O2 consumption during exercise in dogs--roles of splenic contraction and alpha-adrenergic vasoconstriction

1986 ◽  
Vol 251 (3) ◽  
pp. H502-H509 ◽  
Author(s):  
J. C. Longhurst ◽  
T. I. Musch ◽  
G. A. Ordway
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptor ◽  
Maximal Exercise ◽  
Adrenergic Blockade ◽  
Receptor Blockade ◽  
O2 Consumption ◽  
Alpha Adrenergic Receptor ◽  
O2 Extraction ◽  
Adrenergic Receptor Blockade

To examine the influence of alpha-adrenergic vasoconstriction on the aerobic capacity of dogs, we calculated O2 consumption (VO2) by the Fick method during submaximal and maximal exertion before and during alpha-adrenergic blockade with phentolamine. Regional blood flow was measured with radioactive microspheres. alpha-Adrenergic receptor blockade reduced VO2 by 12.9% during submaximal and 17.9% during maximal exercise. Arterial and venous lactic acid approximately doubled during both levels of stress in the presence of alpha-adrenergic receptor blockade. Calculated VO2 decreased because arteriovenous O2 (A-V)O2 extraction was reduced by 11.6% during submaximal exercise. During maximal exercise a 16.7% decrease in (A-V)O2 extraction and a 5.7% decrease in cardiac output contributed to the decrease in maximal VO2. During both levels of stress, (A-V)O2 extraction was reduced because arterial O2 content was decreased. Since circulating hematocrits during exercise were reduced by alpha-adrenergic receptor blockade (43-38%), we postulate that splenic contraction likely was inhibited. Additionally, distribution of blood flow to skeletal muscle and visceral organs was unaltered by alpha-blockade. To examine the importance of splenic contraction during maximal exercise, we examined hemodynamic and metabolic responses before and after splenectomy. Compared with the spleen-intact condition, splenectomized dogs demonstrated a 12.6% reduction in VO2 as a result of 7.7 and 5.5% reductions in (A-V)O2 extraction and cardiac output, respectively. (A-V)O2 extraction was reduced because arterial O2 content and circulating hematocrit during exercise were decreased. Therefore, in the exercising dog, alpha-adrenergic receptor blockade reduces O2 consumption and causes a shift to anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of heat stress on vascular capacitance

1994 ◽  
Vol 266 (5) ◽  
pp. H2122-H2129 ◽  
Author(s):  
A. Deschamps ◽  
S. Magder
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heat Stress ◽  
Blood Volume ◽  
Adrenergic Receptor ◽  
Venous Return ◽  
Receptor Blockade ◽  
Ganglionic Blockade ◽  
Unstressed Volume ◽  
Adrenergic Receptor Blockade

In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core temperatures. We repeated the measurements at high core temperatures with ganglionic blockade, alpha-adrenergic receptor blockade, or beta-adrenergic receptor blockade to determine the efferent neurohumoral pathway. When core temperature was increased from 37.8 +/- 0.2 to 41.9 +/- 0.1 degrees C, total splanchnic blood volume decreased 23% (4.6 +/- 1.4 ml/kg) and splanchnic unstressed volume decreased 38.5%. None of the other determinants of venous return changed. Ganglionic blockade shifted the total and unstressed splanchnic blood volume during heat stress back to normothermic values. However, beta- and alpha-blockade did not affect splanchnic volumes. We conclude that a decrease in splanchnic unstressed volume is an important factor for the increased venous return during heat stress. Although mediated through sympathetic ganglions, this decrease is not abolished by alpha- or beta-receptor blockade.

Alpha-adrenergic receptor subtypes in the cerebral circulation of newborn piglets

1987 ◽  
Vol 252 (6) ◽  
pp. R1092-R1098
Author(s):  
L. C. Wagerle ◽  
M. Delivoria-Papadopoulos
Keyword(s):  
Blood Flow ◽  
Choroid Plexus ◽  
Adrenergic Receptor ◽  
Masseter Muscle ◽  
Newborn Piglet ◽  
Receptor Subtypes ◽  
Receptor Blockade ◽  
Newborn Piglets ◽  
Alpha Adrenergic Receptor ◽  
Adrenergic Receptor Blockade

The purpose of this study was to identify the alpha-adrenergic receptor subtype mediating cerebral vasoconstriction during sympathetic nerve stimulation in the newborn piglet. The effect of alpha 1- and alpha 2- antagonists prazosin and yohimbine on the cerebrovascular response to unilateral electrical stimulation (15 Hz, 15 V) of the superior cervical sympathetic trunk was studied in 25 newborn piglets. Regional cerebral blood flow was measured with tracer microspheres (15 +/- 1 micron). Sympathetic stimulation decreased blood flow to the ipsilateral cerebrum hippocampus, choroid plexus, and masseter muscle by 15 +/- 2, 10 +/- 2, 51 +/- 5, and 94 +/- 5%, respectively. alpha 1-Adrenergic receptor blockade with prazosin (0.5 mg/kg, n = 10) inhibited the sympathetic vasoconstriction in the cerebrum, hippocampus, and masseter muscle (7 +/- 2, 4 +/- 3, and 55 +/- 9%, respectively) and abolished it in the choroid plexus. alpha 2-Adrenergic receptor blockade with yohimbine (0.5 mg/kg, n = 6 and 1.0 mg/kg, n = 5) had no effect. Following the higher dose of yohimbine, however, blood flow to all brain regions was increased by approximately two-fold, possibly due to enhanced cerebral metabolism. These data demonstrate that vascular alpha 1-adrenergic receptors mediate vasoconstriction to neuroadrenergic stimulation in cerebral resistance vessels in the newborn piglet.

