Arterial-venous Oxygen Difference Research Articles

Effect of arm training on central and peripheral circulatory function

LOFTIN, M., R. A. BOILEAU, B. H. MASSEY, and T. G. LOHMAN. Effect of arm training on central and peripheral circulatory function. Med. Sci. Sports Exerc., Vol. 20, No. 2, pp. 136–141, 1988. The purpose of this study was to examine the effect of endurance arm training on metabolic and circulatory function during arm and leg exercise. Thirty-eight females (aged 18 to 35 yr) participated in the study, with 19 subjects in the training group and 19 in a control group. Both a specific and general training response was observed at the conclusion of the 5-wk training period. As a result of training, during peak arm exercise, significant increases (P < 0.05) were observed for oxygen uptake (VO2), ventilation, cardiac output, stroke volume, arterial-venous oxygen difference, cumulative work, and total performance time. During peak leg exercise following arm training, significant increases (P < 0.05) were observed for VO2, ventilation, cardiac output, cumulative work, and total performance time. Standardized partial regression coefficients were used to examine the relative influence of the metabolic and circulatory components which define VO2. Prior to training during arm work, the arterial- venous oxygen difference accounted for the largest proportion of variance in VO2; but after training, stroke volume contributed the largest portion of variance. On the other hand, during leg exercise, stroke volume accounted for the largest portion of variation in leg VOz both before and after arm training. The data suggest that endurance arm training as prescribed in this study elicits significant circulorespiratory function adaptations to support improved performance in both arm and leg work. Further, the findings suggest both a specific and general training effect, with the more dominant effect specific to arm work. Moreover, the results indicate that central circulatory function (stroke volume) plays a more dominant role in arm exercise after training, suggesting that metabolic and circulatory responses during arm work become more like responses observed during leg work.

Effect of arm training on central and peripheral circulatory function.

The purpose of this study was to examine the effect of endurance arm training on metabolic and circulatory function during arm and leg exercise. Thirty-eight females (aged 18 to 35 yr) participated in the study, with 19 subjects in the training group and 19 in a control group. Both a specific and general training response was observed at the conclusion of the 5-wk training period. As a result of training, during peak arm exercise, significant increases (P less than 0.05) were observed for oxygen uptake (VO2), ventilation, cardiac output, stroke volume, arterial-venous oxygen difference, cumulative work, and total performance time. During peak leg exercise following arm training, significant increases (P less than 0.05) were observed for VO2, ventilation, cardiac output, cumulative work, and total performance time. Standardized partial regression coefficients were used to examine the relative influence of the metabolic and circulatory components which define VO2. Prior to training during arm work, the arterial-venous oxygen difference accounted for the largest proportion of variance in VO2; but after training, stroke volume contributed the largest portion of variance. On the other hand, during leg exercise, stroke volume accounted for the largest portion of variation in leg VO2 both before and after arm training. The data suggest that endurance arm training as prescribed in this study elicits significant circulorespiratory function adaptations to support improved performance in both arm and leg work. Further, the findings suggest both a specific and general training effect, with the more dominant effect specific to arm work.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of a Pyridoxalated-Hemoglobin-Polyoxyethylene Conjugate (PHP) as an Oxygen Carrying Plasma Expander in Lethal Anemia

