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.

Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion

1985 ◽  
Vol 249 (6) ◽  
pp. H1070-H1077 ◽  
Author(s):  
I. Y. Liang ◽  
C. E. Jones
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Adrenergic Blockade ◽  
Adrenergic Antagonist

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6–8 min of prazosin infusion (0.6–0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

Intramyocardial Pressure and Coronary Extravascular Resistance

1985 ◽  
Vol 107 (1) ◽  
pp. 46-50 ◽  
Author(s):  
P. D. Stein ◽  
H. N. Sabbah ◽  
M. Marzilli
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Driving Pressure ◽  
Ventricular Pressure ◽  
Intramyocardial Pressure ◽  
Extravascular Resistance

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastole, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blood flow.

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.

Intramyocardial pressure gradients in working and nonworking isolated cat hearts

1994 ◽  
Vol 266 (3) ◽  
pp. H1233-H1241 ◽  
Author(s):  
L. S. Mihailescu ◽  
F. L. Abel
Keyword(s):  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Mechanical Resistance ◽  
Coronary Perfusion ◽  
Pressure Gradients ◽  
Intramyocardial Pressure ◽  
Krebs Henseleit Buffer ◽  
Transmural Gradient

This study presents an improved method for the measurement of intramyocardial pressure (IMP) using the servo-nulling mechanism. Glass micropipettes (20-24 microns OD) were used as transducers, coated to increase their mechanical resistance to breakage, and placed inside the left ventricular wall with a micropipette holder and manipulator. IMP was measured at the base of the left ventricle in working and nonworking isolated cat hearts that were perfused with Krebs-Henseleit buffer. In working hearts a transmural gradient of systolic IMP oriented from endocardium toward the epicardium was found; the endocardial values for systolic IMP were slightly higher than systolic left ventricular pressure (LVP), by 11-18%. Increases in afterload induced increases in IMP, without changing the systolic IMP-to-LVP ratio. In nonworking hearts with drained left ventricles, the systolic transmural gradient for IMP described for working hearts persisted, but at lower values, and was directly dependent on coronary perfusion pressure. Systolic IMP-to-LVP ratios were always > 1. The diastolic IMP of both working and nonworking hearts exhibited irregular transmural gradients. Our results support the view that generated systolic IMP is largely independent of LVP development.

Transmural distribution of blood flow during activation of coronary muscarinic receptors

1981 ◽  
Vol 240 (6) ◽  
pp. H941-H946 ◽  
Author(s):  
G. J. Gross ◽  
J. D. Buck ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Muscarinic Receptors ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Tissue Blood Flow ◽  
Coronary Perfusion ◽  
Coronary Vasodilator ◽  
Blood Flow Ratio

The role of coronary muscarinic receptors in the distribution of transmural blood flow across the left ventricular wall of the working heart was studied in anesthetized open-chest dogs. Tissue blood flow in subepicardium, midmyocardium, and subendocardium was determined with radioactive microspheres before and during activation of muscarinic vasodilator receptors by intracoronary infusions of acetylcholine. Myocardial and coronary vascular beta-receptors were blocked by sotalol (2.0 mg/kg iv). Equivalent submaximal coronary vasodilator doses of acetylcholine and adenosine were compared for effects on transmural blood flow. Intracoronary infusions of acetylcholine (5.0 and 10.7 micrograms/min) produced a dose-related increase in the subendocardial-subepicardial blood flow ratio (endo/epi) from 1.07 to 1.32 and 1.57, respectively. A progressively larger decrease in coronary vascular resistance occurred in the subendocardium than midmyocardium or subepicardium following acetylcholine administration. In contrast, intracoronary administration of adenosine (54.4 micrograms/min) produced no change in endo/epi. Atropine effectively blocked acetylcholine-induced coronary vasodilation but not vasodilation produced by adenosine. Neither agent affected heart rate, left ventricular pressure, coronary perfusion pressure, or myocardial contractility. These results suggest that activation of muscarinic coronary vasodilator receptors redistributes blood flow preferentially to the subendocardium independent of cardiac mechanical influences.

Effects of aminophylline on behaviorally induced coronary blood flow increases

1987 ◽  
Vol 253 (3) ◽  
pp. H548-H555
Author(s):  
G. E. Billman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Left Ventricular Pressure ◽  
Aversive Conditioning ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adenosine Antagonist ◽  
Blood Flow Increase ◽  
Myocardial Oxygen Supply

