentiate RV and LV elastin accumulation during the initial weeks of volume overload since both enalapril and losartan block this increase.

Aging↗
PubMed1997

Early changes in the functions of cardiac sarcoplasmic reticulum in volume-overloaded cardiac hypertrophy in rats.

By sequestering activator calcium, the sarcoplasmic reticulum (SR) plays the central role in the excitation-contraction (E-C) cycle of cardiac muscle. Hence, functional changes in the SR in diseased myocardium might critically determine its mechanical characteristics. Previously, we demonstrated that both Ca2+ release and uptake were increased in SR isolated from hearts showing compensatory left ventricular (LV) hypertrophy taken from pressure-overloaded rats. However, it has not been elucidated whether such alterations also occur in the volume-overloaded myocardium. Rats in which volume-overloaded hypertrophy had been induced by aortocaval shunt 12 weeks prior to the investigation were compared to sham-operated controls in terms of SR Ca2+ uptake and release, and density of Ca2+ releasing channels (ryanodine receptors, RyR). Isometric tension and intracellular Ca2+ transients were also measured using the bioluminescent Ca2+ indicator, aequorin, in isolated LV papillary muscles. The extent of hypertrophy was verified by measuring the ratio of biventricular weight to body weight. In vivo, the aortocaval shunt rats showed normal LV contractility and slightly depressed LV relaxation, indicating a compensatory (adaptive) stage of LV function. In contrast, Ca2+ release, uptake, and maximal number of [3H]-ryanodine binding sites were all significantly lower in aortocaval shunt rats than in controls. Both the Ca2+ transients and isometric relaxation of the isolated myocardium were significantly prolonged in aortocaval shunt rats, though their amplitudes were similar in the two groups. Thus, the volume-overloaded cardiac hypertrophy, even at its hemodynamically compensatory (adaptive) stage, (i) was accompanied by abnormal Ca2+ handling, as indicated by prolonged intracellular Ca2+ transients and isometric tension traces, (ii) seems to involve subcellular mechanisms related to decreases in SR Ca2+ release and uptake functions, as well as to a decrease in the number of RyR. Therefore, changes in the intracellular processes underlying cardiac E-C coupling, including SR function, precede the development of this type of heart disease.

Animals↗
PubMed1991

A new cross sectional echocardiographic method for estimating the volume of large pericardial effusions.

OBJECTIVE: To evaluate a new cross sectional echocardiographic method for estimating the volume of pericardial effusions. DESIGN: The volume of pericardial fluid removed by surgical drainage or paracentesis was compared with the volume estimated by the echocardiographic method. The pericardial sac volume and cardiac volume were calculated by applying the formula for the volume of a prolate ellipse (pi x 4/3 x L/2 x D1/2 x D2/2) where L is the major axis and D1 and D2 are the minor axes. The pericardial fluid volume was calculated as the pericardial sac volume minus the cardiac volume. PATIENTS: 13 patients with 14 large pericardial effusions (one recurrence) all of whom had tamponade and cross sectional echocardiography just before therapeutic full drainage of the effusion. RESULTS: The volumes of pericardial fluid drained ranged from 0.5 to 2.11. The correlation between these actual volumes and the volumes estimated by echocardiography was excellent (r = 0.97); the correlation was good in four patients with intrapericardial adhesions. CONCLUSIONS: Because of certain approximations in measuring quantity of pericardial fluid drained, the echocardiographic estimations cannot be claimed to be definite. The data, however, indicate that the echocardiographic method is sufficiently reliable to provide useful estimates for practical clinical purposes.

Echocardiography↗
PubMed2000

Positional localization: three-dimensional transthoracic echocardiographic techniques for the measurement of cardiac mass, volume, and function.

An accurate and reproducible determination of cardiac volume and mass is important for the selection and timing of therapeutic interventions. Quantitative three-dimensional echocardiography has evolved to provide these measurements with the use of a noninvasive, readily available, and inexpensive technique. We introduce and review the principle of positional localization as well as the clinical application of this technique for the measurement of cardiac volume and mass.

Cardiac Volume↗
PubMed1977

Effect of high-altitude exposure for 10 days on stroke volume and cardiac output.

Resting stroke volume and cardiac output of 50 normal healthy sea-level residents (group A) were estimated by the noninvasive technique of electrical impedance plethysmography. They were then airlifted to an altitude of 3,658 m and serial estimations carried out at 0-4 h and 5-8 h and on the 2nd, 3rd, 4th, 5th, and 10th days. The subjects were brought back to sea level and studied for up to 5 days. Thirty permanent residents of high altitude (group B) and sixteen lowlanders temporarily resident at high altitude (group C) were also subjected to similar studies. It was found that resting stroke volume and cardiac output of group A started falling immediately on arrival at high altitude, reached the minimum on the 3rd day and tended to improved on the 4th and 5th day, but showed a secondary fall on the 10th day. The reduction in stroke volume in this group was not fully compensated by tachycardia. On return to sea level the cardiac output normalized immediately, the stroke volume on the 2nd day. At sea level goup A had values similar to group B and at high altitude to group C.

Adult↗
PubMed1993

Renin-angiotensin system and minoxidil-induced cardiac hypertrophy in rats.

Besides cardiac volume overload, cardiac sympathetic activity and the renin-angiotensin system (RAS) are activated by arterial vasodilators such as minoxidil. To evaluate the possible involvement of the RAS in the development of minoxidil-induced cardiac hypertrophy, we assessed in normotensive rats minoxidil-induced changes in cardiac and plasma renin activity (PRA) and the potential of chronic treatment with the angiotensin-converting enzyme (ACE) inhibitor enalapril and the nonpeptide angiotensin II receptor blocker losartan to prevent minoxidil-induced cardiac hypertrophy. PRA increased in parallel with the increase in cardiac filling pressures and development of cardiac hypertrophy, whereas the increase in cardiac renin activity was delayed as compared with these changes. Losartan did not decrease left ventricular end-diastolic pressure (LVEDP) but prevented the remodeling of the heart by minoxidil. In contrast, enalapril nearly normalized LVEDP but did not affect the hypertrophic response of the heart. The losartan data indicate that the RAS is involved in the minoxidil-induced cardiac hypertrophy either directly (e.g., by mediating the hypertrophic response of the heart to cardiac volume overload) or indirectly (e.g., by potentiating cardiac sympathetic activity). The ineffectiveness of enalapril has no obvious explanation but may possibly indicate ineffective blockade of angiotensin II formation in the heart in this model.

Angiotensin II↗