AbstractPHP, mean molecular weight of approximately 90,000 daltons, is produced by chemical modifications of outdated human red cell hemoglobin (Hb). The P50 value of PHP is 22 ± 0.7mmHg. Eleven healthy mongrel dogs were exposed to severe anemia to a hematocrit of 5 ± 2% by normovolemic exchange (ET) with PHP (n=5) or a plasma expander, Hespan (Control, n=6). Hb concentration in the preparation is 6.0 g/dl. All the animals with PHP tolerated the procedure well and have survived for 1 year at sacrifice while five of the controls died within a week (p=0.004). Reductions in hematological and coagulation parameters occurred following ET and these parameters returned to the normal ranges by 4 weeks post ET. Renal function parameters (serum urea and creatinine) remained in the normal range throughout the experimental period. A transient slight increase in the hepatic enzyme SGOT was observed. Open biopsies of major organs at 2 weeks post ET showed vacuolated cells in the liver and kidneys. Normal histology was noted at and after 3 months. Oxygen transport properties as examined by arterial-venous oxygen differences, oxygen delivery and oxygen extraction showed that PHP continued to transport oxygen up to 48 hours studied post ET. PHP functioned as effectively as red blood cells at 6 hours in oxygen delivery to the tissues. PHP effectively supported life at lethal levels of anemia and is physiologically well accepted.

Arterial blood gas derived variables as estimates of intrapulmonary shunt in critically ill children.

Oxygen transport data, prospectively collected from 52 critically ill children, were analyzed to determine whether any derived variable accurately estimated intrapulmonary shunt (Qsp/Qt). Arterial hemoglobin saturation was more closely correlated with Qsp/Qt than was PaO2, alveolar-arterial oxygen gradient, arterial mixed venous oxygen difference (C[a-v]O2), arterial/alveolar oxygen ratio, and the ratio of PaO2 to inspired oxygen (FIO2) (r = 0.8, p less than .0001). When C(a-v)O2 was normal, hemoglobin saturation became a very accurate (r = 0.96) assessment of Qsp/Qt. We conclude that various arterial blood gas derived variables do not accurately reflect Qsp/Qt in critically ill children. In these patients, a pulmonary artery catheter is needed to accurately assess intrapulmonary shunt.

Cerebral oxidative metabolism in the fetal lamb: Relationship to electrocortical state

Cerebral oxidative metabolism and blood flow were measured in 14 chronically prepared fetal lambs with changes in fetal electrocortical activity. Myocardial blood flow was also measured with changes in fetal state in order to determine whether metabolic changes observed were organ specific. Samples of preductal arterial and sagittal vein blood were analyzed for oxygen content, blood gases, and pH. Blood flow was measured with a radioactive microsphere technique. Cerebral oxidative metabolism increased significantly from 126 ± 7 μmol/100 gm/min during the high-voltage electrocortical state to 152 ± 7 μmol/100 gm−1/min−1 (p < 0.05) during the low-voltage electrocortical state. The increase in cerebral oxidative metabolism was sustained by an increase in blood flow, 148 ± 7 ml/100 gm/min to 173 ± 10 ml/100 gm/min (p < 0.01), whereas the arterial venous oxygen difference remained unchanged. Changes in myocardial blood flow were in the opposite direction, with a decrease noted during the low-voltage electrocortical state, and were correlated with changes in fetal heart rate. We conclude that cerebral oxidative metabolism is increased during the fetal low-voltage electrocortical state and suggests an important role for the increased incidence of this state during the accelerated growth and development of the brain during the perinatal period.

Maximal perfusion of skeletal muscle in man.

Five subjects exercised with the knee extensor of one limb at work loads ranging from 10 to 60 W. Measurements of pulmonary oxygen uptake, heart rate, leg blood flow, blood pressure and femoral arterial-venous differences for oxygen and lactate were made between 5 and 10 min of the exercise. Flow in the femoral vein was measured using constant infusion of saline near 0 degrees C. Since a cuff was inflated just below the knee during the measurements and because the hamstrings were inactive, the measured flow represented primarily the perfusion of the knee extensors. Blood flow increased linearly with work load right up to an average value of 5.7 l min-1. Mean arterial pressure was unchanged up to a work load of 30 W, but increased thereafter from 100 to 130 mmHg. The femoral arterial-venous oxygen difference at maximum work averaged 14.6% (v/v), resulting in an oxygen uptake of 0.80 l min-1. With a mean estimated weight of the knee extensors of 2.30 kg the perfusion of maximally exercising skeletal muscle of man is thus in the order of 2.5 l kg-1 min-1, and the oxygen uptake 0.35 l kg-1 min-1. Limitations in the methods used previously to determine flow and/or the characteristics of the exercise model used may explain why earlier studies in man have failed to demonstrate the high perfusion of muscle reported here. It is concluded that muscle blood flow is closely related to the oxygen demand of the exercising muscles. The hyperaemia at low work intensities is due to vasodilatation, and an elevated mean arterial blood pressure only contributes to the linear increase in flow at high work rates. The magnitude of perfusion observed during intense exercise indicates that the vascular bed of skeletal muscle is not a limiting factor for oxygen transport.