Effect of β-Adrenergic Receptor Blockade on Blood Flow to Collateral-Dependent Myocardium During Exercise

Circulation ◽  
1995 ◽  
Vol 91 (5) ◽  
pp. 1560-1567 ◽  
Author(s):  
Jay H. Traverse ◽  
John D. Altman ◽  
James Kinn ◽  
Dirk J. Duncker ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Adrenergic Receptor Blockade

scholarly journals Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses

2004 ◽  
Vol 25 (22) ◽  
pp. 2034-2039 ◽  
Author(s):  
E BARBATO ◽  
J BARTUNEK ◽  
W AARNOUDSE ◽  
M VANDERHEYDEN ◽  
F STAELENS ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Alpha Adrenergic Receptor ◽  
Hyperaemic Response ◽  
Coronary Stenoses ◽  
Adrenergic Receptor Blockade

Gastrointestinal blood flow and oxygen consumption in awake newborn piglets: effect of feeding

1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
O2 Consumption ◽  
Gi Tract ◽  
Local Blood Flow ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Gastrointestinal Blood Flow ◽  
O2 Delivery ◽  
Effect Of Feeding

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.

Distribution of cardiac output during induced isometric exercise in dogs

1979 ◽  
Vol 236 (2) ◽  
pp. H218-H224 ◽  
Author(s):  
S. C. Crayton ◽  
R. Aung-Din ◽  
D. E. Fixler ◽  
J. H. Mitchell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptor ◽  
Isometric Exercise ◽  
Peripheral Resistance ◽  
Minute Volume ◽  
Adrenergic Blockade ◽  
Limb Muscles ◽  
Anesthetized Dogs ◽  
Distribution Of Cardiac Output

Studies were designed to characterize the distribution of cardiac output during induced isometric exercise in anesthetized dogs. The response to isometric exercise involved significant increases in heart rate (+12 +/- 3%(SE)), mean arterial pressure (+13 +/- 2%), cardiac output (+26 +/- 8%), and respiratory minute volume (+75 +/- 26%); total peripheral resistance did not change significantly. Significant changes in blood flow were observed during isometric exercise in kidneys (-18 +/- 6%) and contracting limb muscles (+453 +/- 154%). Flow to liver (hepatic artery), spleen, brain, and myocardium remained near control values. Section of spinal dorsal roots L6-L7 abolished the responses to isometric exercise except for the increase in flow to exercising limb muscles. Alpha-adrenergic receptor blockade abolished the decrease in renal blood flow during isometric exercise; however, the increase in flow to exercising limb muscles was not affected by either alpha- or beta-adrenergic blockade.

Enhanced contribution of NO to exercise-induced coronary responses after α-adrenergic receptor blockade

2002 ◽  
Vol 282 (2) ◽  
pp. H508-H515 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Michel Lavallée
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
No Formation ◽  
Exercise Induced ◽  
Adrenergic Effects ◽  
Adrenergic Receptor Blockade

We hypothesized that nitric oxide (NO), in addition to β-adrenergic effects, may contribute to exercise-induced coronary responses after α-adrenergic receptor blockade. Data were analyzed as relationships between coronary sinus (CS) O2 saturation (CS O2sat) or coronary blood flow (CBF) and myocardial O2 consumption (MV˙o 2). As MV˙o 2 increased, CS O2sat fell more ( P < 0.05) after N ω-nitro-l-arginine methyl ester (l-NAME; slope = −2.9 ± 0.4 × 10−2 %saturation · μl O2 · min−1 · g−1) than before (slope = −2.1 ± 0.3 × 10−2%saturation · μl O2 · min−1 · g−1). The slope of CBF versus MV˙o 2 was not altered. After blockade of α-adrenergic receptors alone (phentolamine), CS O2sat failed to decrease as MV˙o 2 increased (slope = −0.1 ± 0.5 × 10−2 %saturation · μl O2 · min−1 · g−1).l-NAME given after phentolamine led to substantial decreases in CS O2sat ( P < 0.01) as MV˙o 2 increased (slope = −2.1 ± 0.4 × 10−2 percent saturation · μl O2 −1 · min−1 · g−1). CBF responses to exercise were smaller ( P < 0.01) after phentolamine + l-NAME (slope = 6.1 ± 0.1 × 10−3 ml/μl O2) than after phentolamine alone (slope = 6.9 ± 0.2 × 10−3 ml/μl O2). Thus a significant portion of exercise-induced coronary responses after α-adrenergic receptor blockade involves NO formation.

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