Progressively heterogeneous mismatch of regional oxygen delivery to consumption during graded coronary stenosis in pig left ventricle

2015 ◽  
Vol 309 (10) ◽  
pp. H1708-H1719 ◽  
Author(s):  
David J. C. Alders ◽  
A. B. Johan Groeneveld ◽  
Thomas W. Binsl ◽  
Johannes H. G. M. van Beek
Keyword(s):  
Blood Flow ◽  
Coronary Stenosis ◽  
Oxygen Supply ◽  
Perfusion Pressure ◽  
Oxygen Extraction ◽  
Adenosine Infusion ◽  
Coronary Perfusion ◽  
Metabolic Demand ◽  
Tissue Samples ◽  
Group I

In normal hearts, myocardial perfusion is fairly well matched to regional metabolic demand, although both are distributed heterogeneously. Nonuniform regional metabolic vulnerability during coronary stenosis would help to explain nonuniform necrosis during myocardial infarction. In the present study, we investigated whether metabolism-perfusion correlation diminishes during coronary stenosis, indicating increasing mismatch of regional oxygen supply to demand. Thirty anesthetized male pigs were studied: controls without coronary stenosis ( n = 11); group I, left anterior descending (LAD) coronary stenosis leading to coronary perfusion pressure reduction to 70 mmHg ( n = 6); group II, stenosis with perfusion pressure of about 35 mmHg ( n = 6); and group III, stenosis with perfusion pressure of 45 mmHg combined with adenosine infusion ( n = 7). [2-13C]- and [1,2-13C]acetate infusion was used to calculate regional O2 consumption from glutamate NMR spectra measured for multiple tissue samples of about 100 mg dry mass in the LAD region. Blood flow was measured with microspheres in the same regions. In control hearts without stenosis, regional oxygen extraction did not correlate with basal blood flow. Average myocardial O2 delivery and consumption decreased during coronary stenosis, but vasodilation with adenosine counteracted this. Regional oxygen extraction was on average decreased during stenosis, suggesting adaptation of metabolism to lower oxygen supply after half an hour of ischemia. Whereas regional O2 delivery correlated with O2 consumption in controls, this relation was progressively lost with graded coronary hypotension but partially reestablished by adenosine infusion. Therefore, coronary stenosis leads to heterogeneous metabolic stress indicated by decreasing regional O2 supply to demand matching in myocardium during partial coronary obstruction.

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.

Abstract 17334: The Detrimental Effect of Chest Compression Interruptions on Coronary Perfusion Pressure Dynamics

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Norman A Paradis ◽  
Karen L Moodie ◽  
Christopher L Kaufman ◽  
Joshua W Lampe
Keyword(s):  
Blood Flow ◽  
Chest Compression ◽  
Detrimental Effect ◽  
Perfusion Pressure ◽  
Vena Cava ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Over Time

Introduction: Guidelines for treatment of cardiac arrest recommend minimizing interruptions in chest compressions based on research indicating that interruptions compromise coronary perfusion pressure (CPP) and blood flow and reducing the likelihood of successful defibrillation. We investigated the dynamics of CPP before, during, and after compression interruptions and how they change over time. Methods: CPR was performed on domestic swine (~30 Kg) using standard physiological monitoring. Blood flow was measured in the abdominal aorta (AAo), the inferior vena cava, the right common carotid and external jugular. Ventricular fibrillation (VF) was electrically induced. Mechanical chest compressions (CC) were started after four minutes of VF. CC were delivered at a rate of 100 compressions per minute (cpm) and at a depth of 2” for a total of 12 min. CPP was calculated as the difference between aortic and right atrial pressure at end-diastole per Utstein guidelines. CPP was determined for 5 compressions prior to the interruption, every 2 seconds during the CC interruption, and for 7 compressions after the interruption. Per protocol, 12 interruptions occurred at randomized time points. Results: Across 12 minutes of CPR, averaged CPP prior to interruption was significantly greater than the averaged CPP after the interruption (22.4±1.0 vs. 15.5±0.73 mmHg). As CPR continued throughout the 12 minutes, CPP during compressions decreased (First 6 min = 24.1±1.4 vs. Last 6 min = 20.1±1.3 mmHg, p=0.05), but the effect of interruptions remained constant resulting in a 20% drop in CPP for every 2 seconds irrespective of the prior CPP. The increase (slope) of CPP after resumption of compressions was significantly reduced over time (First 6 min = 1.47±0.18 vs. Last 6 min = 0.82±0.13 mmHg/compression). Conclusions: Chest compression interruptions have a detrimental effect on coronary perfusion and blood flow. The magnitude of this effect increases over time as a resuscitation effort continues. These data confirm the importance of providing uninterrupted CPR particularly in long duration resuscitations.

Vasodilation or altered perfusion pressure moves 15-micrometers spheres trapped in the gut wall

1982 ◽  
Vol 243 (1) ◽  
pp. H123-H127
Author(s):  
L. C. Maxwell ◽  
A. P. Shepherd ◽  
G. L. Riedel
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Venous Blood ◽  
Intestinal Blood Flow ◽  
Experimental Conditions ◽  
Tissue Samples ◽  
Intestinal Segments ◽  
Microsphere Method ◽  
Adjacent Segments ◽  
Isoproterenol Infusion

