Regional plasma catecholamine removal and release at rest and exercise in dogs

1988 ◽  
Vol 254 (4) ◽  
pp. R663-R672
Author(s):  
F. Peronnet ◽  
L. Beliveau ◽  
G. Boudreau ◽  
F. Trudeau ◽  
G. Brisson ◽  
...  

Dynamics of circulating catecholamines (CA) were studied at rest (heart rate = 104 +/- 3 beats/min) and during mild treadmill exercise (heart rate = 168 +/- 5 beats/min) in 60 dogs. Plasma epinephrine (E) and norepinephrine (NE) removal from circulation and release into circulation were estimated from plasma CA arteriovenous differences across the regional vascular beds studied (pulmonary, myocardial, hepatosplanchnic, renal, and skeletal muscle vascular beds) and from regional blood flows. Regional plasma E fractional extraction (PEFE) was used as an index of NE removal from plasma. Arterial plasma CA increased significantly from rest to exercise (P less than 0.05). A significant PEFE was observed at rest and exercise across all studied vascular beds but the pulmonary bed. When plasma flow was taken into account, the largest contributors to plasma CA removal were the hepatosplanchnic vascular bed at rest and skeletal muscle vascular beds during exercise. At rest, the hepatosplanchnic vascular bed was a major contributor to the plasma NE pool. During exercise, main contributors to NE release into plasma were skeletal muscle vascular beds. Circulating CA kinetics did not appear to vary from rest to exercise. Clearance and apparent distribution space were estimated to be, respectively, 1.5 l/min and 2 liters for circulating E and 2 l/min and 5 liters for NE at rest and exercise. Circulating E and NE half times were estimated to be approximately 1 and 1.8 min, respectively.

1980 ◽  
Vol 58 (4) ◽  
pp. 411-415 ◽  
Author(s):  
U. Ackermann ◽  
A. T. Veress

Radioactively labelled microspheres (15 μm diameter) were used to measure cardiac output (CO) distribution and blood flows in spleen, kidneys, and skeletal muscle before and after normovolemic anemia or polycythemia in anesthetized rats. Hematocrits were changed from 45 to 33% or from 45 to 59% by an exchange transfusion of homologous plasma or packed cells. Anemia was accompanied by a 39% increase in CO while polycythemia showed a 25% decrease. Following hemodilution the spleen as well as skeletal muscle received greater than normal fractions of CO and in each the flow increase was greater than expected from the fall in viscosity. The renal fraction of CO was unchanged. Following hemoconcentration "greater-than-normal" fractions of CO were distributed towards spleen and kidney. In these tissues the changes in flow were significantly greater than the change in resistance due to viscosity. Skeletal muscle flow changes appeared to have been due mostly to increased viscosity. These observations imply that during acute, isovolemic changes in hematocrit, the flow changes of individual vascular beds cannot be explained by viscosity changes alone but the importance of nervous control or of local metabolic factors remains to be investigated.


1985 ◽  
Vol 249 (3) ◽  
pp. H485-H491 ◽  
Author(s):  
R. F. Tuma ◽  
G. L. Irion ◽  
U. S. Vasthare ◽  
L. A. Heinel

The purpose of this investigation was to characterize the changes in regional blood flow and central hemodynamic measures that occur in the rat as a result of the aging process. The isotope-labeled microsphere technique was used to measure cardiac output and regional blood flows in conscious and anesthetized adult (12 mo) and senescent (24 mo) Fischer 344 virgin female rats. No significant changes were observed in central hemodynamic measurements or regional blood flows in conscious rats with the exception of a 25% reduction in splenic blood flow. Pentobarbital anesthesia significantly reduced cardiac index and heart rate but elevated total peripheral resistance and mean arterial blood pressure. There was a decrease in blood flow to skeletal muscle, spleen, duodenum, stomach, and brain tissue samples and increased hepatic arterial blood flow in both age groups. The use of anesthesia caused a greater reduction in the cardiac index and brain blood flow in the senescent anesthetized rats than in the adult rats. Heart and kidney blood flows were decreased by anesthesia in the senescent rats but not in the adult rats. Skeletal muscle blood flow, however, was significantly greater in the senescent anesthetized rats than in the younger anesthetized animals. Although body weight and organ weights of the liver, spleen, kidneys, stomach, heart, and brain were significantly greater for the senescent rats, no differences could be demonstrated in tibial length or lean body mass.


1982 ◽  
Vol 243 (5) ◽  
pp. H830-H836 ◽  
Author(s):  
R. J. Ferguson ◽  
A. W. Taylor ◽  
P. Cote ◽  
J. Charlebois ◽  
Y. Dinelle ◽  
...  

