Exercise, dobutamine, and combined atropine, norepinephrine, and epinephrine compared

1985 ◽  
Vol 58 (6) ◽  
pp. 2047-2053 ◽  
Author(s):  
G. C. Haidet ◽  
T. I. Musch ◽  
G. A. Ordway ◽  
J. H. Mitchell

We compared the cardiovascular effects evoked in conscious dogs by 1) submaximal exercise; 2) infusion of dobutamine (40 micrograms X kg-1 X min-1); and 3) infusion of a combination of atropine (0.15 mg/kg), norepinephrine (0.19 micrograms X kg-1 X min-1), and epinephrine (0.05 micrograms X kg-1 X min-1). Myocardial O2 demand, as estimated by the double product (heart rate X systolic blood pressure), was similar during all three interventions. Cardiac output and heart rate increased significantly (P less than 0.05) during each of the three interventions. Arteriovenous O2 difference and total body O2 consumption, however, increased only during submaximal exercise. Although myocardial blood flow increased similarly during each of the three interventions, blood flow to skeletal muscle and the tongue increased only during exercise. Exercise and the combined infusion of atropine, norepinephrine, and epinephrine produced similar increases in blood flow to the diaphragm and similar decreases in blood flow to the stomach. These changes in blood flow were associated with appropriate changes in vascular resistance. Additionally, blood flow to the brain, kidney, adrenal glands, liver, and intestine did not change during any of the three interventions. Thus, in dogs, submaximal exercise, infusion of dobutamine, and infusion of a combination of atropine, norepinephrine, and epinephrine to evoke a given level of estimated myocardial O2 consumption produce similar increases in cardiac output, heart rate, and myocardial blood flow. In contrast, the changes in total body O2 consumption, arteriovenous O2 difference, regional blood flow, and regional vascular resistance that occur during each of these three interventions are different.

1989 ◽  
Vol 256 (6) ◽  
pp. H1651-H1658
Author(s):  
C. L. Rosen ◽  
A. Cote ◽  
G. G. Haddad

To investigate the effects of enkephalins on cardiac output and regional blood flow, we administered D-Ala-D-Leu-enkephalin (DADLE) intracisternally (ic) to 14 chronically instrumented unanesthetized dogs. Measurements were made at base line, 20, 45, and 75 min after DADLE (25 or 125 micrograms/kg) and 15 min after naloxone (5 micrograms/kg ic). After 125 micrograms/kg DADLE, all animals developed hypoventilation, bradycardia, and decreased O2 consumption without hypotension. Cardiac output decreased (-34%), but brain blood flow increased (+110%). Blood flow decreased to the diaphragm (-38%), heart (-21%), skeletal muscle (-40%), skin (-67%), pancreas (-79%), and gastrointestinal tract (-26%). After 25 micrograms/kg DADLE, there were no consistent changes in cardiac output or regional blood flow. Four additional animals (without DADLE) were exposed to altered inspired gases to reproduce the blood gas changes after DADLE. These animals developed hyperventilation without bradycardia and increased brain (+114%) and diaphragm (+649%) blood flow. We conclude that centrally administered enkephalins produce 1) a parallel decrease in ventilation, heart rate, O2 consumption, and cardiac output and 2) a major blood flow redistribution, primarily dictated by the effects of opioids on ventilation, heart rate, and metabolism.


1991 ◽  
Vol 70 (3) ◽  
pp. 1129-1136 ◽  
Author(s):  
E. E. Wolfel ◽  
B. M. Groves ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. S. Mazzeo ◽  
...  

Arterial O2 delivery during short-term submaximal exercise falls on arrival at high altitude but thereafter remains constant. As arterial O2 content increases with acclimatization, blood flow falls. We evaluated several factors that could influence O2 delivery during more prolonged submaximal exercise after acclimatization at 4,300 m. Seven men (23 +/- 2 yr) performed 45 min of steady-state submaximal exercise at sea level (barometric pressure 751 Torr), on acute ascent to 4,300 m (barometric pressure 463 Torr), and after 21 days of residence at altitude. The O2 uptake (VO2) was constant during exercise, 51 +/- 1% of maximal VO2 at sea level, and 65 +/- 2% VO2 at 4,300 m. After acclimatization, exercise cardiac output decreased 25 +/- 3% compared with arrival and leg blood flow decreased 18 +/- 3% (P less than 0.05), with no change in the percentage of cardiac output to the leg. Hemoglobin concentration and arterial O2 saturation increased, but total body and leg O2 delivery remained unchanged. After acclimatization, a reduction in plasma volume was offset by an increase in erythrocyte volume, and total blood volume did not change. Mean systemic arterial pressure, systemic vascular resistance, and leg vascular resistance were all greater after acclimatization (P less than 0.05). Mean plasma norepinephrine levels also increased during exercise in a parallel fashion with increased vascular resistance. Thus we conclude that both total body and leg O2 delivery decrease after arrival at 4,300 m and remain unchanged with acclimatization as a result of a parallel fall in both cardiac output and leg blood flow and an increase in arterial O2 content.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 257 (1) ◽  
pp. H25-H32 ◽  
Author(s):  
A. L. Siren ◽  
G. Feuerstein

