scholarly journals Effects of Myosin Isozyme Shift on Curvilinearity of the Left Ventricular End-Systolic Pressure-Volume Relation of In Situ Rat Hearts.

1998 ◽  
Vol 48 (6) ◽  
pp. 445-455 ◽  
Author(s):  
Shinyu LEE ◽  
Yoshimi OHGA ◽  
Hideo TACHIBANA ◽  
Yi SYUU ◽  
Haruo ITO ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Rat Hearts ◽  
Volume Relation ◽  
Myosin Isozyme

Reversible effects of isoproterenol-induced hypertrophy on in situ left ventricular function in rat hearts

2004 ◽  
Vol 287 (1) ◽  
pp. H277-H285 ◽  
Author(s):  
Yutaka Kitagawa ◽  
Daisuke Yamashita ◽  
Haruo Ito ◽  
Miyako Takaki
Keyword(s):  
Cardiac Hypertrophy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Osmotic Minipump ◽  
Good Index ◽  
Rat Hearts ◽  
Lv Volume ◽  
Work Capability

The aim of the present study was to evaluate specifically left ventricular (LV) function in rat hearts as they transition from the normal to hypertrophic state and back to normal. Either isoproterenol (1.2 and 2.4 mg·kg−1·day−1 for 3 days; Iso group) or vehicle (saline 24 μl·day−1 for 3 days; Sa group) was infused by subcutaneous implantation of an osmotic minipump. After verifying the development of cardiac hypertrophy, we recorded continuous LV pressure-volume (P-V) loops of in situ ejecting hypertrophied rat hearts. The curved LV end-systolic P-V relation (ESPVR) and systolic P-V area (PVA) were obtained from a series of LV P-V loops in the Sa and Iso groups 1 h or 2 days after the removal of the osmotic minipump. PVA at midrange LV volume (PVAmLVV) was taken as a good index for LV work capability ( 13 , 15 , 20 , 21 ). However, in rat hearts during remodeling, whether PVAmLVV is a good index for LV work capability has not been determined yet. In the present study, in contrast to unchanged end-systolic pressure at midrange LV volume, PVAmLVV was significantly decreased by isoproterenol treatment relative to saline; however, these measurements were the same 2 days after pump removal. Simultaneous treatment with a β1-blocker, metoprolol (24 mg·kg−1·day−1), blocked the formation of cardiac hypertrophy and thus PVAmLVV did not decrease. The reversible changes in PVAmLVV reflect precisely the changes in LV work capability in isoproterenol-induced hypertrophied rat hearts mediated by β1-receptors. These results indicate that the present approach may be an appropriate strategy for evaluating the effects of antihypertrophic and antifibrotic modalities.

Targeted gene transfer increases contractility and decreases oxygen cost of contractility in normal rat hearts

2007 ◽  
Vol 292 (5) ◽  
pp. H2356-H2363 ◽  
Author(s):  
Susumu Sakata ◽  
Djamel Lebeche ◽  
Naoya Sakata ◽  
Yuri Sakata ◽  
Elie R. Chemaly ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Energy Utilization ◽  
Water Volume ◽  
Rat Hearts ◽  
Significant Difference ◽  
Cardiac Gene ◽  
Normal Rat ◽  
Volume Relation

The aim of this study was to examine how global cardiac gene transfer of sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) can influence left ventricular (LV) mechanical and energetic function, especially in terms of O2 cost of LV contractility, in normal rats. Normal rats were randomized to receive an adenovirus carrying the SERCA2a (SERCA) or β-galactosidase (β-Gal) gene or saline by a catheter-based technique. LV mechanical and energetic function was measured in cross-circulated heart preparations 2–3 days after the infection. The end-systolic pressure-volume relation was shifted upward, end-systolic pressure at 0.1 ml of intraballoon water volume was higher, and equivalent maximal elastance, i.e., enhanced LV contractility, was higher in the SERCA group than in the normal, β-Gal, and saline groups. Moreover, the LV relaxation rate was faster in the SERCA group. There was no significant difference in myocardial O2 consumption per beat-systolic pressure-volume area relation among the groups. Finally, O2 cost of LV contractility was decreased to subnormal levels in the SERCA group but remained unchanged in the β-Gal and saline groups. This lowered O2 cost of LV contractility in SERCA hearts indicates energy saving in Ca2+ handling during excitation-contraction coupling. Thus overexpression of SERCA2a transformed the normal energy utilization to a more efficient state in Ca2+ handling and superinduced the supranormal contraction/relaxation due to enhanced Ca2+ handling.