To determine whether the microsphere method for measuring the intramural distribution of intestinal blood flow is affected by perfusion pressure or vasodilation, we infused radioactive 9- and 15-micrometers spheres into adjacent segments of isolated canine small bowel. After sphere infusion the blood supply of the control loop was occluded, and the vasculature of the experimental loop was either dilated by infusing isoproterenol or was subjected to increased perfusion pressure. Intestinal segments were dissected into mucosal, submucosal, and muscularis samples. Venous blood was collected during sphere infusions and experimental perturbations. Accumulations of spheres in tissue samples and venous blood were assessed in a gamma radioactivity counter. Isoproterenol caused previously infused spheres to leave submucosa and redistributed them primarily to mucosa with few additional spheres reaching venous blood. An increase in perfusion pressure also dislodged spheres from submucosa, but these did reach venous blood. The combined estimate of mucosal plus submucosal blood flow was relatively unaffected by isoproterenol infusion but was significantly altered by increased perfusion pressure. These results have the following implications for microsphere studies of the intramural distribution of intestinal blood flow: 1) tissue must be sampled after each sphere infusion unless the possibility of sphere migration has been experimentally eliminated and 2) even a two-compartment fractionation of blood flow into muscularis and mucosal-plus-submucosal compartments is not valid under some experimental conditions.

The physiologic reserve in oxygen carrying capacity: studies in experimental hemodilution

1986 ◽  
Vol 64 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Supply ◽  
The Body ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Whole Body ◽  
Oxygen Extraction Ratio ◽  
Acute Anemia ◽  
Total Body Oxygen

The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. Several factors are discussed which contribute to the increase in cardiac output during acute anemia including the reduction in blood viscosity, sympathetic innervation of the heart, and increased venomotor tone. The latter has been shown to be dependent on intact aortic chemoreceptors. With respect to peripheral vascular responses, the rise in coronary and cerebral blood flows which occur following hemodilution is proportionally greater than the increase in cardiac output while the opposite is true for kidney, liver, spleen, and intestine. Skeletal muscle does not contribute to a redistribution of blood flow to more vital areas during acute anemia despite its relatively large anaerobic capacity. Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.

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.

Characteristics of coronary blood flow and transmural distribution in miniature pigs

1978 ◽  
Vol 235 (5) ◽  
pp. H601-H609 ◽  
Author(s):  
M. Sanders ◽  
F. C. White ◽  
T. M. Peterson ◽  
C. M. Bloor
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Oxygen Demand ◽  
Coronary Artery Occlusion ◽  
Adenosine Infusion ◽  
Myocardial Oxygen Demand ◽  
Heavy Exercise ◽  
Miniature Pigs

The relationship between phasic systolic and diastolic coronary blood flow and its transmural distribution has been studied in 29 Yucatan miniature pigs at rest and during heavy exercise, with and without adenosine infusion (1.5 mg . kg-1 . min-1) and with and without a subtotal coronary artery occlusion. Altered factors that affected coronary flow included vascular resistance, perfusion pressure, myocardial oxygen demand, and extra-vascular pressure. The data indicate that, at rest, endomural perfusion is significantly dependent on diastolic blood flow. However, the ability of the myocardial vessels to autoregulate during systole as well as during diastole was clearly shown with the use of adenosine infusion. This ability to regulate flow intrinsically appeared to transcend the endocardial dependency on diastolic perfusion under certain stressful conditions, e.g., during heavy exercise, when the diastolic duration was significantly reduced. Systolic transmural perfusion may then become a significant factor in meeting the blood flow demands of the myocardium. However, due to gradients in vascular resistance, perfusion pressure, and oxygen demand, the coronary reserve of the epicardium appears to be greater than that of the endocardium under any condition.

Persistent right coronary flow reserve at low perfusion pressure

1989 ◽  
Vol 256 (4) ◽  
pp. H1176-H1184 ◽  
Author(s):  
H. Murakami ◽  
S. J. Kim ◽  
H. F. Downey
Keyword(s):  
Blood Flow ◽  
Coronary Flow Reserve ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Adenosine Infusion ◽  
Blood Flows ◽  
Flow Reserve ◽  
Anesthetized Dogs ◽  
Myocardial O2 Consumption ◽  
O2 Supply

To determine whether right coronary (RC) flow reserve persists at perfusion pressures below the apparent autoregulatory range, the RC artery of 18 anesthetized dogs was cannulated and perfused at controlled pressures. RC blood flow (RCBF) fell from 65.3 +/- 6.1 to 33.7 +/- 2.3 ml.min-1.100 g-1 as RC perfusion pressure (RCPP) was reduced from 80 to 40 mmHg. At 40 mmHg, intracoronary adenosine increased RCBF by 97.9 +/- 10.6 ml.min-1.100 g-1 (P less than 0.001). RCBF fell to 9.5 +/- 1.7 ml.min-1.100 g-1 at 20 mmHg, and RCBF did not significantly increase during adenosine, although RC vasodilation was observed in four dogs. Regional right ventricular (RV) blood flows at RCPP of 80 and 40 mmHg were measured by radioactive microsphere technique. Before adenosine infusion, RCBF was distributed uniformly across the RV free wall at normal and low perfusion pressures. During adenosine infusion, blood flow in both regions increased significantly, but the flow reserve was greater in the subendocardial region at both normal and reduced pressures. RV myocardial O2 consumption (MVo2) was decreased significantly at 40 mmHg, however, there was no evidence of ischemia at this pressure, since the RV lactate extraction ratio was normal (n = 8). Thus RV O2 demand fell when RC O2 supply was reduced, although a flow reserve was available. RV MVo2 was restored to normal when right coronary flow reserve was mobilized by adenosine infusion. For RCBF from 65 to 365 ml.min-1.100 g-1, RC venous O2 content rose and RV MVo2 was essentially constant.(ABSTRACT TRUNCATED AT 250 WORDS)

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