scholarly journals Influence of dual ETA/ETB-receptor blockade on coronary responses to treadmill exercise in dogs

2000 ◽  
Vol 89 (5) ◽  
pp. 2041-2048 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Peter Cernacek ◽  
Michel Lavallée
Keyword(s):  
Coronary Sinus ◽  
Adrenergic Receptor ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Receptor Blockade ◽  
Etb Receptor ◽  
Dual Blockade ◽  
The Relationship

We hypothesized that endothelin (ET) release during exercise may be triggered by α-adrenergic-receptor activation and thereby influence coronary hemodynamics and O2 metabolism in dogs. Exercise resulted in coronary blood flow increases (to 1.88 ± 0.26 from 1.10 ± 0.12 ml · min−1 · g−1) and in a fall ( P < 0.01) in coronary sinus O2saturation (17.4 ± 1.5 to 9.6 ± 0.7 vol%), whereas myocardial O2 consumption (MV˙o 2) increased (109 ± 13% from 145 ± 16 μl O2 · min−1 · g−1). Tezosentan, a dual ETA/ETB-receptor blocker, slightly reduced mean arterial pressure (MAP) and increased heart rate throughout exercise. The relationship between coronary sinus O2 saturation and MV˙o 2 was shifted upward ( P < 0.05) after tezosentan administration; i.e., as MV˙o 2 increased during exercise, coronary sinus O2 saturation was disproportionately higher after ET-receptor blockade. After propranolol, tezosentan resulted in significant decreases ( P < 0.05) in left ventricular pressure, the first derivative of left ventricular pressure over time, and MAP during exercise. As MV˙o 2 increased during exercise, coronary sinus O2 saturation levels after tezosentan became superimposable over those observed before ET-receptor blockade. Thus dual blockade of ETA/ETBreceptors alters coronary hemodynamics and O2 metabolism during exercise, but ET activity failed to increase beyond baseline levels.

Coronary Sinus Assessment of Left Ventricular Pressure in Man

1984 ◽  
pp. 424-429 ◽  
Author(s):  
David P. Faxon ◽  
A. K. Jacobs ◽  
S. M. McSweeney ◽  
W. D. Coats ◽  
M. A. Kellett ◽  
...  
Keyword(s):  
Coronary Sinus ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure

Stopped-flow epicardial lymph pressure is affected by left ventricular pressure in anesthetized goats

1993 ◽  
Vol 264 (5) ◽  
pp. H1624-H1628 ◽  
Author(s):  
Y. Han ◽  
I. Vergroesen ◽  
J. A. Spaan
Keyword(s):  
Control Level ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beating Heart ◽  
Ventricular Pressure ◽  
Stopped Flow ◽  
Pressure Waveform ◽  
Descending Aorta ◽  
Aortic Clamping ◽  
The Relationship

We measured epicardial lymph pressure (Plymph) in the anesthetized goat (n = 5 goats). To study the transmission of systolic left ventricular pressure (PLV) to Plymph, the effect of an increase in PLV caused by clamping of the descending aorta on Plymph was evaluated. Peak systolic PLV was 131 +/- 4 (+/- SE) mmHg during control (43 beats) and 188 +/- 4 mmHg when elevated due to aortic clamping (157 beats). Peak systolic Plymph was 24.8 +/- 1.0 and 34.8 +/- 1.1 mmHg during control and elevated PLV, respectively. In the first beat of elevated PLV, peak Plymph did not change, although the pressure waveform did. In the subsequent beats, Plymph increased proportionally with increased PLV. When PLV was decreased back to control, Plymph also decreased but did not reach control level until after three beats. The relationship between normalized Plymph and normalized PLV is given by Plymph = 0.70 x PLV + 0.09. The results show that PLV does affect Plymph in a normal beating heart.

Transcardiac gradients of circulating apelin: extraction by normal hearts vs. release by hearts failing due to pressure overload

2010 ◽  
Vol 109 (6) ◽  
pp. 1744-1748 ◽  
Author(s):  
Satu Helske ◽  
Petri T. Kovanen ◽  
Jyri Lommi ◽  
Heikki Turto ◽  
Markku Kupari
Keyword(s):  
Coronary Sinus ◽  
Aortic Root ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Control Group ◽  
Electrophysiological Studies ◽  
Plasma Apelin

Apelin is a newly discovered inotropic peptide tentatively linked up with the pathophysiology of heart failure (HF). To further assess the role of apelin in HF, we measured its transcardiac arteriovenous gradients in patients with left ventricular pressure overload with or without HF and in patients with structurally normal hearts. Blood samples from the aortic root and coronary sinus were drawn from 49 adult patients undergoing preoperative cardiac catheterization for severe aortic valve stenosis (AS). Similar samples were taken from 12 control patients with structurally normal hearts undergoing electrophysiological studies. Plasma apelin was determined by enzyme immunoassay. In the control group, apelin decreased from a median of 0.39 (0.16–1.94) ng/ml in the aortic root to 0.18 (0.13–1.04) ng/ml in the coronary sinus ( P = 0.004). In AS patients free of HF ( n = 33), apelin concentration remained unaltered across the heart, but in those with HF ( n = 15) apelin rose from a median of 0.26 (0.20–0.82) ng/ml in the aorta to 0.45 (0.24–1.17) ng/ml in the coronary sinus ( P = 0.002). The transcardiac apelin gradients differed statistically highly significantly across the three groups ( P = 0.00005), and each of the two-group differences was also statistically significant ( P < 0.05). In conclusion, left ventricular pressure overload changes the transcardiac arteriovenous differences of circulating apelin. Although normal hearts extract apelin from the coronary blood, hearts failing due to left ventricular pressure overload release apelin into the circulation. Loss of cardiac apelin may be involved in the mechanisms of HF development in AS.