It has been proposed that adenosine is a metabolic vasodilator that matches myocardial oxygen supply to demand by regulating coronary blood flow. In the present study, the adenosine antagonist aminophylline (Am) was used to evaluate the role adenosine plays in the coronary blood flow increase elicited by a controlled aversive stress, namely, classical aversive conditioning (a 30-s tone reinforced with a 1-s shock). Fifteen mongrel dogs were chronically instrumented to measure left circumflex coronary blood flow (CBF), left ventricular pressure (LVP), and heart rate. Am significantly (P greater than 0.01) attenuated the CBF response to the aversive stress without affecting the prestress levels (pre-Am control 40.9 +/- 2.4, peak 64.6 +/- 3.3 ml/min; post-Am control 41.7 +/- 2.2, peak 55.0 +/- 2.5 ml/min). The maximal CBF increase was reduced by 38.9 +/- 6.7% when compared with the control (no drug) condition. In a similar manner, neither heart rate nor LVP was affected by Am. However, Am significantly increased prestress level of first derivative of left ventricular pressure with reference to time [LV dP/dt] (pre-Am control 3,793.5 +/- 289.8 and Am 4,599.6 +/- 331.2 mmHg/s, respectively). These data suggest that adenosine contributes significantly to the regulation of CBF during a controlled emotional stress.

Direct cardiac effects of vasopressin: role of V1- and V2-vasopressinergic receptors

1988 ◽  
Vol 255 (2) ◽  
pp. H261-H265 ◽  
Author(s):  
B. R. Walker ◽  
M. E. Childs ◽  
E. M. Adams
Keyword(s):  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Cardiac Effects ◽  
Coronary Vasoconstriction ◽  
Langendorff Preparation ◽  
Wide Range ◽  
Male Wistar Rats

Experiments were performed to determine the possible direct effects of arginine vasopressin (AVP) on cardiac function in the nonworking Langendorff preparation. Hearts were isolated from male Wistar rats, and the coronary arteries were retrograde perfused at a constant rate through the aorta with a Krebs-Henseleit solution, which was continuously bubbled with 95% O2–5% CO2. The hearts were paced at 280 beats/min and measurements made of peak ventricular pressure (PVP), first derivative of left ventricular pressure (dP/dtmax), and coronary perfusion pressure (CPP). By maintaining constant coronary flow, the direct cardiac effects of AVP could be determined independent of changes in myocardial O2 delivery elicited by potential coronary vasoconstriction. Myocardial function was assessed at AVP concentrations of 0, 10, 25, 50, 100, 200, 400, and 500 pg/ml. Progressive coronary vasoconstriction was observed with increasing AVP concentration. In contrast, PVP and dP/dtmax increased at 50 and 100 pg/ml of AVP but fell at 400 and 500 pg/ml. The maximal PVP and dP/dtmax responses were at 50 pg/ml (+16 +/- 3 and +44 +/- 4%, respectively), whereas at 500 pg/ml both PVP and dP/dtmax were reduced below control (-30 +/- 4 and -34 +/- 5%, respectively). Pretreatment with the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (40 ng/ml) totally blocked both the coronary vasoconstrictor and contractility responses to AVP. Furthermore, infusion of a specific V2-agonist was without effect even at high doses. These data suggest that although AVP causes dose-related coronary vasoconstriction over a wide range of AVP concentrations, the hormone may exert a positive inotropic effect at doses mimicking circulating levels encountered in a number of pathophysiological situations.(ABSTRACT TRUNCATED AT 250 WORDS)

Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline

1989 ◽  
Vol 257 (4) ◽  
pp. H1043-H1048 ◽  
Author(s):  
H. M. Wei ◽  
Y. H. Kang ◽  
G. F. Merrill
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Vasodepressor Response

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.

Influence of low perfusion pressure on effect of endothelin on coronary vascular bed

1991 ◽  
Vol 260 (3) ◽  
pp. H893-H901 ◽  
Author(s):  
J. P. Clozel ◽  
U. Sprecher
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Perfusion Pressure ◽  
Coronary Spasm ◽  
Electromagnetic Flowmeter ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Cross Sectional ◽  
Coronary Vasoconstriction

The goal of this study was to evaluate the influence of low coronary perfusion pressure on the coronary vasoconstriction induced by endothelin. For this purpose, the circumflex coronary arteries of 12 open-chest dogs were cannulated and perfused at a controlled pressure. Total coronary blood flow was measured with an electromagnetic flowmeter and the transmural distribution of coronary blood flow with the radioactive microspheres technique. In addition, the circumflex coronary artery diameter was measured by sonomicrometry with piezoelectric crystals, and the coronary cross-sectional area was calculated. At a coronary perfusion pressure of 100 mmHg, endothelin induced a marked coronary vasoconstriction and a redistribution of coronary blood flow toward the endocardium. At a low coronary perfusion pressure of 40 mmHg, these effects of endothelin were still present. The constriction of the large coronary artery occurred even with a lower dose of endothelin at a low coronary perfusion pressure compared with the normal perfusion pressure. This was not the case when angiotensin II was given the same way. We conclude that endothelin is a potent coronary vasoconstrictor even at a low perfusion pressure. Thus one may speculate that endothelin plays a role in the coronary spasm which has been shown in patients with angina pectoris.

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