Rest and exercise hemodynamics in pulmonary stenosis: comparison of children and adults

To better understand the hemodynamics of pulmonary stenosis (PS), 24 adults and 53 children with similar degrees of PS who had undergone cardiac catheterization at rest and during supine exercise were retrospectively studied. Three groups were defined. Group I consisted of 9 adults and 18 children with a pulmonary valve area of less tjan 0.5 cm 2/m 2; group II, 6 adults and 25 children with a pulmonary valve area of 0.5 to 1.0 cm 2/m 2; and group III, 9 adults and 10 children with pulmonary valve area of more than 1.0 cm 2/m 2. The mean ages of the adults were 29, 26 and 22 years for groups I, II, and III, respectively. The mean ages of the children were 11, 10 and 9 years for groups I, II and III, respectively. The pertinent data collected from catheterization included oxygen consumption, cardiac rate and index, arterial venous oxygen difference, stroke index, right ventricular (RV) systolic pressure and RV end-diastolic pressure. Adults and children in groups II and III had a appropriate response to exercise. Group I children responded abnormally by increasing their RV end-diastolic pressure and decreasing their stroke index. In group I adults both of these variables increased. Group I adults exhibited a significantly lower cardiac index at rest and exercise secondary to a significantly lower absolute cardiac rate. Long-standing severe PS results in hemodynamic compromise. Hence, early relief of PS is recommended.

Effects of milrinone on coronary hemodynamics and myocardial energetics in patients with congestive heart failure.

To examine the effect of milrinone on myocardial energetics in patients with congestive heart failure, we measured systemic, pulmonary, and coronary hemodynamics in 18 patients before and after intravenous administration of milrinone (125 +/- 36 micrograms/kg). There was a 45% increase in cardiac index (2.1 +/- 0.5 to 3.0 +/- 0.6 liters/min/m2; p = .0001), a 39% fall in the pulmonary capillary wedge pressure (28 +/- 8 to 17 +/- 8 mm Hg; p = .0001), and a 42% increase in left ventricular external work (3758 +/- 1419 to 5340 +/- 1598 g-m/min; p = .0001). Both the heart rate-blood pressure product (9624 +/- 2272 to 9380 +/- 2428 mm Hg-beats/min; p = NS) and regional left ventricular myocardial oxygen consumption (7.6 +/- 2.9 to 8.1 +/- 3.1 ml O2/min; p = NS) were unchanged after milrinone, resulting in a 45% increase in calculated left ventricular external efficiency (p = .004). Although myocardial oxygen consumption did not change, regional great cardiac venous blood flow increased significantly (73 +/- 32 to 85 +/- 34 ml/min; p = .02) as a result of a 30% reduction in regional coronary vascular resistance (1.32 +/- 0.99 to 0.93 +/- 0.54 mm Hg-min/ml; p = .004), a decrease comparable to the concurrent 37% and 38% falls seen in systemic and pulmonary vascular resistance, respectively. These changes were associated with an 11% fall in the transcoronary arterial-venous oxygen difference (111 +/- 24 to 99 +/- 21 ml/O2/liter; p = .0001), which is consistent with a primary coronary vasodilator effect of milrinone.(ABSTRACT TRUNCATED AT 250 WORDS)

