The effects of hyperoxia on oxygen uptake during acute anemia

1984 ◽  
Vol 62 (7) ◽  
pp. 809-814 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain ◽  
W. N. Stainsby
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Cardiovascular Responses ◽  
Capillary Blood ◽  
Whole Body ◽  
Normobaric Hyperoxia ◽  
Blood Exchange ◽  
Variable Section ◽  
Bilateral Vagotomy

The effects of normobaric hyperoxia on the oxygen uptake [Formula: see text] and cardiovascular responses of the whole body and hindlimb during anemia were investigated. Anesthetized, paralyzed dogs were ventilated for 20-min periods with room air (normoxia), 100% O2 (hyperoxia), and returned to room air. Anemia (hematocrit = 15%) was then induced by isovolemic dextran-for-blood exchange and the normoxia, hyperoxia, normoxia sequence was repeated. Whole body [Formula: see text] and cardiac output rose following anemia, and then fell (p < 0.05) with hyperoxia during anemia. These responses were not abolished by β-blockade with propranolol (1 mg/kg, iv) or bilateral vagotomy. The hindlimb data for blood flow and [Formula: see text] were similar in direction to those of the whole body but were more variable. Section of the sciatic and femoral nerves did not appear to have significant effect on the limb responses to hyperoxia. The decrease in whole body and hindlimb [Formula: see text] with hyperoxia during anemia may have resulted from a redistribution of capillary blood flow away from exchange vessels in response to the elevated [Formula: see text].

Whole body and hindlimb cardiovascular responses of the anesthetized dog during CO hypoxia

1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
The Body ◽  
Whole Body ◽  
Total Resistance ◽  
Intact Group ◽  
Anesthetized Dogs

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.

Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose

1993 ◽  
Vol 264 (4) ◽  
pp. E504-E513 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
The Body ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Co2 Production ◽  
Arterial Blood ◽  
Splanchnic Oxygen

The contribution of the splanchnic tissues to the initial 2-h rise in whole body energy expenditure after ingestion of glucose or fructose was examined in healthy subjects. Indirect calorimetry and catheter techniques were employed to determine pulmonary gas exchange, cardiac output, splanchnic blood flow, splanchnic oxygen uptake, and blood temperatures before and for 2 h after ingestion of 75 g of either fructose or glucose in water solution or of water only. Fructose ingestion was found to increase total oxygen uptake by an average of 9.5% above basal levels; the corresponding increase for glucose was 8.8% and for water only 2.5%. The respiratory exchange ratio increased from 0.84 in the basal state to 0.97 at 45 min after fructose ingestion and rose gradually after glucose to 0.86 after 120 min. The average 2-h thermic effect, expressed as percent of ingested energy, was 5.0% for fructose and 3.7% for glucose (not significant). Splanchnic oxygen consumption did not increase measurably after ingestion of either fructose or glucose. The arterial concentration of lactate rose, arterial pH fell, and PCO2 remained essentially unchanged after fructose ingestion. Glucose, but not fructose, elicited increases in cardiac output (28%) and splanchnic blood flow (56%). Fructose, but not glucose, increased arterial blood temperature significantly. It is concluded that both fructose and glucose-induced thermogenesis occurs exclusively in extrasplanchnic tissues. Compared with glucose, fructose ingestion is accompanied by a more marked rise in CO2 production, possibly reflecting an increased extrasplanchnic oxidation of lactate and an accumulation of heat in the body.

Effects of alpha -adrenergic blockade during acute anemia

1982 ◽  
Vol 52 (1) ◽  
pp. 16-20 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Volume Expansion ◽  
Cardiovascular Responses ◽  
Whole Body ◽  
Peripheral Blood Flow ◽  
Adrenergic Blockade ◽  
Acute Anemia ◽  
Alpha Blockade ◽  
Total Body Oxygen

Studies were carried out in seven anesthetized paralyzed dogs to examine the importance of alpha -adrenergic tone in the cardiovascular responses during acute anemia. Data were obtained 1) at normal hematocrit (Hct), 2) during anemia produced by isovolemic hemodilution with dextran (Hct, 13–15%), 3) during anemia after alpha -blockade (alpha -bl) with phenoxybenzamine (3 mg/kg), and 4) following volume expansion during anemia with a red blood cell dextran solution. Cardiac output (QT), limb and total body oxygen uptake (VO2), and limb blood flow (QL) were determined. Both QT and QL increased during anemia (P less than 0.01), whereas limb resistance (RL) and total peripheral resistance (TPR) were decreased (P less than 0.01). No further change in either RL or TPR occurred with alpha -blockade anemia, but both QT and QL decreased (P less than 0.01). Whole-body VO2 increased during anemia and then declined with alpha -bl and anemia. Following volume expansion during anemia with alpha -bl, QT, QL, and whole-body VO2 increased. We conclude that alpha -adrenergic sympathetic tone to capacitance vessels is essential for the cardiac output increased during anemia, but has little or no effect on resistance vessels and hence distribution of peripheral blood flow.

