Cardiac contraction affects deep myocardial vessels predominantly

1991 ◽  
Vol 261 (5) ◽  
pp. H1417-H1429 ◽  
Author(s):  
M. Goto ◽  
A. E. Flynn ◽  
J. W. Doucette ◽  
C. M. Jansen ◽  
M. M. Stork ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Intraventricular Injection ◽  
Cardioplegic Solution ◽  
Pentobarbital Sodium ◽  
Perfusion Fixation ◽  
Myocardial Flow

To evaluate the roles of intramyocardial forces and systolic ventricular pressure in myocardial flow in the different layers separately, we measured myocardial flow in rabbit hearts during stable systolic contracture with left ventricular pressures of 60 (n = 5) and 0 mmHg (n = 5) and during stable diastolic arrest (n = 5). We also measured the number and size of the intramyocardial vessels after perfusion fixation (systolic arrest, n = 5; diastolic arrest, n = 5). In 25 rabbits, hearts were excised and perfused from the aortic root. Systolic arrest was achieved by perfusion of a low-Ca2+ Tyrode solution containing 2.0 mM Ba2+. Diastolic arrest was achieved by intraventricular injection of 700-1,000 mg pentobarbital sodium and was maintained by perfusion with St. Thomas cardioplegic solution. At perfusion pressure of 100 mmHg, subendocardial flow was lower than subepicardial flow during systolic arrest regardless of left ventricular pressure, whereas during diastolic arrest, subendocardial flow was higher than subepicardial flow. Subendocardial-to-subepicardial flow ratios for a physiological range of perfusion pressures were lower during systolic arrest with low rather than with high left ventricular pressure. Small arteriolar and capillary densities showed no difference between subendocardium and subepicardium. During systolic arrest, diameters of subendocardial terminal arterioles (4.6 +/- 1.3 microns) and capillaries (4.0 +/- 1.3 microns) were smaller than those in the subepicardium (8.8 +/- 1.7 and 7.1 +/- 1.6 microns, respectively; P less than 0.0001), whereas during diastolic arrest, diameters of subendocardial terminal arterioles (10.1 +/- 2.0 microns) and capillaries (7.6 +/- 1.8 microns) were slightly larger than those in the subepicardium (9.5 +/- 1.5 and 6.7 +/- 1.0 microns, respectively; P less than 0.01). We conclude that cardiac contraction predominantly affects subendocardial vessels and impedes subendocardial flow more than subepicardial flow regardless of left ventricular pressure.

Coronary oscillatory flow amplitude is more affected by perfusion pressure than ventricular pressure

1990 ◽  
Vol 258 (6) ◽  
pp. H1889-H1898 ◽  
Author(s):  
R. Krams ◽  
P. Sipkema ◽  
N. Westerhof
Keyword(s):  
Oscillatory Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Waterfall Model ◽  
Developed Pressure ◽  
Phasic Flow

In this study on the isolated, maximally vasodilated, blood-perfused cat heart we investigated the relation between left ventricular developed pressure (delta Piv) and coronary oscillatory flow amplitude (diastolic minus systolic flow, delta F) at different levels of constant perfusion pressure (Pp). We hypothesized that the effect of cardiac contraction on the phasic flow results from the changing elastic properties of cardiac muscle. The coronary vessel compartment can, as can the left ventricular lumen compartment, be described by a time-varying elastance. This concept predicts that the effect of left ventricular pressure on delta F is small, whereas the effect of Pp is considerable. Both the waterfall model and the intramyocardial pump model predict the inverse. The relation between delta Piv and delta F at a Pp of 10 kPa is delta F = (4.71 +/- 3.08).delta Piv + 337 +/- 75 (slope in ml.min-1.100 g-1.kPa-1 and intercept in ml.min-1.100 g-1; n = 7); the relation between (constant levels of) Pp and delta F at a constant delta Piv of 10 kPa is delta F = 51.Pp + 211 (slope in ml.min-1.100 g-1.kPa-1 and intercept in ml.min-1.100 g-1; n = 6). The differences in slope are best predicted by the time-varying elastance concept.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