Dobutamine and hydralazine: Comparative influences of positive inotropy and vasodilation on coronary blood flow and myocardial energetics in nonischemic congestive heart failure

Coronary blood flow and myocardial energetics were assessed after the administration of a parenteral inotrope (dobutamine hydrochloride) and an oral vasodilator agent (hydralazine) in 10 patients with nonischemic congestive heart failure. Dobutamine (5 micrograms/kg per min) and hydralazine (1 mg/kg) when group-matched elicited an identical increase in cardiac index and stroke volume index. Both agents augmented coronary blood flow while reducing coronary vascular resistance. Both forms of therapy elicited a significant increase in myocardial oxygen consumption. Dobutamine, demonstrating a balanced effect on the coronary circulation, induced a proportional increase in coronary blood flow and myocardial oxygen consumption, with the arterial-venous oxygen difference across the coronary vascular bed remaining unchanged. Hydralazine enhanced the myocardial oxygen supply versus demand ratio; despite a significant increase in myocardial oxygen consumption, the arterial-venous oxygen difference and the myocardial extraction ratio diminished. Both forms of therapy enhanced cardiac performance without inducing any electrocardiographic or clinical evidence of ischemia. Dobutamine, a positive inotropic agent, elicited a balanced effect on the coronary circulation while hydralazine, a vasodilator agent, induced a greater increase in coronary flow than in myocardial oxygen demand.

Adaptive cardiovascular modifications in the western chipmunks genusEutamias

Metabolic and cardiovascular parameters were studied in four western chipmunks, genusEutamias, to elucidate the mechanisms underlying the maintenance of normal aerobic metabolism while the heart rate were profoundly depressed (Jones and Wang, 1976). It was postulated that cardiovascular adaptations involving either an increase of stroke volume and/or an increase of arterial-venous oxygen difference (A-V O2) must have evolved to account for such alterations (Jones and Wang, 1976). Simultaneous measurements of O2 consumption, heart rate and A-V O2 were made in anesthetized animals at thermal neutral temperature of 25°C. The mean cardiac output ranged between 16.2–23.5 ml/min, and the calculated stroke volume was between 0.032–0.057 ml/beat, not atypical for similar sized mammals (Table 1). Measurements of heart weight as an indirect indicator for stroke volume also indicated normal stroke volume in the chipmunks (Table 2). The mean A-V O2, on the other hand, was between 5.6–10.4 vol % (Table 1), comparatively greater than the 4–6 vol % typical of resting mammals. The measured hematocrit, hemoglobin concentration, red blood cell counts, and blood volume, were within the range of values for similar sized mammals (Table 3), suggesting normal O2 capacity as well as O2 content carried in blood. Taken together, it was concluded that the major cardiovascular modification in the chipmunks while accomplishing normal aerobic metabolism under profoundly depressed heart rates is by the increased ability to extract O2 across the capillary beds. Possible mechanisms relating to this adaptation are discussed.

Redistribution of cardiac output in response to heating in Iguana iguana

1. 1. In Iguana iguana and Tupinambis nigropunctatus heating resulted in lower arterial-venous oxygen differences than were seen in controls at a similar temperature. Oxygen pulse values changed in a similar manner. 2. 2. Ventricular systemic output increased as much as 2.3 times during heatigg when compared with values during non-heating, control conditions. 3. 3. In three iguanas right-to-left shunting or bypassing the pulmonary circuit in response to heating averaged 20.3 per cent of ventricular systemic output. In one tegu it averaged 8.3 per cent. 4. 4. Increased heart rate with sustained, increased or decreased stroke volume was responsible for the increase in observed ventricular output under conditions of heating.

HIGH-PRESSURE OXYGEN AS AN ADJUNCT IN EXPERIMENTAL BACTEREMIC SHOCK.