Cardiovascular and skeletal muscle adaptations were studied before and after 6 mo of physical training in patients with coronary artery disease and exertional angina pectoris. Symptom-limited exercise capacity increased by 41% (470 +/- 30 to 665 +/- 35 kg.m.min-1; n = 29, P less than 0.001) with training as did skeletal muscle succinate dehydrogenase activity (1.75 +/- 0.24 to 3.31 +/- 0.24 IU; n = 23, P less than 0.001) and the areas of muscle fibers (type I from 43.6 +/- 3.3 to 54.4 +/- 3.3 micrometers 2 X 10(2); n = 21, P less than 0.05 and type II from 43.9 +/- 2.4 to 57.2 +/- 5.1 micrometers 2 X 10(2); P less than 0.01). At the same submaximal exercise intensity (mean 355 +/- 100 km.m.min-1), plasma catecholamines (1.31 +/- 0.14 to 1.07 +/- 0.09 ng.ml-1; n = 13, P less than 0.05), heart rate (115 +/- 3 to 97 +/- 3 beats/min; n = 29, P less than 0.001), and systolic blood pressure (171 +/- 4 to 143 +2- 4 mmHg; n = 29, P less than 0.001) were significantly reduced after training. Maximal coronary sinus blood flow (192 +/- 10 to 208 +/- 9 ml.min-1; n = 29, P less than 0.05) and left ventricular oxygen consumption (23.2 +/- 1.5 to 25.8 +/- 1.6 ml.min-1; n = 24, P less than 0.05) were increased by 8 and 11%, respectively, after training. The improvement in exercise capacity with training in patients with exercise is secondary to a reduction in myocardial oxygen requirements during subangina levels of exercise and partly to a small increase in maximal myocardial oxygen consumption. The skeletal muscle adaptations with training were not related to other indices of training such as the reduced exercise heart rate or increased symptom-limited exercise capacity.


1980 ◽  
Vol 59 (s6) ◽  
pp. 355s-356s ◽  
Author(s):  
J. F. Liard

1. Mean arterial pressure, cardiac output (electromagnetic flow-meter) and regional blood flows (15 μm radioactive microspheres) were measured repeatedly in eight dogs receiving a salt and water load after renal mass reduction as well as in six control animals. 2. As previously observed, hypertension developed in the salt-loaded dogs with an initial increase in cardiac output followed by a secondary rise in total peripheral resistance. 3. Much of the early increase in cardiac output was distributed to the skeletal muscle vascular bed. 4. Total peripheral resistance changes did not reflect the resistance of individual vascular beds in the early stages of salt and water load hypertension; indeed, resistance in the muscle vascular bed was decreased and that in the splanchnic area and the bone increased on the first day of salt and water load when total peripheral resistance was unchanged.


1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.


1995 ◽  
Vol 79 (4) ◽  
pp. 1255-1259 ◽  
Author(s):  
E. Weitzberg ◽  
A. Hemsen ◽  
J. M. Lundberg ◽  
G. Ahlborg

To investigate splanchnic and renal vascular effects and elimination of endothelin-3 (ET-3), ET-3 (10 pmol.kg-1.min-1 iv for 20 min) was given to six healthy male volunteers. Arterial plasma ET-3-like immunoreactivity (ET-3-Li) increased 10-fold to 111 +/- 31 pmol/l (P < 0.01). The initial half-life of plasma ET-3-Li determined in three subjects was 1.7 +/- 0.2 min. The fractional extraction of ET-3-Li was 68 +/- 7% in the splanchnic and 63 +/- 4% in the renal vascular beds. Mean arterial blood pressure fell from 86 +/- 4 to 94 +/- 4 mmHg (10%) (P < 0.05). Splanchnic and renal blood flows fell by 43 +/- 3% (P < 0.05) and 29 +/- 4% (P < 0.05), respectively, during the infusion. Splanchnic and renal vascular resistances rose by 92 +/- 22% (P < 0.05) and 58 +/- 7% (P < 0.05). In conclusion, ET-3 infusion in humans induces splanchnic and renal vasoconstriction of similar magnitude as previously shown during endothelin-1 infusion, presumably by ETB receptor activation. Plasma ET-3 is efficiently extracted in the splanchnic and renal vascular regions.


