Mechanical restitution of isolated human ventricular myocardium subjected to in vivo pressure and volume overload

1992 ◽  
Vol 26 (10) ◽  
pp. 978-982 ◽  
Author(s):  
I. C Cooper ◽  
C. H Fry ◽  
M. M Webb-Peploe
Keyword(s):  
Volume Overload ◽  
Ventricular Myocardium ◽  
Mechanical Restitution ◽  
Human Ventricular Myocardium

Impact of acute and enduring volume overload on mechanotransduction and cytoskeletal integrity of canine left ventricular myocardium

2007 ◽  
Vol 292 (5) ◽  
pp. H2324-H2332 ◽  
Author(s):  
Dirk W. Donker ◽  
Jos G. Maessen ◽  
Fons Verheyen ◽  
Frans C. Ramaekers ◽  
Roel L. H. M. G. Spätjens ◽  
...  
Keyword(s):  
Protein Expression ◽  
Volume Overload ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Mechanical Stimuli ◽  
Hypertrophic Growth ◽  
Lim Protein ◽  
Ventricular Mechanics

It is poorly understood how mechanical stimuli influence in vivo myocardial remodeling during chronic hemodynamic overload. Combined quantitation of ventricular mechanics and expression of key proteins involved in mechanotransduction can improve fundamental understanding. Adult anesthetized dogs ( n = 20) were studied at sinus rhythm (SR) and 0, 3, 10, and 35 days of complete atrioventricular block (AVB). Serial left ventricular (LV) myofiber mechanics were measured. Repeated LV biopsies were analyzed for mRNA and/or protein expression of β1D-integrin, melusin, Akt, GSK3β, muscle LIM protein (MLP), four-and-a-half LIM protein 2 (fhl2), desmin, and calpain. Upon AVB, increased ejection strain (0.29 ± 0.01 vs. 0.13 ± 0.02, SR) and end-diastolic stress (4.8 ± 1.1 vs. 2.7 ± 0.4 kPa) dominated mechanical changes. Brain natriuretic peptide plasma levels were correspondingly high (33 ± 4 vs. 19 ± 1 pg/ml, SR). β1D-Integrin protein expression increased chronically after AVB. Melusin was temporarily overexpressed (+33 ± 9%, 3 days AVB vs. SR), followed by elevated ratios of phosphorylated (P)-Akt to Akt and P-GSK3β to GSK3β (+26 ± 6% and +30 ± 8% at 10 days AVB vs. SR). These changes corresponded to peak hypertrophic growth at 3 to 10 days. MLP increased gradually to maxima at chronic AVB (+36 ± 7%). In contrast, fhl2 (−22 ± 3%, 3 days) and desmin (−30 ± 9%, 10 days AVB) transiently declined but recovered at chronic AVB. Calpain protein expression remained unaltered. In conclusion, volume overload after AVB causes a transient compromise of cytoskeletal integrity based, at least partly, on transcriptional downregulation. Subsequent cytoskeletal reorganization coincides with the upregulation of melusin, P-Akt, P-GSK3β, and MLP, indicating a strong drive to compensated hypertrophy.

β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

2014 ◽  
Vol 112 (11) ◽  
pp. 951-959 ◽  
Author(s):  
Morten Eriksen ◽  
Arnfinn Ilebekk ◽  
Alessandro Cataliotti ◽  
Cathrine Rein Carlson ◽  
Torstein Lyberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Β2 Adrenergic Receptor ◽  
Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

ACE inhibitors and cardiac ACE mRNA in volume overload-induced cardiac hypertrophy

1997 ◽  
Vol 273 (2) ◽  
pp. H641-H646 ◽  
Author(s):  
W. Lear ◽  
M. Ruzicka ◽  
F. H. Leenen
Keyword(s):  
Cardiac Hypertrophy ◽  
Ace Inhibitors ◽  
Cardiac Tissue ◽  
Ace Inhibitor ◽  
Internal Standard ◽  
Phosphoglycerate Kinase ◽  
Volume Overload ◽  
Ang Ii ◽  
Aortocaval Shunt