The effect of intravenous injections (0.1–3 nmol/kg) of platelet-activating factor (PAF) on blood pressure, heart rate, cardiac output, and blood flow (hindquarter, renal, mesenteric) were studied in conscious rats. PAF decreased blood pressure and total peripheral resistance (TPR) but increased heart rate; cardiac output was reduced by the highest dose. Low doses of PAF increased blood flow and decreased vascular resistance in all vascular beds, whereas high doses reduced mesenteric blood flow in part by increasing mesenteric vascular resistance. The hypotensive and cardiac effects of PAF were blocked by intravenous infusions of the selective PAF-receptor antagonists, 15 mg/kg BN 52021 and 1 mg/kg SDZ 63–441. BN 52021 also attenuated the hindquarter and renal responses to PAF, but the mesenteric responses remained relatively unchanged. The results indicate that PAF is a potent vasodilator of mesenteric greater than hindquarter = renal vessels at low doses and a cardiac depressant at high doses. A therapeutic role for the PAF antagonists BN 52021 and SDZ 63–441 is suggested in endotoxemia, anaphylaxis, and other disease states in which increased release of PAF contributes to key hemodynamic derangements.


1985 ◽  
Vol 59 (1) ◽  
pp. 183-189 ◽  
Author(s):  
T. I. Musch ◽  
G. C. Haidet ◽  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8–12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.


1981 ◽  
Vol 51 (2) ◽  
pp. 447-451 ◽  
Author(s):  
J. M. Hagberg ◽  
J. P. Mullin ◽  
M. D. Giese ◽  
E. Spitznagel

This investigation was undertaken to determine the effect of pedal frequency on submaximal exercise responses. Seven well-trained competitive cyclists were studied riding their road-racing bicycles on a motor-driven treadmill at 80% of maximum O2 consumption (VO2 max) using different gear ratios. Cyclists were also studied during a series of unloaded trials to assess the effects of varying rates of limb movements independent of external work load. Heart rate (HR) increased, whereas net HR (after subtracting the HR during unloaded cycling) decreased with increasing pedal frequency during loaded cycling. Expiratory flow (VE), O2 consumption (VO2), blood lactate, net VO2 (after subtracting the VO2 of unloaded cycling), and net VE (after subtracting the VE during unloaded cycling) were quadratically related to pedal frequency. The quadratic relationships evident after corrections were made for the additional work needed to move the legs more frequently may be explained at the lower pedaling rates by a less uniform pattern of blood flow caused by increasing the force requirement per pedal stroke and, at the higher pedal frequencies, by the recruitment of additional musculature to stabilize the trunk. The average of preferred frequency for the group, which was also the most economical pedaling rate judged by most of the variables was 91 rpm, although the preferred pedaling rate for each subject ranged from 72 to 102 rpm.


1986 ◽  
Vol 61 (6) ◽  
pp. 2012-2017 ◽  
Author(s):  
N. Imai ◽  
J. I. Paley ◽  
H. S. Barold ◽  
C. S. Liang

To determine whether the increase in cardiac output during mild to moderate exercise is related to an increase in the tissue redox potential, we compared the responses of cardiac output, total body oxygen consumption, and arterial blood lactate-to-pyruvate ratio (a measure of NADH/NAD) to treadmill exercise between dogs treated with normal saline and those treated with a hydrogen acceptor, new methylene blue. Normal saline was infused into the left atrium in the first group of dogs at a rate of 0.38 ml/min throughout the treadmill exercise (2.5 mph and 5.0 mph on a 6% incline, each for 20 min). In the second group, methylene blue was administered as a loading dose (4 mg/kg) before exercise, followed by a continuous infusion (0.15 mg X kg-1 X min-1) throughout exercise. A similar infusion of methylene blue was given to a third group of dogs without exercise; it reduced the arterial lactate-to-pyruvate ratio from 6.70 +/- 0.35 to 4.12 +/- 0.27 but had no or little effects on cardiac output, heart rate, arterial pressure, and left ventricular dP/dt and (dP/dt)/P. Treadmill exercise doubled cardiac output and increased total body O2 consumption three- to fourfold in the first two groups but increased arterial blood lactate-to-pyruvate ratio only in group 1 (6.0 +/- 0.54 to 9.97 +/- 0.91). The relationship between cardiac output and total body O2 consumption was unaffected by the simultaneous administration of methylene blue during exercise. Groups 1 and 2 also did not differ in their heart rate, left ventricular dP/dt and (dP/dt)/P, and plasma catecholamine responses to exercise.(ABSTRACT TRUNCATED AT 250 WORDS)


2007 ◽  
Vol 292 (5) ◽  
pp. E1401-E1409 ◽  
Author(s):  
Emma O'Donnell ◽  
Paula J. Harvey ◽  
Jack M. Goodman ◽  
Mary Jane De Souza