Impairment of contraction increases sensitivity of epicardial lymph pressure for left ventricular pressure

1998 ◽  
Vol 274 (1) ◽  
pp. H187-H192 ◽  
Author(s):  
Jurgen W. G. E. Vanteeffelen ◽  
Daphne Merkus ◽  
Luc J. Bos ◽  
Isabelle Vergroesen ◽  
Jos A. E. Spaan
Keyword(s):  
Time Derivative ◽  
Left Ventricular Pressure ◽  
Relative Increase ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Local Contraction ◽  
Lymphatic Vasculature ◽  
Anesthetized Dogs ◽  
Lidocaine Administration

In the present study, cardiac contraction was regionally impaired to investigate the relationship between contractility [maximum first time derivative of left ventricular pressure (dPLV/d tmax)] and PLVon epicardial lymph pressure (Plymph) generation. Measurements were performed in open-chest anesthetized dogs under control conditions and while local contraction was abolished by intracoronary administration of lidocaine. Lidocaine significantly lowered dPLV/d tmaxand PLVpulse to 77 ± 9 (SD; n = 5) and 82 ± 5% of control, respectively, whereas Plymphpulse increased to 186 ± 101%. The relative increase of maximum Plymphto PLVrelated inversely to the change in dPLV/d tmaxafter lidocaine administration. Additional data were obtained when PLVwas transiently increased by constriction of the descending aorta. The ratio of pulse Plymphto PLVduring aortic clamping increased after lidocaine administration, from 0.063 ± 0.03 to 0.15 ± 0.09. The results suggest that transmission of PLVto the cardiac lymphatic vasculature is enhanced when regional contraction is impaired. These findings imply that during normal, unimpaired contraction lymph vessels are shielded from high systolic PLVby the myocardium itself.

scholarly journals Why is the subendocardium more vulnerable to ischemia? A new paradigm

2011 ◽  
Vol 300 (3) ◽  
pp. H1090-H1100 ◽  
Author(s):  
Dotan Algranati ◽  
Ghassan S. Kassab ◽  
Yoram Lanir
Keyword(s):  
Heart Rate ◽  
Network Flow ◽  
Perfusion Pressure ◽  
Compressive Loading ◽  
Flow Simulation ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
New Paradigm ◽  
Vessel Wall Thickness

Myocardial ischemia is transmurally heterogeneous where the subendocardium is at higher risk. Stenosis induces reduced perfusion pressure, blood flow redistribution away from the subendocardium, and consequent subendocardial vulnerability. We propose that the flow redistribution stems from the higher compliance of the subendocardial vasculature. This new paradigm was tested using network flow simulation based on measured coronary anatomy, vessel flow and mechanics, and myocardium-vessel interactions. Flow redistribution was quantified by the relative change in the subendocardial-to-subepicardial perfusion ratio under a 60-mmHg perfusion pressure reduction. Myocardial contraction was found to induce the following: 1) more compressive loading and subsequent lower transvascular pressure in deeper vessels, 2) consequent higher compliance of the subendocardial vasculature, and 3) substantial flow redistribution, i.e., a 20% drop in the subendocardial-to-subepicardial flow ratio under the prescribed reduction in perfusion pressure. This flow redistribution was found to occur primarily because the vessel compliance is nonlinear (pressure dependent). The observed thinner subendocardial vessel walls were predicted to induce a higher compliance of the subendocardial vasculature and greater flow redistribution. Subendocardial perfusion was predicted to improve with a reduction of either heart rate or left ventricular pressure under low perfusion pressure. In conclusion, subendocardial vulnerability to a acute reduction in perfusion pressure stems primarily from differences in vascular compliance induced by transmural differences in both extravascular loading and vessel wall thickness. Subendocardial ischemia can be improved by a reduction of heart rate and left ventricular pressure.

scholarly journals Arrhythmia analysis in Langendorff perfused hearts

2019 ◽  
Author(s):  
Hedvig Takács
Keyword(s):  
Heart Rate ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Observer Agreement ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Isolated Hearts ◽  
Definition Of

