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.  

scholarly journals Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

2014 ◽  
Vol 35 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Christopher K Willie ◽  
Philip N Ainslie ◽  
Ivan Drvis ◽  
David B MacLeod ◽  
Anthony R Bain ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Breath Hold ◽  
Cerebral Oxygen ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
End Tidal ◽  
The Brain

The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers ( n=17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing (‘clamp’) was then used to replicate an identical temporal pattern of decreasing arterial PO2 (PaO2) and increasing arterial PCO2 (PaCO2) while breathing. End-apnea PaO2 ranged from 23  to 37 mm Hg (30±7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54±24% versus 34±26%, respectively; however, CBF increased similarly between apnea and clamp (93.6±28% and 83.4±38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

scholarly journals Effects of Hematocrit Variations on Cerebral Blood Flow and Oxygen Transport in Ischemic Cerebrovascular Disease

1981 ◽  
Vol 1 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Masahito Kusunoki ◽  
Kazufumi Kimura ◽  
Masaichi Nakamura ◽  
Yoshinari Isaka ◽  
Shotaro Yoneda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Oxygen Transport ◽  
Oxygen Delivery ◽  
Inverse Correlation ◽  
Arterial Oxygen ◽  
Brain Oxygenation ◽  
Arterial Oxygen Content ◽  
Ischemic Cerebrovascular Disease

The contribution of hematocrit (Ht) changes on cerebral blood flow (CBF) and brain oxygenation in ischemic cerebrovascular disease is still controversial. In the present study, effects of Ht variations on CBF and oxygen delivery were investigated in patients with ischemic cerebrovascular disease. CBF was measured by the Xe-133 intracarotid injection method in 27 patients, whose diagnoses included completed stroke, reversible ischemic neurological deficit, and transient ischemic attack. Ht values in the patients ranged from 31 to 53%. There was a significant inverse correlation between CBF and Ht in these Ht ranges. Oxygen delivery, i.e., the product of arterial oxygen content and CBF, increased with Ht elevation and reached the maximum level in the Ht range of 40–45% and then declined. The CBF-Ht and oxygen transport-Ht relations observed in our study were similar to those in the glass-tube model studies by other workers rather than to those in intact animal experiments. From these results, it is conceivable that in ischemic cerebrovascular disease, the vasomotor adjustment was impaired in such a manner that the relations among Ht, CBF, and oxygen delivery were different from those in healthy subjects. Further, an “optimal hematocrit” for brain oxygenation was also discussed.

Effects of l-Epinephrine and l-Norepinephrine on the Splanchnic Bed of Intact Dogs

1957 ◽  
Vol 189 (3) ◽  
pp. 576-579 ◽  
Author(s):  
E. Allbaugh Farrand ◽  
R. Larsen ◽  
Steven M. Horvath
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Splanchnic Blood Flow ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Metabolic Functions ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Change In Mean ◽  
Infusion Period

The changes in splanchnic blood flow and related metabolic functions which occurred as the result of the infusion of 0.1 µg/kg/min. of l-epinephrine and l-norepinephrine for 10 minutes were measured in anesthetized dogs. l-Epinephrine elicited a marked increase in estimated splanchnic blood flow and no change in mean arterial pressure. While a significantly increased mean arterial blood pressure was observed following the administration of l-norepinephrine, no change in estimated splanchnic blood flow occurred. Arterial oxygen content was increased significantly with both drugs. Utilization of oxygen by the splanchnic bed was not changed during the infusion of either drug but was increased during the postepinephrine infusion period.

scholarly journals The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Cerebrovascular Function

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.

Heliox increases quadriceps muscle oxygen delivery during exercise in COPD patients with and without dynamic hyperinflation

2012 ◽  
Vol 113 (7) ◽  
pp. 1012-1023 ◽  
Author(s):  
Zafeiris Louvaris ◽  
Spyros Zakynthinos ◽  
Andrea Aliverti ◽  
Helmut Habazettl ◽  
Maroula Vasilopoulou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Oxygen Delivery ◽  
Quadriceps Muscle ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Muscle Oxygen ◽  
Peripheral Muscle ◽  
Copd Patients ◽  
Gastric Pressure