α1-Adrenergic receptor responses in α1AB-AR knockout mouse hearts suggest the presence of α1D-AR

2003 ◽  
Vol 284 (4) ◽  
pp. H1104-H1109 ◽  
Author(s):  
Lynne Turnbull ◽  
Diana T. McCloskey ◽  
Timothy D. O'Connell ◽  
Paul C. Simpson ◽  
Anthony J. Baker
Keyword(s):  
Adrenergic Receptor ◽  
Coronary Flow ◽  
Wild Type Mouse ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Mouse Heart ◽  
Double Knockout ◽  
Experimental Conditions ◽  
Perfused Hearts

Two functional α1-adrenergic receptor (AR) subtypes (α1Aand α1B) have been identified in the mouse heart. However, it is unclear whether the third known subtype, α1D-AR, is also present. To investigate this, we determined whether there were α1-AR responses in hearts from a novel mouse model lacking α1A- and α1B-ARs (double knockout) (ABKO). In Langendorff-perfused hearts, α1-ARs were stimulated with phenylephrine. For ABKO hearts, phenylephrine reduced left ventricular pressure and coronary flow (to 87 ± 2% and 86 ± 4% of initial, respectively, n = 11, P < 0.01). These effects were blocked by prazosin and 8-{2-[4-(2-methoxyphenyl)-1-piperazinyl]-8-azaspirol[4,5]decane-7,9-dione} dihydrochloride, suggesting that α1D-AR-mediated responses were present. In contrast, right ventricular trabeculae from ABKO hearts did not respond to phenylephrine, suggesting that in ABKO perfused hearts, the effects of phenylephrine were not mediated by direct actions on cardiomyocytes. A novel finding was that α1-AR stimulation caused positive inotropy in the wild-type mouse heart, in contrast to negative inotropy observed in mouse cardiac muscle strips. We conclude that mouse hearts lacking α1A- and α1B-ARs retain functional α1-AR responses involving decreases of coronary flow and ventricular pressure that reflect α1D-AR-mediated vasoconstriction. Furthermore, α1-AR inotropic responses depend critically on the experimental conditions.

scholarly journals New Amino-steroid-anthracenone with Biological Activity Against Ischemia-reperfusion Injury in a Wistar Rat Model

2018 ◽  
Vol 8 (1) ◽  
pp. 10-20 ◽  
Author(s):  
Figueroa-Valverde Lauro ◽  
Rosas-Nexticapa Marcela ◽  
Mateu-Armand Virginia ◽  
Herrera-Meza Socorro ◽  
Díaz-Cedillo Francisco ◽  
...  
Keyword(s):  
Biological Activity ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Infarct Area ◽  
Camp Levels

Objective: The main objective of this study was to evaluate the biological activity of an ASA (Amino-Steroid-Anthracenone derivative) against heart failure caused by the ischemia- reperfusion injury (translated as infarct area). Methods: Biological activity exerted by ASA (0.001-100 nM) on infarct area was determined using an ischemia-reperfusion injury model. In addition, to characterize the molecular mechanism involved in the effect exerted by ASA on left ventricular pressure, some drugs such as estrone (0.001-100 nM), tamoxifen (1 nM), butoxamine (1 nM) and ZM-241385 (1 nM) were used. Results: The experimental data showed that ASA decreased the infarction area significantly (p = 0.05) compared to estrone. Other results indicated that ASA decreased left ventricular pressure and this effect was inhibited by ZM-241385. In addition, ASA increased cAMP levels in a time-dependent manner compared to control conditions. Conclusion: The results showed that ASA decreases ischemia-reperfusion injury (translated as infarct area) via A2 adenosine receptor activation and these phenomena involve changes in cAMP levels.

scholarly journals Activity Exerted by a Testosterone Derivative on Myocardial Injury Using an Ischemia/Reperfusion Model

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Figueroa-Valverde Lauro ◽  
Díaz-Cedillo Francisco ◽  
García-Cervera Elodia ◽  
Pool-Gómez Eduardo ◽  
López-Ramos Maria ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Perfusion Pressure ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Dependent Manner ◽  
Coronary Resistance ◽  
Testosterone Derivative

Some reports indicate that several steroid derivatives have activity at cardiovascular level; nevertheless, there is scarce information about the activity exerted by the testosterone derivatives on cardiac injury caused by ischemia/reperfusion (I/R). Analyzing these data, in this study, a new testosterone derivative was synthetized with the objective of evaluating its effect on myocardial injury using an ischemia/reperfusion model. In addition, perfusion pressure and coronary resistance were evaluated in isolated rat hearts using the Langendorff technique. Additionally, molecular mechanism involved in the activity exerted by the testosterone derivative on perfusion pressure and coronary resistance was evaluated by measuring left ventricular pressure in the absence or presence of the following compounds: flutamide, prazosin, metoprolol, nifedipine, indomethacin, and PINANE TXA2. The results showed that the testosterone derivative significantly increasesP=0.05the perfusion pressure and coronary resistance in isolated heart. Other data indicate that the testosterone derivative increases left ventricular pressure in a dose-dependent manner (0.001–100 nM); however, this phenomenon was significantly inhibitedP=0.06by indomethacin and PINANE-TXA2  P=0.05at a dose of 1 nM. In conclusion, these data suggest that testosterone derivative induces changes in the left ventricular pressure levels through thromboxane receptor activation.

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