Quinapril, an angiotensin-converting enzyme (ACE) inhibitor with high affinity for cardiac ACE, prevents increases in both plasma and cardiac angiotensin II (ANG II) and development of cardiac hypertrophy after aortocaval shunt in rats. In contrast, enalapril, an ACE inhibitor with low affinity for cardiac ACE, only prevents the increase in plasma ANG II. In the present study, we assessed whether these differences between enalapril and quinapril reflect different inhibition of cardiac tissue ACE and local ANG II by measuring their effects on cardiac ACE mRNA. Treatment with enalapril (250 mg/l) and quinapril (200 mg/l in drinking water) was started 3 days before the shunt and sham surgery. After 1 wk of aortocaval shunt, the hearts were excised and the left ventricle and right ventricle were weighed and used for reverse transcriptase-polymerase chain reaction (RT-PCR) assays for ACE and phosphoglycerate kinase-1 (internal standard). Quinapril, but not enalapril, inhibited the development of cardiac hypertrophy by aortocaval shunt. The shunt increased ACE mRNA in both left and right ventricles about twofold. In animals with aortocaval shunt, quinapril markedly further upregulated ACE mRNA in both ventricles, whereas enalapril did not cause significant changes. In sham rats, both ACE inhibitors increased ACE mRNA, but the increase was more pronounced by treatment with quinapril. These studies show that in vivo ACE inhibitors with low (enalapril) vs. high (quinapril) affinity for cardiac ACE differ in their effects on cardiac ACE mRNA. This difference is more pronounced in volume overload-induced cardiac hypertrophy, presumably reflecting their different effects on cardiac ANG II.

Demonstration of hysteresis in refractoriness of canine ventricular myocardium

1988 ◽  
Vol 255 (6) ◽  
pp. H1342-H1348
Author(s):  
C. Giorgi ◽  
M. Vermeulen ◽  
R. Cardinal ◽  
P. Savard ◽  
R. Nadeau ◽  
...  
Keyword(s):  
Pulse Width ◽  
Cycle Length ◽  
Ventricular Myocardium ◽  
Ventricular Muscle ◽  
Cycle Lengths ◽  
Long Pulse ◽  
Basic Cycle Length ◽  
Canine Ventricular Myocardium

The properties and determinants of hysteresis during ventricular effective refractory period (VERP) measurements by an extrastimulus technique were determined in 15 anesthetized open-chest dogs as well as in isolated ventricular muscle (n = 6). VERP was determined both by decreasing the S1-S2 interval and also by increasing S1S2. Hysteresis was then calculated by subtracting the VERP obtained with the decreasing S1S2 from the VERP obtained with the increasing S1S2. The effects of basic cycle length, pulse width, stimulation intensity, and the number of basic drives on VERP and hysteresis were evaluated. VERP was shorter for long pulse width, high stimulation intensities, and shorter basic cycle lengths. These modifications were not associated with significant changes of hysteresis. VERP was shorter during decreasing S1S2 than during increasing S1S2. Hysteresis was greater with 6 basic drive cycles than with 12 (P less than 0.001) in both in vivo and in vitro preparations. The data suggest that 1) hysteresis occurs during VERP measurements; 2) hysteresis is independent of stimulation modality; and 3) hysteresis decreases with the number of basic drive cycles.

scholarly journals NT pro- B-type Natriuretic Peptide in the Small Ventricular Septal Defect in Children

2021 ◽  
Vol 9 (B) ◽  
pp. 1677-1680
Author(s):  
Rahmat Budi Kuswiyanto ◽  
Putria Apandi ◽  
Dany Hilmanto ◽  
Muhammad Hasan Bashari ◽  
Sri Endah Rahayuningsih
Keyword(s):  
Natriuretic Peptide ◽  
Transcatheter Closure ◽  
Volume Overload ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Natriuretic Peptide Level ◽  
Peptide Level ◽  
Before And After ◽  
Male Patients

Background: Brain natriuretic peptide is a cardiac hormone secreted from the left ventricular myocardium due to ventricular expansion and volume overload. A recent study shows that small VSD will have risk of ventricular dysfunction in adulthood. Another complications such as endocarditis, congestive heart failure, aortic regurgitation, arrhythmia also we should be aware. Evaluations of the plasma B-type natriuretic peptide level (NT pro BNP) are currently being considered as methods to identify the possible presence of ventricular dilation in small VSD. Objective: To evaluate the change in plasma B-type natriuretic peptide after transcatheter closure of VSD. Methods: A pretest-posttest design was conducted on VSD patients before and after transcatheter closure. Plasma B-type natriuretic peptide level were measured before and 30 days after the transcatheter closure of VSD. Result: A total of 32 peri membranous VSD patients were included in this study with 62.5 % female patients (n=20) and 37.5 % male patients (n=12). A significant decrease was observed in the median NT pro BNP level when the level before closure of 1.08 (0.74 – 3.47) ng/ml was compared to the level after closure of 0.91 (0.68 – 2.07) ng/ml (p<0.05). Conclusion: Significant decreases in NT pro BNP level are seen in small VSD patients 30 days after transcatheter closure. Patients with small peri membranous VSD are generally considered to need occlusion for their childhood defect.  

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