Central and peripheral adaptations of the gas transport system to one-leg training

1981 ◽  
Vol 59 (11) ◽  
pp. 1146-1154 ◽  
Author(s):  
S. G. Thomas ◽  
D. A. Cunningham ◽  
M. J. Plyley ◽  
D. R. Boughner ◽  
R. A. Cook
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Endurance Training ◽  
Maximal Oxygen Uptake ◽  
Enzyme Activities ◽  
Cardiovascular Responses ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Enzyme Analysis ◽  
Ergometer Exercise

The role of central and peripheral adaptations in the response to endurance training was examined. Changes in cardiac structure and function, oxygen extraction, and muscle enzyme activities following one-leg training were studied.Eleven subjects (eight females, three males) trained on a cycle ergometer 4 weeks with one leg (leg 1), then 4 weeks with the second leg (leg 2). Cardiovascular responses to exercise with both legs and each leg separately were evaluated at entry (T1), after 4 weeks of training (T2), and after a second 4 weeks of training (T3). Peak oxygen uptake ([Formula: see text] peak) during exercise with leg 1 (T1 to T2 increased 19.8% (P < 0.05) and during exercise with leg 2 (T2 to T3 increased 16.9% (P < 0.05). Maximal oxygen uptake with both legs increased 7.9% from T1 to T2 and 9.4% from T2 to T3 (P < 0.05). During exercise at 60% of [Formula: see text] peak, cardiac output [Formula: see text] was increased significantly only when the trained leg was exercised. [Formula: see text] increased 12.2% for leg 1 between T1 and T2 and 13.0% for leg 2 between T2 and T3 (P < 0.05). M-mode echocardiographic assessment of left ventricular internal diameter at diastole and peak velocity of circumferential fibre shortening at rest or during supine cycle ergometer exercise at T1 and T3 revealed no training induced changes in cardiac dimensions or function. Enzyme analysis of muscle biopsy samples from the vastus lateralis (At T1, T2, T3) revealed no consistent pattern of change in aerobic (malate dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase) or anaerobic (phosphofructokinase, lactate dehydroginase, and creatine kinase) enzyme activities. Increases in cardiac output and maximal oxygen uptake which result from short duration endurance training can be achieved, therefore, without measurable central cardiac adaptation. The absence of echocardio-graphically determined changes in cardiac dimensions and contractility and the absence of an increase in cardiac output during exercise with the nontrained leg following training of the contralateral limb support this conclusion.

A simple module for on-line computation of stroke volume and cardiac output

1975 ◽  
Vol 38 (5) ◽  
pp. 927-929 ◽  
Author(s):  
G. Pinardi ◽  
A. Sainz ◽  
E. Santiago
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Data Analysis ◽  
Stroke Volume ◽  
Simple Module ◽  
Cardiovascular Responses ◽  
Aortic Blood Flow ◽  
Aortic Blood ◽  
On Line ◽  
Aortic Blood Flow Velocity

An easily constructed, low-priced, simple, and reliable module to obtain stroke volume and cardiac output by analog integration of aortic blood flow velocity signals is described. Rapid data analysis of physiologic and pharmacologic cardiovascular responses in dogs is greatly facilitated by on line computation of these parameters.

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.

Oxygen uptake and blood flow in canine skeletal muscle during moderate and severe anemia

1983 ◽  
Vol 61 (2) ◽  
pp. 178-182 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Oxygen Transport ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Arterial Oxygen ◽  
Acute Anemia ◽  
Moderate Anemia ◽  
The Mean

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius–plantaris muscle group was isolated. Cardiac output [Formula: see text], muscle blood flow [Formula: see text], total body and muscle oxygen uptake [Formula: see text] were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle [Formula: see text], [Formula: see text], and [Formula: see text] were increased in both groups at 30 min of anemia. By 60 min, [Formula: see text] and [Formula: see text] declined to preanemic control values in the moderate anemia group; whole body [Formula: see text] was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle [Formula: see text] showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle [Formula: see text] during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle [Formula: see text] response was related to the decrease in arterial oxygen transport.

scholarly journals Cardiovascular effects of the respiratory muscle metaboreflexes in dogs: rest and exercise

2003 ◽  
Vol 95 (3) ◽  
pp. 1159-1169 ◽  
Author(s):  
Joshua R. Rodman ◽  
Kathleen S. Henderson ◽  
Curtis A. Smith ◽  
Jerome A. Dempsey
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Lactic Acid ◽  
Respiratory Muscle ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Vascular Conductance ◽  
Iliac Arteries ◽  
Muscle Metaboreflex ◽  
Arterial Blood

