Effects of metabolic acidosis and alkalosis on coronary blood flow and myocardial metabolism in the intact dog

1961 ◽  
Vol 200 (3) ◽  
pp. 628-632 ◽  
Author(s):  
A. V. N. Goodyer ◽  
W. F. Eckhardt ◽  
R. H. Ostberg ◽  
M. J. Goodkind
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Coronary Blood Flow ◽  
Venous Blood ◽  
Left Ventricular ◽  
Myocardial Uptake ◽  
Severe Metabolic Acidosis ◽  
Glucose Levels ◽  
Arterial Blood

Severe metabolic acidosis and alkalosis were induced in anesthetized dogs by the infusion of solutions of hydrochloric acid and sodium bicarbonate. Infusions of sodium chloride were administered to other dogs under the same experimental circumstances. Measurements were made of arterial blood pressure, heart rate, cardiac output and coronary blood flow, arterial blood pH, and the content of oxygen, total CO2, lactate, pyruvate and glucose in both arterial and coronary venous blood. The cardiac output and coronary blood flow were decreased by acidosis and increased by alkalosis, the changes induced by alkalosis. There were no significant changes of left ventricular efficiency. Acidosis increased blood glucose concentrations and interfered with the increased myocardial uptake of glucose expected at higher arterial glucose levels. Alkalosis increased blood lactate and pyruvate levels and, correspondingly, the myocardial uptake of these carbohydrate substrates. It is concluded that cardiac dynamic function (as indicated by measurements of cardiac efficiency and output and arterial pressure) is much less affected by severe metabolic acidosis in the intact animal than in the isolated perfused organ.

Continuous Airway Pressure Breathing With the Head-Box in the Newborn Lamb: Effects on Regional Blood Flows

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Airway Pressure ◽  
Left Ventricular Pressure ◽  
Blood Gases ◽  
Ocular Blood Flow ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Blood Flows ◽  
Arterial Blood

Continuous airway pressure delivered by a head-box is an accepted means of treating clinical hyaline membrane disease. To investigate hemodynamic alterations resulting from its use, eight newborn lambs, 1 to 6 days of age, were studied at 6 and 11 mm Hg of positive pressure, while spontaneously breathing room air. Organ blood flows and cardiac output were measured with 25 µ-diameter radioactive microspheres. Heart rate, left ventricular pressure, and arterial blood gases did not change during the study. Jugular venous pressures increased from 6.4 mm Hg to 18.6 and 24.2 mm Hg at 6 and 11 mm Hg, respectively (P < .005). Cardiac output decreased approximately 20% at either intrachamber pressure setting. Renal blood flow fell 21% at 11 mm Hg. No significant changes in blood flow were found in the brain, gastrointestinal tract, spleen, heart, or liver when compared to control flows. Of particular interest was the finding of a 28% reduction in ocular blood flow at 6 mm Hg and 52% at 11 mm Hg. From these results, we conclude that substantial cardiovascular alterations may occur during the application of head-box continuous airway pressure breathing, including a significant reduction in ocular blood flow.

Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stig Müller ◽  
Ole-Jakob How ◽  
Stig E Hermansen ◽  
Truls Myrmel
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Arterial Blood ◽  
Time Flow ◽  
The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Acute Heart Failure ◽  
Coronary Blood Flow ◽  
Drug Effects ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Energetic Cost ◽  
Lv Function

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.

Effects of protoveratrine on coronary blood flow of the renal hypertensive dog

1963 ◽  
Vol 204 (5) ◽  
pp. 895-898 ◽  
Author(s):  
James W. West ◽  
Elwood L. Foltz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Saturation ◽  
Coronary Blood Flow ◽  
Arterial Oxygen Saturation ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Venous Oxygen Saturation

In renal hypertension, protoveratrine decreased coronary blood flow, cardiac oxygen consumption, arterial and venous oxygen saturation, coronary arteriovenous oxygen difference, mean arterial blood pressure, cardiac output, cardiac work, cardiac efficiency, cardiac rate, total peripheral resistance, coronary resistance, respiratory rate, and minute volume. The decrease was significant in all functions except coronary blood flow, coronary venous oxygen saturation, and cardiac output. The results of these experiments indicate that in the renal hypertensive animal, a therapeutically beneficial effect was derived from protoveratrine on the circulation by its ability to decrease the work of the heart (lowering the elevated mean arterial pressure) and the coronary vascular resistance while maintaining coronary blood flow and cardiac output within normal levels. The less advantageous effect of protoveratrine on circulation resulted from its respiratory inhibiting effect which reduced the arterial blood oxygen saturation. Although a small decline in coronary venous oxygen saturation was noted, the coronary flow and oxygen delivery in face of the reduced arterial oxygen saturation was apparently adequate to maintain a normal cardiac activity.

Regulation of coronary flow

2021 ◽  
pp. 11-13
Author(s):  
Nico Bruining ◽  
Eric Boersma ◽  
Dirk J. Duncker
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Arterial Blood ◽  
Arterial Inflow ◽  
Systolic Phase ◽  
Vascular Beds

This chapter describes the regulation of coronary blood flow. The left ventricle generates the systemic arterial blood pressure that is required to maintain coronary blood flow. The coronary circulation is unique among regional vascular beds in that its perfusion is impeded during the systolic phase of the cardiac cycle by the surrounding contracting cardiac muscle. Systolic contraction increases left ventricular wall tension and compresses the intramyocardial microvessels, thereby impeding coronary arterial inflow. This compression is not uniformly distributed across the left ventricular wall, resulting in a redistribution of blood flow from the subendocardium to subepicardium.

scholarly journals Modulation of Myocardial Oxygen Delivery in Response to Isovolemic Hemodilution

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Blake R. Simon ◽  
Hana E. Baker ◽  
Conner C. Earl ◽  
Adam G. Goodwill ◽  
Sam Luebbe ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Oxygen Delivery ◽  
Venous Blood ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Neural Pathways ◽  
Isovolemic Hemodilution ◽  
Arterial Oxygen Content ◽  
Arterial Blood

Background and Hypothesis: Prior studies have established that progressive increases in coronary blood flow are sufficient to maintain myocardial oxygen delivery in response to reductions in arterial oxygenation. However, the precise mechanisms responsible for anemic coronary vasodilation remain poorly understood. This investigation tested the hypothesis that autonomic neural pathways contribute to the maintenance of myocardial oxygen delivery in response to graded reductions in arterial hematocrit.  Experimental Design: Experiments were conducted in open-chest anesthetized swine while assessing coronary blood flow and coronary arterial and venous blood gases in response to progressive hemodilution. Isovolemic hemodilution was achieved via simultaneous removal of 250mL of arterial blood and addition of 250mL of a synthetic plasma expander (Hespan) in swine that received either vehicle or a combination of atropine (0.5mg/kg) and propranolol (1mg/kg) (Atro/Pro).  Results: Relative to vehicle control swine, treatment with Atro/Pro increased heart rate by ~50±4 beats/min and arterial pressure by ~10±1 mmHg.  However, Atro/Pro did not significantly alter increases in coronary blood flow in response to isovolemic hemodilution (hematocrits ranging from ~35±1% to ~15±1%). Coronary venous PO2, an index of myocardial oxygenation, was also unchanged by hemodilution in both vehicle and Atro/Pro treated swine.   Conclusion and Potential Impact: These data suggest that autonomic neural pathways do not play a significant role in the maintenance of myocardial oxygen delivery in response to graded reduction in arterial oxygen content. Understanding of how myocardial oxygen supply is ultimately sensed and regulated in response to reductions in tissue oxygenation remains elusive.  

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