A Brief Regional Ischemic-reperfusion Enhances Propofol-induced Depression in Left Ventricular Function of in situ  Rat Hearts

2004 ◽  
Vol 101 (4) ◽  
pp. 879-887 ◽  
Author(s):  
Naoya Kuzumoto ◽  
Yutaka Kitagawa ◽  
Koichi Uemura ◽  
Takashi Ueyama ◽  
Ken-ichi Yoshida ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Inhibitory Effects ◽  
Ischemic Reperfusion ◽  
Kinase C ◽  
Rat Hearts

Background Propofol is short-acting intravenous general anesthetics that reduces cardiovascular hemodynamics. The effects of propofol on intrinsic myocardial contractility, however, remain debatable. The aim of the current study was to test the hypothesis that inhibitory effects of propofol on left ventricular (LV) contractility and mechanical work capability of in situ ejecting rat hearts are attenuated after a brief regional ischemia and reperfusion. Methods The authors obtained steady-state LV pressure-volume loops and intermittently obtained LV end-systolic pressure-volume relation and evaluated effects of propofol on LV function by end-systolic pressure (ESPmLVV), systolic pressure-volume area (PVAmLVV) at midrange LV volume (mLVV). Results Propofol (5.2 +/- 0.3 approximately 11.1 +/- 3.7 microg.ml) significantly decreased ESP0.08 to 78 +/- 12% approximately 64 +/- 13% of prepropofol and PVA0.08 to 76 +/- 13%approximately 63 +/- 16% of prepropofol in normal hearts, whereas propofol at a lower concentration (4.1 +/- 1.0 microg/ml) did not. Although brief ischemic-reperfusion per se did not affect LV function, propofol after that, even at a lower concentration (4.1 +/- 1.0 microg/ml), significantly decreased ESP0.08 to 70 +/- 27% of prepropofol and PVA0.08 to 68 +/- 33% of prepropofol. Pretreatment with a protein kinase C (PKC) inhibitor, bisindolylmaleimide reduced the propofol (4.1 +/- 1.0 microg/ml)-induced greater decreases in ESP0.08 and PVA0.08 after brief ischemic-reperfusion to 94 +/- 33% and 92 +/- 39% of prepropofol. In the propofol-infused hearts after brief ischemic-reperfusion, protein kinase C-epsilon translocation to the nucleus-myofibril fraction was found. Conclusion In contrast to the study hypothesis, brief ischemic-reperfusion enhanced the inhibitory effects of propofol on LV systolic function; this enhancement is attributable to activation of protein kinase C.

scholarly journals Linearity of the left ventricular end-systolic pressure-volume relation in patients with severe heart failure

1989 ◽  
Vol 14 (1) ◽  
pp. 127-134 ◽  
Author(s):  
Constantine N. Aroney ◽  
Howard C. Herrmann ◽  
Marc J. Semigran ◽  
G. William ◽  
Charles A. Boucher ◽  
...  
Keyword(s):  
Heart Failure ◽  
Severe Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Relation

Inotropic effects of ejection are myocardial properties

1994 ◽  
Vol 266 (3) ◽  
pp. H1202-H1213 ◽  
Author(s):  
P. P. De Tombe ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Negative Effects ◽  
Inotropic Effects ◽  
Contraction Duration ◽  
Loading System ◽  
Positive Effect ◽  
Isolated Rat

