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

1069: Ejaculatory Disorder Induced by Alpha-Adrenergic Receptor Blockade is not Retrograde Ejaculation

2005 ◽  
Vol 173 (4S) ◽  
pp. 290-290 ◽  
Author(s):  
Shin-ichi Hisasue ◽  
Ryoji Furuya ◽  
Naoki Itoh ◽  
Ryuichi Kato ◽  
Ko Kobayashi ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Retrograde Ejaculation ◽  
Receptor Blockade ◽  
Alpha Adrenergic Receptor ◽  
Ejaculatory Disorder ◽  
Adrenergic Receptor Blockade

scholarly journals Vascular responses after alpha adrenergic receptor blockade

1968 ◽  
Vol 47 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Francois M. Abboud ◽  
Phillip G. Schmid ◽  
John W. Eckstein
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Vascular Responses ◽  
Alpha Adrenergic Receptor ◽  
Adrenergic 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)

Effects of alpha-adrenergic receptor blockade on coronary circulation in conscious dogs

1982 ◽  
Vol 243 (1) ◽  
pp. H94-H98
Author(s):  
P. Macho ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Adrenergic Receptor ◽  
Coronary Circulation ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Alpha Adrenergic Receptor ◽  
Adrenergic Receptor Blockade

The effects of three alpha-adrenergic-receptor blocking agents (phentolamine, prazosin, and trimazosin) were compared on the coronary circulation and left ventricular (LV) function in chronically instrumented conscious dogs. The three alpha-adrenergic-receptor blocking agents were administered in equidepressor doses (mean arterial pressure fell by approximately 20%) and in the presence of beta-adrenergic-receptor blockade and constant heart rate. LV systolic pressure, LV end-diastolic pressure, and LV end-diastolic diameter also fell similarly with the three drugs. Phentolamine decreased the time rate of change of LV pressure (LV dP/dt) by 21 +/- 3%, whereas trimazosin and prazosin decreased LV dP/dt only by 14 +/- 2 and 11 +/- 2%, respectively. LV velocity was not changed with trimazosin and prazosin but decreased with phentolamine by 12 +/- 4%. The three drugs exerted differential effects on the coronary circulation. Only trimazosin increased coronary blood flow (18 +/- 5%). Trimazosin decreased late diastolic coronary resistance (LDCR) by 35 +/- 2%, which was significantly more than reductions in LDCR induced by prazosin (22 +/- 2%) and by phentolamine (11 +/- 3%). A test dose of phenylephrine (5.0 micrograms/kg) increased mean arterial pressure by 53 +/- 3.5 mmHg. After trimazosin, prazosin, and phentolamine, the same dose of phenylephrine increased mean arterial pressure by 24 +/- 2.1, 14 +/- 1.6, and 1.9 +/- 0.6 mmHg, respectively. The response after phentolamine was significantly less than with trimazosin (P less than 0.01) and prazosin (P less than 0.02). Thus the capacity of these three alpha-adrenergic-receptor blocking drugs to dilate coronary vessels is inversely proportional to their capability to block exogenous alpha-adrenergic-receptor agonists.

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