The cardiovascular consequences of hypoestrogenism in premenopausal women are unclear. Accordingly, the influence of menstrual status and endogenous estrogen (E2) exposure on blood pressure (BP), heart rate (HR), and calf blood flow in young (18–35 yr) regularly exercising premenopausal women with exercise-associated menstrual aberrations was investigated. Across consecutive menstrual cycles, daily urinary ovarian steroid levels were analyzed, and the area under the curve was calculated to determine menstrual status and E2exposure. BP, HR, blood flow, vascular conductance, and resistance were measured at baseline and following ischemic calf exercise. Exercising subjects consisted of 14 ovulatory (ExOv), 10 short-term (anovulatory and ≤100 days amenorrhea; ST-E2Def), and 8 long-term (>100 days amenorrhea; LT-E2Def) E2-deficient women. Nine sedentary ovulatory subjects (SedOv) were also studied. All groups were similar in age (24.8 ± 0.7 yr), height (164.8 ± 1.3 cm), weight (57.9 ± 0.9 kg), and body mass index (21.3 ± 0.3 kg/m2). E2-deficient groups had lower ( P < 0.002) E2exposure compared with ovulatory groups. Resting systolic BP, HR, blood flow, and vascular conductance were lower ( P < 0.05) and vascular resistance higher ( P < 0.05) in LT-E2Def compared with both ovulatory groups. Peak ischemic blood flow, vascular conductance, and HR were also lower ( P < 0.05) and vascular resistance higher ( P < 0.05) in LT-E2Def compared with all other groups. Our findings show that exercising women with long-term E2deficiency have impaired regional blood flow and lower systolic BP and HR compared with exercising and sedentary ovulatory women. These cardiovascular alterations represent markers of altered vascular function and autonomic regulation of which the long-term effects remain unknown.


1976 ◽  
Vol 40 (2) ◽  
pp. 191-195 ◽  
Author(s):  
D. L. Foreman ◽  
M. Sanders ◽  
C. M. Bloor

To determine the influence of exercise on cerebral blood flow, we ran 14 swine at 3–6 mph and at 0–10% grades on a treadmill for 30 min at moderate and severe levels of exercise. Measuring heart rate, cardiac output, and aortic pressure via implanted probes, we injected 15-mum radiolabeled microspheres via the left atrium before and during exercise. We measured their distribution by gamma spectrometry, determining total cerebral blood flow, regional blood flow, and ratio of flow to gray and white matter. Heart rate, cardiac output, and aortic pressure rose progressively with increasing exercise. Total cerebral flow resembled that reported in humans, i.e., it did not change significantly with exercise. Regional flow distribution also failed to change significantly with exercise. The ratio of gray to white matter flow did not change except to the cerebellum where it rose significantly from resting values at both moderate and severe exercise. Gray matter received more flow than white matter during all three conditions of observation. Cerebral blood flow was remarkably constant during even severe exercise.


1993 ◽  
Vol 74 (1) ◽  
pp. 147-152 ◽  
Author(s):  
C. Duggal ◽  
M. H. Weil ◽  
R. J. Gazmuri ◽  
W. Tang ◽  
S. Sun ◽  
...  

Quantitative measurement of regional blood flow during cardiac arrest and resuscitation has been confined to large animals. We report on a rodent model utilizing radioactive microspheres during cardiac arrest and resuscitation for investigation of regional blood flow. Ventricular fibrillation was electrically induced in 10 pentobarbital-anesthetized Sprague-Dawley rats. Resuscitation was attempted by precordial compression followed by external direct current countershock. During precordial compression, cardiac output corresponded to 12% of prearrest flow. Similarly low flows were observed in the myocardium and brain. However, much lower flows were observed in the adrenal glands, kidneys, intra-abdominal viscera, skin, and skeletal muscle. Five of ten animals were successfully resuscitated. During precordial compression, resuscitated animals had significantly higher cardiac output (13.1 +/- 4.1 vs. 8.6 +/- 1.46 ml/min), myocardial blood flow (0.70 +/- 0.24 vs. 0.22 +/- 0.15 ml.min-1.g-1), cerebral blood flow (0.17 +/- 0.04 vs. 0.06 +/- 0.02 ml.min-1.g-1), and adrenal blood flow (1.09 +/- 0.60 vs. 0.27 +/- 0.16 ml.min-1.g-1). Thirty minutes after successful resuscitation, cardiac output and myocardial, cerebral, renal, and adrenal blood flows and blood flow to splanchnic viscera (with the exception of the spleen) had returned to > or = 70% of prearrest flows. These studies confirm the conclusion of earlier investigations in larger animals that visceral blood flow during cardiac arrest and precordial compression is preferentially distributed to the brain and myocardium. Successful cardiac resuscitation is contingent on threshold levels of myocardial blood flow that exceed 0.4 ml.min-1.g-1.


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