Recent studies in isolated and in vivo canine hearts have suggested that the left ventricular end-systolic pressure (LVPes) of ejecting beats is the net result of a balance between positive and negative effects of ejection. At present, it is unknown whether these ejection effects are merely a ventricular chamber property or represent a fundamental myocardial property. Accordingly, we examined the effects of ejection in eight isolated rat cardiac trabeculae at the sarcomere level. We approximated in situ sarcomere shortening patterns using an iterative computer loading system. Six isovolumic contractions were compared with four ejecting contractions. The superfusing solution contained either 0.7 mM Ca2+ or 0.65 mM Sr2+ plus 0.15 mM Ca2+. With Ca2+, simulated LVPes ("LVP"es) of ejecting contractions was significantly lower than isovolumic "LVP"es (-5.3 +/- 5.6%), whereas with Sr2+, ejecting "LVP"es was significantly higher than isovolumic "LVP"es (+4.5 +/- 7.5%). Contraction duration and time to end systole were markedly prolonged in ejecting vs. isovolumic contractions with either Ca2+ or Sr2+. As a consequence, comparison of simulated LVP between ejecting and isovolumic beats throughout the contraction, i.e., at the same simulated LVV and time, revealed only a positive effect of ejection with either Ca2+ (+18.8 +/- 5.5%) or Sr2+ (+23.4 +/-9.3%). We conclude that both positive and negative effects of ejection are basic myocardial properties.

Abstract P144: Effects of Alamandine in Post-ischemic Function

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jonathas F Almeida ◽  
Robson A Santos
Keyword(s):  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Baseline Period ◽  
Left Ventricular ◽  
Biologically Active ◽  
Ventricular Systolic Pressure ◽  
Infarcted Area ◽  
Rat Hearts ◽  
Ischemic Period ◽  
Isolated Rat

Alamandine, a biologically active peptide of the renin-angiotensin system (RAS), was recently described and characterized. Further it has been shown to present effects similar to those elicited by Ang-(1-7). It has been described that Ang-(1-7) decreases the incidence and duration of ischemia-reperfusion arrhythmias and improved the post-ischemic function in isolated perfused rat hearts. In this study we aimed to evaluate the effects of Alamandine in isolated rat hearts subjected to myocardial infarction (MI). Wistar rats weighing between 250-300g were euthanized and their hearts were placed on Langendorff apparatus to evaluate the cardiac parameters. Hearts were submitted to 30min of stabilization, 30min of partial ischemia by occlusion of the left descending coronary artery and 30min of reperfusion. Drugs (alamandine 22pM, d-pro7-ang-(1-7) 220pM) were added to the perfusion setting from the beginning of the experiment until the end. 2,3,5-trypheniltetrazolium chloride were used to evaluate the extension of infarcted area. In control hearts (CON), there was a decrease on the left ventricular systolic pressure (LVSP) on ischemic period (54,6 ± 6,9mmHg) compared to the baseline period (84,6 ± 11,6mmHg). Alamandine (ALA) attenuated that decrease in the ischemic period (66,9 ± 7,9mmHg) vs (82,3 ± 8,9mmHg). Further, ischemia led to a decrease in the left ventricular developed pressure (dLVP), dP/dt maximum and minimum when compared to baseline values. ALA, once more, kept the ischemic parameters of dLVP and dP/dt max and min (58,9 ± 8mmHg; 1629 ± 202,2mmHg/s; 1101 ± 130mmHg/s, respectively) similar to those of baseline period (68,9 ± 8,92; 1682 ± 248,8; 1179 ± 118,6 mmHg, respectively). Ischemia/reperfusion induced an arrhythmia severity index (ASI) in control hearts (4,9 ± 1,26) higher than in hearts treated with ALA (1,10 ± 0,58). ALA also reduced infarcted area (19,64 ± 2,61%) compared with CON (33,85 ± 4,55%). All those effects were blocked by D-PRO7-Ang-(1-7). In conclusion, our data shown that Alamandine exert cardioprotective effects in post-ischemic function in isolated rat hearts by preventing LVSP, dLVP , dP/dt max and min decrease. Furthermore it reduced the infarcted area and I/R arrhythmias, apparently involving MrgD receptor participation.