In this work, we used the isolated, Langendorff perfused heart model for arrhythmia investigations, and the data of the arrhythmia analysis served for clarifying and characterising the physiology of the model and also, to validate arrhythmia definitions. In our first investigation we examined the relationship between ventricular rhythm and coronary flow autoregulation in Langendorff perfused guinea pig hearts. It is a well-known fact, that heart rate affects coronary flow, but the mechanism is complex, especially in experimental settings. We examined whether ventricular irregularity influences coronary flow independently of heart rate. According to our results, during regular rhythm, left ventricular pressure exceeded perfusion pressure and prevented coronary perfusion at peak systole. However, ventricular irregularity significantly increased the number of beats in which left ventricular pressure remained below perfusion pressure, facilitating coronary perfusion. We found that in isolated hearts, cycle length irregularity increases the slope of the positive linear correlation between mean ventricular rate and coronary flow via producing beats in which left ventricular pressure remains below perfusion pressure. This means that changes in rhythm have the capacity to influence coronary flow independently of heart rate in isolated hearts perfused at constant pressure. In our second investigation we examined whether the arrhythmia definitions of Lambeth Conventions I (LC I) and Lambeth Conventions II (LC II) yield the same qualitative results and whether LC II improves inter-observer agreement. Data obtained with arrhythmia definitions of LC I and LC II were compared within and between two independent observers. Applying ventricular fibrillation (VF) definition of LC II significantly increased VF incidence and reduced VF onset time irrespective of treatment by detecting ‘de novo’ VF episodes. Using LC II reduced the number of ventricular tachycardia (VT) episodes and simultaneously increased the number of VF episodes, and thus, LC II masked the significant antifibrillatory effects of flecainide and the high K+ concentration. When VF incidence was tested, a very strong interobserver agreement was found according to LC I, whereas using VF definition of LC II reduced inter-observer agreement. It is concluded that LC II shifts some tachyarrhythmias from VT to VF class. VF definition of LC II may change the conclusion of pharmacological, physiological and pathophysiological arrhythmia investigations and may reduce inter-observer agreement.

scholarly journals Pharmacodynamics and Pharmacokinetics of Injectable Pimobendan and Its Metabolite, O-Desmethyl-Pimobendan, in Healthy Dogs

2021 ◽  
Vol 8 ◽  
Author(s):  
Poonavit Pichayapaiboon ◽  
Lalida Tantisuwat ◽  
Pakit Boonpala ◽  
Nakkawee Saengklub ◽  
Tussapon Boonyarattanasoonthorn ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Maximum Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial

Objectives: This study was designed to thoroughly evaluate the effects of bolus pimobendan at a dose of 0.15 mg/kg on cardiac functions, hemodynamics, and electrocardiographic parameters together with the pharmacokinetic profile of pimobendan and its active metabolite, o-desmethyl-pimobendan (ODMP), in anesthetized dogs.Methods: Nine beagle dogs were anesthetized and instrumented to obtain left ventricular pressures, aortic pressures, cardiac outputs, right atrial pressures, pulmonary arterial pressures, pulmonary capillary wedge pressures, electrocardiograms. After baseline data were collected, dogs were given a single bolus of pimobendan, and the pharmacodynamic parameters were obtained at 10, 20, 30, 60, and 120 min. Meanwhile, the venous blood was collected at baseline and 2, 5, 10, 20, 30, 60, 120, 180, 360, and 1,440 min after administration for the determination of pharmacokinetic parameters.Results: Compared with baseline measurements, the left ventricular inotropic indices significantly increased in response to intravenous pimobendan, as inferred from the maximum rate of rise in the left ventricular pressure and the contractility index. Conversely, the left ventricular lusitropic parameters significantly decreased, as inferred from the maximum rate of fall in the left ventricular pressure and the left ventricular relaxation time constant. Significant increases were also noted in cardiac output and systolic blood pressure. Decreases were observed in the systemic vascular resistance, pulmonary vascular resistance, left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, right atrial pressure, and pulmonary arterial pressure. The heart rate increased, but the PQ interval decreased. There was no arrhythmia during the observed period (2 h). The mean maximum plasma concentration (in μg/L) for ODMP was 30.0 ± 8.8. Pimobendan exerted large volume of distribution ~9 L/kg.Conclusions: Intravenous pimobendan at the recommended dose for dogs increased cardiac contraction and cardiac output, accelerated cardiac relaxation but decreased both vascular resistances. These mechanisms support the use of injectable pimobendan in acute heart failure.