1997 ◽  
Vol 82 (4) ◽  
pp. 1237-1243 ◽  
Author(s):  
Mitsuru Saito ◽  
Ryoko Sone ◽  
Masao Ikeda ◽  
Tadaaki Mano

Saito, Mitsuru, Ryoko Sone, Masao Ikeda, and Tadaaki Mano.Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise. J. Appl. Physiol. 82(4): 1237 – 1243, 1997.—To investigate the effects of exercise duration on muscle sympathetic nerve activity (MSNA), heart rate, blood pressure (BP), tympanic temperature, blood lactate concentration, and thigh electromyogram were measured in eight volunteers during 30 min of cycling in the sitting position at an intensity of 40% of maximal oxygen uptake. MSNA burst frequency increased 18 min after exercise was begun (25 ± 4 bursts/min at baseline and 36 ± 5 bursts/min at 21 min of exercise), reaching 41 ± 5 bursts/min at the end of exercise. Heart rate and systolic BP increased during exercise. Twenty minutes after commencement of exercise, however, both systolic and diastolic BP values tended to drop compared with the initial period of exercise. Tympanic temperature increased in a time-dependent manner, and the increment was significant 12 min after exercise was begun. Blood lactate concentration and integrated electromyogram showed no significant changes during exercise. The increased MSNA during prolonged light-intensity exercise may be a secondary effect of the drop in BP as a result of blood redistribution caused by thermoregulation rather than by metaboreflex.


1963 ◽  
Vol 204 (6) ◽  
pp. 1145-1150 ◽  
Author(s):  
David G. Reynolds ◽  
Charles J. Imig

The effect of sympathectomy on the vascular bed of the dog was studied by analyzing segmental resistance changes occurring in response to intra-arterial injections of epinephrine and norepinephrine. The results indicate that the increase in total vascular bed reactivity is caused by sensitization of only the small vessel and venous segments. In an attempt to test the possibility that vascular smooth muscle develops supersensitivity in a manner similar to that which causes skeletal muscle supersensitivity, experiments were done on dogs which received intravenous injections of norepinephrine (0.5 µg/kg) every 8 hr for 2 weeks following sympathectomy. This procedure resulted in an increase in sensitivity of the arterial and venous segments in both the control and sympathectomized legs. Since this behavior was seen in both the denervated and innervated vascular beds no definite conclusions could be reached.


Drugs ◽  
1985 ◽  
Vol 29 (Supplement 2) ◽  
pp. 154-164 ◽  
Author(s):  
A. Ross Lorimer ◽  
Howard M. McAlpine ◽  
Alan P. Rae ◽  
Ian A. Simpson ◽  
Maureen P. Barbour ◽  
...  

1996 ◽  
Vol 84 (3) ◽  
pp. 596-604 ◽  
Author(s):  
Russell D. Wada ◽  
Hideyoshi Harashima ◽  
William F. Ebling ◽  
Eileen W. Osaki ◽  
Donald R. Stanski

Background The goal of this investigation was to characterize the effects of thiopental on cardia output and regional blood flows in the rat. Blood flows influence thiopental pharmacokinetics. Acquisition of these data may ultimately permit evaluation of the contribution of thiopental-induced alterations in regional blood flows to the disposition and hypnotic effect of this drug. Methods Chronically instrumented unrestrained Wistar rats (n=20) aged 3-4 months received either a dose of thiopental sufficient to induce a brief period of unconsciousness (20 mg.kg(-1)) or a larger dose achieving electroencephalographic burst suppression (45 mg.kg(-1)). Cardiac output and blood flows to 14 tissues were determined at 4 times in each rat for a period of 420 min using injections of radioactive microspheres (expressed as mean +/- SD). Mean arterial pressure, heart rate, and blood gas tensions were determined at all measurement times. Arterial plasma concentrations were sampled at postinfusion times. Results No important changes in systemic cardiovascular measurements were detected after the smaller dose of thiopental. One minute after the larger dose, cardiac output decreased from baseline (123 +/- 14 to 84 +/- ml.min (-1), P&lt; 0.01), flow to muscle and fat decreased, and muscle and fat resistance increased. At 5 min, compared to baseline, no difference in cardiac output was detected (123 +/- vs. 119 +/- ml.min (-1)), intestinal flows increased and intestinal resistances decreased. Cardiac output was again depressed at 30, 90, and 180 min. Brain blood flow decreased 25 +/- 19 % (P&lt; 0.01) from baseline for the duration of the study. Conclusions Thiopental acutely decreases cardiac output, and blood flows to muscle and fat tissue. The temporary return of cardiac output to baseline may be related to intestinal vasodilation. These blood flow alterations may influence the pharmacokinetics of thiopental.


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