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.

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)

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

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.

scholarly journals Selective α1-adrenergic blockade disturbs the regional distribution of cerebral blood flow during static handgrip exercise

2016 ◽  
Vol 310 (11) ◽  
pp. H1541-H1548 ◽  
Author(s):  
Igor A. Fernandes ◽  
João D. Mattos ◽  
Monique O. Campos ◽  
Alessandro C. Machado ◽  
Marcos P. Rocha ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerve ◽  
Adrenergic Receptor ◽  
Sympathetic Nerve Activity ◽  
Flow Distribution ◽  
Receptor Blockade ◽  
Blood Flow Distribution ◽  
Nerve Activity ◽  
Adrenergic Receptor Blockade

Handgrip-induced increases in blood flow through the contralateral artery that supplies the cortical representation of the arm have been hypothesized as a consequence of neurovascular coupling and a resultant metabolic attenuation of sympathetic cerebral vasoconstriction. In contrast, sympathetic restraint, in theory, inhibits changes in perfusion of the cerebral ipsilateral blood vessels. To confirm whether sympathetic nerve activity modulates cerebral blood flow distribution during static handgrip (SHG) exercise, beat-to-beat contra- and ipsilateral internal carotid artery blood flow (ICA; Doppler) and mean arterial pressure (MAP; Finometer) were simultaneously assessed in nine healthy men (27 ± 5 yr), both at rest and during a 2-min SHG bout (30% maximal voluntary contraction), under two experimental conditions: 1) control and 2) α1-adrenergic receptor blockade. End-tidal carbon dioxide (rebreathing system) was clamped throughout the study. SHG induced increases in MAP (+31.4 ± 10.7 mmHg, P < 0.05) and contralateral ICA blood flow (+80.9 ± 62.5 ml/min, P < 0.05), while no changes were observed in the ipsilateral vessel (−9.8 ± 39.3 ml/min, P > 0.05). The reduction in ipsilateral ICA vascular conductance (VC) was greater compared with contralateral ICA (contralateral: −0.8 ± 0.8 vs. ipsilateral: −2.6 ± 1.3 ml·min−1·mmHg−1, P < 0.05). Prazosin was effective to induce α1-blockade since phenylephrine-induced increases in MAP were greatly reduced ( P < 0.05). Under α1-adrenergic receptor blockade, SHG evoked smaller MAP responses (+19.4 ± 9.2, P < 0.05) but similar increases in ICAs blood flow (contralateral: +58.4 ± 21.5 vs. ipsilateral: +54.3 ± 46.2 ml/min, P > 0.05) and decreases in VC (contralateral: −0.4 ± 0.7 vs. ipsilateral: −0.4 ± 1.0 ml·min−1·mmHg−1, P > 0.05). These findings indicate a role of sympathetic nerve activity in the regulation of cerebral blood flow distribution during SHG.

Neurally mediated cardiac effects of forskolin in conscious dogs

1996 ◽  
Vol 271 (4) ◽  
pp. H1473-H1482 ◽  
Author(s):  
M. Iwase ◽  
Y. Ishikawa ◽  
Y. T. Shen ◽  
R. P. Shannon ◽  
N. Sato ◽  
...  
Keyword(s):  
Heart Rate ◽  
Adenylyl Cyclase ◽  
Adrenergic Receptor ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Ganglionic Blockade ◽  
Adrenergic Receptor Blockade

Because major cardiovascular disease states are characterized by defects in adenylyl cyclase regulation, it becomes important to understand the mechanisms by which adenylyl cyclase activators affect inotropy and chronotropy in intact conscious animals. Accordingly, we examined the inotropic and chronotropic responses to forskolin in 11 normal conscious, chronically instrumented dogs and 3 dogs with ventricular denervation (VD). Left ventricular first derivative of pressure (LV dP/dt) increased by 96 +/- 7%, P < 0.05, in response to forskolin (50 nmol.kg-1.min-1) in normal dogs and by significantly less, 52 +/- 14%, in VD dogs. Circulating norepinephrine (NE) levels increased similarly in both groups (from 226 +/- 18 to 389 +/- 33 pg/ml in normal dogs, from 177 +/- 23 to 329 +/- 71 pg/ml in VD dogs). In the presence of ganglionic blockade, the increase in LV dP/dt in response to forskolin was reduced (+62 +/- 4%) in normal dogs but was unchanged in VD dogs (+52 +/- 12%). Ganglionic blockade abolished the increase in circulating NE levels in both groups. Increases in heart rate in the presence of ganglionic blockade (+54 +/- 6 beats/min) were less than in the presence of atropine alone (+92 +/- 10 beats/min). Notably, the LV dP/dt and heart rate responses to forskolin were further attenuated by beta-adrenergic receptor blockade in the presence and absence of ganglionic blockade. Morphine also attenuated the increases in both LV dP/dt and plasma NE in response to forskolin. Increases in LV dP/dt in response to NKH-477 (30 micrograms/kg), a water-soluble forskolin derivative, were similar before and after ganglionic blockade (+63 +/- 8 and +51 +/- 10%, respectively). However, in vitro experiments in LV sarcolemmal membrane preparations demonstrated that stimulation of adenylyl cyclase by forskolin and NKH-477 was not affected by beta-adrenergic receptor blockade. These results indicate that in conscious dogs, inotropic and chronotropic effects of forskolin are not only due to direct activation of adenylyl cyclase, but the effects also are mediated by neural mechanisms and potentiated by the prevailing level of sympathetic tone.

Alpha 1-adrenergic receptor blockade reduces afferent and efferent glomerular arteriolar resistances in SHR

1991 ◽  
Vol 261 (3) ◽  
pp. R576-R580 ◽  
Author(s):  
K. Uchino ◽  
T. Nishikimi ◽  
E. D. Frohlich
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Adrenergic Receptor ◽  
Filtration Rate ◽  
Receptor Blockade ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Wistar Kyoto ◽  
Adrenergic Receptor Blockade

To assess the effects of alpha 1-adrenergic receptor blockade on intrarenal hemodynamics of spontaneously hypertensive rats (SHR), terazosin (0.015 or 0.03 mg/kg body wt) or saline was injected into SHR or normotensive Wistar-Kyoto rats (WKY) (age 16-18 wk). Single-nephron glomerular filtration rate (SNGFR) and renal glomerular filtration rate were determined with [3H]inulin infusion; effective renal blood flow was measured with p-aminohippurate. Intrarenal efferent arteriolar, proximal tubular, stop-flow pressures measurements, and tubular fluid and efferent arteriolar samplings were obtained by micropuncture techniques. Terazosin reduced arterial pressure significantly in both rat strains, but only in SHR did alpha 1-inhibition decrease glomerular hydrostatic pressure (from 58.0 +/- 1.5 to 46.6 +/- 1.1 mmHg; P less than 0.05). Terazosin did not change SNGFR or single-nephron blood flow in either strain. As a result, only in SHR did efferent glomerular arteriolar resistances decrease (0.262 +/- 0.021 to 0.193 +/- 0.014 mmHg.ml-1.min; P less than 0.05). Glomerular ultrafiltration coefficient increased only in SHR (0.034 +/- 0.005 to 0.104 +/- 0.01; P less than 0.05). These results provide further support to the concept of alpha 1-adrenergic receptor hyperresponsiveness of efferent glomerular arteriolar in SHR but not WKY.

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.

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