Isolated working rat heart perfusion with perfluorochemical emulsion Fluosol-43

1982 ◽  
Vol 242 (4) ◽  
pp. H485-H489 ◽  
Author(s):  
L. D. Segel ◽  
S. V. Rendig
Keyword(s):  
Lactate Concentration ◽  
Systolic Pressure ◽  
Colloid Osmotic Pressure ◽  
Left Ventricular ◽  
Mechanical Function ◽  
External Work ◽  
Bicarbonate Buffer ◽  
Rat Hearts ◽  
Perfluorochemical Emulsion ◽  
Perfused Hearts

Isolated working rat hearts were perfused with the perfluorochemical emulsion Fluosol-43 to determine whether it would support prolonged, stable cardiac function. The perfluorochemical emulsion provides a controlled perfusate composition, relatively high oxygen capacity, and a colloid osmotic pressure that is similar to that of plasma. Electrically paced (325 beats/min) hearts were perfused for 6 h at 35 degrees C in a recirculating system. Hemodynamic and mechanical function of seven Krebs-Henseleit-perfused hearts declined significantly more than that of seven Fluosol-43-perfused hearts over the 6-h period. The percent of initial function remaining at 6 h for Krebs-Henseleit-perfused vs. Fluosol-43-perfused hearts was 70.3 +/- 5.0 vs. 95.4 +/- 1.1% (P less than 0.001) for left ventricular peak systolic pressure; 55.6 +/- 7.7 vs. 97.5 +/- 2.4% (P less than 0.001) for dP/dtmax; 27.1 +/- 7.2 vs. 60.6 +/- 5.2% (P less than 0.005) for cardiac output; 11.0 +/- 6.3 vs. 67.2 +/- 3.4% (P less than 0.001) for external work efficiency; and 17.4 +/- 8.4 vs. 67.7 +/- 4.5% (P less than 0.001) for stroke rhythmic than Fluosol-43-perfused hearts during the last 3 h of perfusion. Perfusate lactate concentration was 4.5-fold higher in the Krebs-Henseleit perfusate than in the Fluosol-43 perfusate at 6 h, reflecting greater anaerobic metabolism in the Krebs-Henseleit-perfused hearts. Thus isolated rat hearts perfused with Fluosol-43 have greater maintenance of hemodynamic and mechanical function over a longer time period than hearts perfused with Krebs-Henseleit bicarbonate buffer.

Similar normalized Emax and O2 consumption-pressure-volume area relation in rabbit and dog

1988 ◽  
Vol 255 (2) ◽  
pp. H366-H374 ◽  
Author(s):  
Y. Goto ◽  
B. K. Slinker ◽  
M. M. LeWinter
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Energy Conversion Efficiency ◽  
Left Ventricular ◽  
Energy Transduction ◽  
Base Line ◽  
Contractile State ◽  
Primary Determinant ◽  
Heart Size ◽  
Volume Relation

The end-systolic pressure-volume relation (ESPVR), a measure of ventricular contractile state, and systolic pressure-volume area (PVA), a primary determinant of cardiac oxygen consumption per beat (VO2), have been derived from the pressure-volume diagram of the cross-circulated dog left ventricle. The slope of the PVA-VO2 relation represents the efficiency of chemomechanical energy transduction of the contractile machinery. To see whether these relationships were similar in other animals, we studied the isovolumic ESPVR and the VO2-PVA relation in nine excised, cross-circulated rabbit left ventricles. The base-line ESPVR was linear (r = 0.94-0.99) with the slope (Emax) and volume-axis intercept (V0) equal to 83.4 +/- 18.3 mmHg/ml and 0.43 +/- 0.17 ml, respectively. When normalized for left ventricular weight, Emax (4.1 +/- 1.1 mmHg.ml-1.100 g) and V0 (8.9 +/- 3.7 ml/100 g) were similar to values reported for the dog left ventricle. The correlation between PVA and VO2 was linear (r = 0.93-1.00), and the slope (1.90 X 10(-5) +/- 0.44 X 10(-5) ml O2.mmHg-1.ml-1) and VO2-axis intercept (0.040 +/- 0.009 ml O2.beat-1.100 g-1) were similar to values found in the dog left ventricle. Hence, despite the greatly different heart size, the base-line contractile state and chemomechanical energy conversion efficiency of the excised, cross-circulated rabbit left ventricle are similar to those of the dog left ventricle.

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