Septic shock is a syndrome resulting from sepsis, usually gram-negative bacilli invading the blood stream. It is the result of a complex interaction between host and parasite. The mortality in this syndrome is high and any adjunct which may directly benefit the host or discourage the bacteria might be of eventual clinical value. High-pressure oxygen (OHP) has reduced the mortality in a modified Fine hemorrhagic shock preparation from 70% to 20%, presumably by making more oxygen available to the tissues through physical solution in water. 1 In a bacteremic shock preparation utilizing canine fecal peritonitis, OHP merely delayed the onset of some of the biochemical harbingers of severe shock, such as an increasing arterial-venous oxygen difference. 2 The following study was developed to further investigate the possible role of OHP in septic shock with emphasis on the known effects on aerobic-facultative anaerobic gram-negative bacteria. 3-7 Materials and Methods In Vitro

Effect of bilateral cervical vagotomy in the dog.

Dogs subjected to bilateral cervical vagotomy were maintained by daily infusions of physiological saline and glucose for several weeks and a few animals survived for periods of more than 1 month. The success of this procedure is interpreted as evidence of water and electrolyte changes being major factors in the usual early demise of vagotimized animals. Cardiac outputs were decreased progressively after vagotomy resultant to increased arterial venous oxygen differences. Only slight additional alterations in the hemodynamic picture were noted as these animals survived the acute reactions to cervical vagotomy.

Effect of hypothermia of 2 to 24 hours on oxygen consumption and cardiac output in the dog.

The changes occurring in cardiac output and oxygen consumption in short periods of hypothermia are the same when either ether or pentobarbital sodium is used as the anesthetic agent during the induction of hypothermia. Following an initial decrease in oxygen consumption, no further change occurred as long as the body temperature was maintained at a constant level. Cardiac output, arterial-venous oxygen difference, and coefficient of oxygen utilization remain unchanged for longer periods of time than most physiologic parameters studied during prolonged hypothermia at constant temperatures. After about 14 hours they also begin to alter so that by 24 hours the changes are profound. Stagnant anoxemia and marked increased in the coefficient of O2 utilization resulting from the markedly lowered cardiac output, which was 5% of the precooled controls, occurred.

Effect of therapeutic doses of ephedrine on renal clearances in normal man.

SummaryEphedrine in therapeutic doses (35 to 75 mg) administered intramuscularly to 7 subjects and intravenously to one failed to cause any consistent or significant change in renal plasma flow, filtration rate, PAH extraction ratio, or renal arterial—venous oxygen difference, despite an increase in mean blood pressure and pulse rate. These results are in agreement with the conclusion of Chasis, Goldring, and Smith(l) that, in marked contrast to adrenaline, ephedrine in therapeutic doses has no or a negligible effect on the renal circulation.

Physiologic studies in mitral valvular disease.

Physiologic findings obtained by cardiac catheterization on 29 patients with mitral valvular disease are discussed. Cardiac outputs, intracardiac pulmonary arterial and pulmonary pressures are determined during rest and exercise. It is shown that the resting cardiac output is reduced in all patients with mitral disease and that exercise results either in a fall or a small increase in the minute volume of circulation. The pulmonary artery and capillary pressures are elevated with rest and rise further with exercise. A clear differentiation by physiologic means between mitral stenosis and mitral insufficiency is difficult. However, in patients with mitral insufficiency the resting cardiac output is lower, the arterial venous oxygen difference is higher and exercise causes a greater fall in the cardiac output. A comparison is made between the physiologic manifestations of mitral disease and myocardial failure: the residual volume of blood of the right ventricle is usually increased in patients with mitral disease and failure and in myocardial failure alone. However, the right ventricular residual volume is normal in mitral disease without evidence of myocardial failure. The pulmonary vascular resistance in mitral disease is usually elevated. It is demonstrated that in a number of patients the pulmonary vascular resistance is not fixed since it decreases during exercise or following valvulotomy of the mitral valve.