Effects of cardiac contraction and cavity pressure on myocardial blood flow

1993 ◽  
Vol 265 (4) ◽  
pp. H1342-H1352 ◽  
Author(s):  
J. W. Doucette ◽  
M. Goto ◽  
A. E. Flynn ◽  
R. E. Austin ◽  
W. K. Husseini ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Cavity Pressure ◽  
Outer Flow ◽  
Global Function ◽  
Local Contraction ◽  
Passive Deformation ◽  
Transmural Flow ◽  
Myocardial Flow

Regional impairment of cardiac contraction uncouples force generation from left ventricular pressure (LVP) and may alter the determinants of the phasic pattern and transmural distribution of coronary flow. In anesthetized, open-chest dogs with maximal coronary vasodilation, we studied the effects of abolishing local contraction and changing cavity pressure on phasic myocardial inflow and net transmural flow in a region of left ventricular free wall. With contraction present, the normalized amplitude of distal phasic coronary velocity (NAmp) was not significantly different at normal vs. low LVP (1.00 vs. 0.92 +/- 0.09, respectively, intracoronary lidocaine, however, NAmp varied with LVP (1.62 +/- 0.25 at normal LVP, 0.85 +/- 0.22 at low LVP, P < 0.0001). With contraction present, inner-to-outer flow ratio was not consistently different at normal vs. low LVP (0.47 +/- 0.15 vs. 0.64 +/- 0.28, respectively, P = NS) but was consistently higher at low than at normal LVP with contraction absent (1.01 +/- 0.30 vs. 1.84 +/- 0.38, respectively, P < 0.0001). During uniform global function, contraction is the main determinant of phasic amplitude and transmural distribution of myocardial flow. When regional contraction is abolished, allowing passive deformation of the wall during systole, LVP assumes a powerful role.

Coronary arterial inflow impediment during systole is little affected by capacitive effects

1993 ◽  
Vol 264 (3) ◽  
pp. H715-H721 ◽  
Author(s):  
P. Bouma ◽  
P. Sipkema ◽  
N. Westerhof
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Experimental Conditions ◽  
Dynamic Contractions ◽  
Arterial Inflow ◽  
Static Contractions

During cardiac contraction coronary arterial inflow is impeded, whereas venous flow is augmented. These effects are assumed to be caused by diameter reductions of intramyocardial blood vessels. The reduction in vascular diameter (and thus vascular volume) during contraction increases coronary resistance and/or decreases back pressure so that flow decreases and the rate of change of volume results in a capacitive flow. The aim of this study was to estimate the contribution of capacitive flow to total coronary inflow impediment. Isolated blood-perfused (100 mmHg and constant), maximally vasodilated, ryanodine-pretreated rat hearts (n = 8) with intraventricular balloons were used. The coronary inflow impediment during isovolumic beats at a heart rate of 2–3 Hz (dynamic contractions) and during prolonged systoles obtained by fast pacing (static contractions, no capacitive flow impediment) were compared. Changing left ventricular balloon volume enabled us to vary left ventricular pressure and to relate systolic flow to systolic left ventricular pressure. We found that for the same contractility (expressed in terms of systolic pressure-volume relationship and maximal elastance) and same left ventricular pressure, the ratio of coronary inflow impediment in dynamic and static contractions is not significantly different from unity (P < 0.005). This implies that under our experimental conditions coronary inflow impediment in dynamic contractions is little affected by capacitive effects.

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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