Some reports suggest that heliox breathing during exercise may improve peripheral muscle oxygen availability in patients with chronic obstructive pulmonary disease (COPD). Besides COPD patients who dynamically hyperinflate during exercise (hyperinflators), there are patients who do not hyperinflate (non-hyperinflators). As heliox breathing may differently affect cardiac output in hyperinflators (by increasing preload and decreasing afterload of both ventricles) and non-hyperinflators (by increasing venous return) during exercise, it was reasoned that heliox administration would improve peripheral muscle oxygen delivery possibly by different mechanisms in those two COPD categories. Chest wall volume and respiratory muscle activity were determined during constant-load exercise at 75% peak capacity to exhaustion, while breathing room air or normoxic heliox in 17 COPD patients: 9 hyperinflators (forced expiratory volume in 1 s = 39 ± 5% predicted), and 8 non-hyperinflators (forced expiratory volume in 1 s = 48 ± 5% predicted). Quadriceps muscle blood flow was measured by near-infrared spectroscopy using indocyanine green dye. Hyperinflators and non-hyperinflators demonstrated comparable improvements in endurance time during heliox (231 ± 23 and 257 ± 28 s, respectively). At exhaustion in room air, expiratory muscle activity (expressed by peak-expiratory gastric pressure) was lower in hyperinflators than in non-hyperinflators. In hyperinflators, heliox reduced end-expiratory chest wall volume and diaphragmatic activity, and increased arterial oxygen content (by 17.8 ± 2.5 ml/l), whereas, in non-hyperinflators, heliox reduced peak-expiratory gastric pressure and increased systemic vascular conductance (by 11.0 ± 2.8 ml·min−1·mmHg−1). Quadriceps muscle blood flow and oxygen delivery significantly improved during heliox compared with room air by a comparable magnitude (in hyperinflators by 6.1 ± 1.3 ml·min−1·100 g−1 and 1.3 ± 0.3 ml O2·min−1·100 g−1, and in non-hyperinflators by 7.2 ± 1.6 ml·min−1·100 g−1 and 1.6 ± 0.3 ml O2·min−1·100 g−1, respectively). Despite similar increase in locomotor muscle oxygen delivery with heliox in both groups, the mechanisms of such improvements were different: 1) in hyperinflators, heliox increased arterial oxygen content and quadriceps blood flow at similar cardiac output, whereas 2) in non-hyperinflators, heliox improved central hemodynamics and increased systemic vascular conductance and quadriceps blood flow at similar arterial oxygen content.

Oxygen delivery at high blood viscosity and decreased arterial oxygen content to brains of conscious rats

2001 ◽  
Vol 280 (6) ◽  
pp. H2591-H2597 ◽  
Author(s):  
A. Rebel ◽  
C. Lenz ◽  
H. Krieter ◽  
K. F. Waschke ◽  
K. Van Ackern ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Content ◽  
Blood Viscosity ◽  
Oxygen Delivery ◽  
Brain Structures ◽  
Arterial Oxygen ◽  
Cerebral Oxygen ◽  
Compensatory Mechanisms ◽  
Arterial Oxygen Content

We addressed the question to which extent cerebral blood flow (CBF) is maintained when, in addition to a high blood viscosity (Bvis) arterial oxygen content (CaO2 ) is gradually decreased. CaO2 was decreased by hemodilution to hematocrits (Hct) of 30, 22, 19, and 15% in two groups. One group received blood replacement (BR) only and served as the control. The second group received an additional high viscosity solution of polyvinylpyrrolidone (BR/PVP). Bvis was reduced in the BR group and was doubled in the BR/PVP. Despite different Bvis, CBF did not differ between BR and BR/PVP rats at Hct values of 30 and 22%, indicating a complete vascular compensation of the increased Bvis at decreased CaO2 . At an Hct of 19%, local cerebral blood flow (LCBF) in some brain structures was lower in BR/PVP rats than in BR rats. At the lowest Hct of 15%, LCBF of 15 brain structures and mean CBF were reduced in BR/PVP. The resulting decrease in cerebral oxygen delivery in the BR/PVP group indicates a global loss of vascular compensation. We concluded that vasodilating mechanisms compensated for Bvis increases thereby maintaining constant cerebral oxygen delivery. Compensatory mechanisms were exhausted at a Hct of 19% and lower as indicated by the reduction of CBF and cerebral oxygen delivery.

Effects of khellin on coronary blood flow and related metabolic functions

1959 ◽  
Vol 196 (2) ◽  
pp. 391-393 ◽  
Author(s):  
Richard L. Farrand ◽  
Steven M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Control Period ◽  
Systemic Arterial Pressure ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Fick Principle ◽  
Metabolic Functions ◽  
Pulmonary Arterial

Khellin, a drug employed as a coronary dilator, was tested to determine its effects on the cardiovascular system of the dog. Ten mongrel dogs were anesthetized with Nembutal and, after control observations were made, given an intravenous administration of 1 mg/kg body weight of khellin. Coronary blood flow and cardiac output samples were drawn during the control period and at 10, 40 and 80 minutes after administration of the drug Cardiac output was calculated by the direct Fick principle and coronary blood flow by the nitrous oxide method. There was a significant (5%) increase in the arterial oxygen content during the 10- and 40-minute intervals, but no change was observed at 80 minutes. An increase in arterial-mixed venous oxygen difference occurred at 40 and 80 minutes. No change in systemic arterial pressure or cardiac output was noted at any time. Coronary blood flow had decreased slightly at 80 minutes. A significant decrease in carbon dioxide content of the arterial, pulmonary arterial and coronary sinus blood was observed, possibly as a consequence of hyperventilation. Khellin appeared to alter the metabolism of the myocardial and splanchnic tissues.

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.

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.

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