In awake dogs, lactic acid was injected into the phrenic and deep circumflex iliac arteries to elicit the diaphragm and abdominal muscle metaboreflexes, respectively. At rest, injections into the phrenic or deep circumflex iliac arteries significantly increased mean arterial blood pressure 21 ± 7% and reduced cardiac output 6 ± 2% and blood flow to the hindlimbs 20 ± 9%. Simultaneously, total systemic, hindlimb, and abdominal expiratory muscle vascular conductances were reduced. These cardiovascular responses were not accompanied by significant changes in the amplitude or timing of the diaphragm electromyogram. During treadmill exercise that increased cardiac output, hindlimb blood flow, and vascular conductance 159 ± 106, 276 ± 309, and 299 ± 90% above resting values, lactic acid injected into the phrenic or deep circumflex iliac arteries also elicited pressor responses and reduced hindlimb blood flow and vascular conductance. Adrenergic receptor blockade at rest eliminated the cardiovascular effects of the respiratory muscle metaboreflex. We conclude that the cardiovascular effects of respiratory muscle metaboreflex activation are similar to those previously reported for limb muscles. When activated via metabolite production, the respiratory muscle metaboreflex may contribute to the increased sympathetic tone and redistribution of blood flow during exercise.

Renal oxygen consumption, thermogenesis, and amino acid utilization during i.v. infusion of amino acids in man

1994 ◽  
Vol 267 (5) ◽  
pp. E648-E655 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Amino Acids ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Amino Acid ◽  
Oxygen Uptake ◽  
Heat Production ◽  
Whole Body ◽  
Arterial Blood ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

The renal contribution to the amino acid-induced whole body thermogenesis was examined. Using indirect calorimetry and catheter techniques, pulmonary and renal oxygen uptake and blood flow, blood temperatures, and net renal exchange of amino acids, glucose and lactate were measured in eight healthy men before and during 3 h of intravenous infusion of 720 kJ of an amino acid solution. During the infusion, the pulmonary oxygen uptake increased from 252 +/- 12 to 310 +/- 8 ml/min, cardiac output increased from 5.9 +/- 0.3 to 6.8 +/- 0.3 l/min, and the arterial blood temperature increased from 36.34 +/- 0.04 to 36.68 +/- 0.07 degrees C. Renal oxygen consumption, heat production, blood flow, and net glucose exchange remained unchanged during the infusion. The net renal uptake of amino acid energy from the blood rose from 2 +/- 2 to 11 +/- 4 W. The total renal energy expenditure was 9-10 W throughout the study period. It is concluded that intravenous amino acid infusion greatly augments the uptake and utilization of amino acids in the kidneys but does not stimulate the renal oxygen consumption, heat production, blood flow, or glucose release.

Effects of oral vs. i.v. glucose administration on splanchnic and extrasplanchnic O2 uptake and blood flow

1996 ◽  
Vol 271 (3) ◽  
pp. E496-E504 ◽  
Author(s):  
T. Brundin ◽  
R. Branstrom ◽  
J. Wahren
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Glucose Infusion ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Oral Glucose ◽  
Intravenous Glucose ◽  
Glucose Administration ◽  
Glucose Ingestion ◽  
Splanchnic Oxygen

The metabolic and circulatory responses to intravenous or oral administration of glucose (75 g) were studied in healthy subjects. Pulmonary oxygen uptake increased promptly after oral but not during intravenous glucose infusion. The average 2-h rise above basal in whole body oxygen uptake was 8 +/- 1% (P < 0.001) after oral glucose and 3 +/- 1% (P < 0.05) during intravenous glucose infusion. After oral glucose, splanchnic oxygen uptake rose initially by approximately 15% (P < 0.01) and then declined; its average 2-h postprandial level was not significantly higher than that in the basal state. During intravenous glucose, splanchnic oxygen uptake decreased gradually during the first 75 min, reaching a level approximately 25% below basal (P < 0.05). Oxygen consumption by extrasplanchnic tissues rose significantly and to a similar extent (8%, 2 h average) with both intravenous and oral glucose. Splanchnic blood flow increased significantly after oral but not during intravenous glucose. It is concluded that 1) intravenous infusion and oral glucose administration elicit extrasplanchnic thermogenic effects of similar magnitude, 2) during intravenous glucose infusion, the extrasplanchnic thermogenic effect is counterbalanced by a simultaneous reduction in splanchnic oxygen uptake, resulting in a minimal (3%) net rise in whole body oxygen uptake, and 3) oral glucose ingestion but not intravenous glucose infusion increases the splanchnic blood flow.

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