Beta 2-adrenergic vascular control in hemorrhage and its influence on cardiac performance

1984 ◽  
Vol 246 (3) ◽  
pp. H351-H359
Author(s):  
D. Gustafsson ◽  
J. Lundvall
Keyword(s):  
Plasma Volume ◽  
Peripheral Resistance ◽  
Tissue Perfusion ◽  
Cardiac Performance ◽  
Severe Bleeding ◽  
Acta Physiol ◽  
Vascular Control ◽  
Adrenergic Control ◽  
Cardiac Filling ◽  
Beta 2

Cardiac output (CO), heart rate, stroke volume (SV), and total peripheral resistance (TPR) were followed in anesthetized cats with intact and selectively blocked beta 2-adrenoceptors. SV and CO decreased and TPR increased initially after bleeding in both groups. After this, animals with intact beta 2-adrenoceptors showed gradual recovery of SV and CO and gradual restoration to control of the initially raised TPR. In beta 2-blocked animals SV and CO instead remained low and TPR high. These patterns of response occurred after mild, moderate, and severe bleeding. Separate experiments indicated that the restoration of TPR with intact beta 2-adrenoceptors mainly can be attributed to beta 2-adrenergic dilator interaction with the vasoconstrictor influences. The previously described beta 2-adrenergic control of plasma volume in hemorrhage (Acta Physiol. Scand. 116: 175-180, 1982) suggests that the increases in SV and CO with intact beta 2-adrenoceptors, in turn, probably are indirect effects on cardiac performance due to improved cardiac filling. A synthesis of present and previous findings thus suggests the existence of a beta 2-adrenergic vascular control in hemorrhage favoring tissue perfusion via decreased resistance and via increased plasma volume and hence SV and CO.

Exercise stroke volume relative to plasma-volume expansion

1988 ◽  
Vol 64 (1) ◽  
pp. 404-408 ◽  
Author(s):  
M. K. Hopper ◽  
A. R. Coggan ◽  
E. F. Coyle
Keyword(s):  
Stroke Volume ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Peripheral Resistance ◽  
Submaximal Exercise ◽  
Upright Position ◽  
Plasma Volume Expansion ◽  
Trained Subjects ◽  
The Difference ◽  
Dextran Solution

The effects of plasma-volume (PV) expansion on stroke volume (SV) (CO2 rebreathing) during submaximal exercise were determined. Intravenous infusion of 403 +/- 21 ml of a 6% dextran solution before exercise in the upright position increased SV 11% (i.e., 130 +/- 6 to 144 +/- 5 ml; P less than 0.05) in untrained males (n = 7). Further PV expansion (i.e., 706 +/- 43 ml) did not result in a further increase in SV (i.e., 145 +/- 4 ml). SV was somewhat higher during supine compared with upright exercise when blood volume (BV) was normal (i.e., 138 +/- 8 vs. 130 +/- 6 ml; P = 0.08). PV expansion also increased SV during exercise in the supine position (i.e., 138 +/- 8 to 150 +/- 8 ml; P less than 0.05). In contrast to these observations in untrained men, PV expansion of endurance-trained men (n = 10), who were naturally PV expanded, did not increase SV during exercise in the upright or supine positions. When BV in the untrained men was increased to match that of the endurance-trained subjects, SV was observed to be 15% higher (165 +/- 7 vs. 144 +/- 5 ml; P less than 0.05), whereas mean blood pressure and total peripheral resistance were significantly lower (P less than 0.05) in the trained compared with untrained subjects during upright exercise at a similar heart rate. The present findings indicate that exercise SV in untrained men is preload dependent and that increases in exercise SV occur in response to the first 400 ml of PV expansion. It appears that approximately one-half of the difference in SV normally observed between untrained and highly endurance-trained men during upright exercise is due to a suboptimal BV in the untrained men.

Heart failure depresses endothelium-dependent responses in canine femoral artery

1989 ◽  
Vol 256 (4) ◽  
pp. H962-H967 ◽  
Author(s):  
L. Kaiser ◽  
R. C. Spickard ◽  
N. B. Olivier
Keyword(s):  
Heart Failure ◽  
Femoral Artery ◽  
Peripheral Resistance ◽  
Vascular Control ◽  
Experimental Heart Failure ◽  
Low Concentrations ◽  
Local Mechanism ◽  
Before And After ◽  
Significant Depression ◽  
Response To Exercise

Vascular responses to many physiological stresses are abnormal in heart failure. Increased peripheral resistance and a reduction in the vasodilator response to exercise and ischemia are examples of this abnormal vascular control. Such abnormal vascular control in heart failure is a result of interplay between neural, hormonal, and local vascular factors. This study was designed to test the hypothesis that a specific local mechanism, endothelium-dependent relaxation to acetylcholine (ACh), is depressed in experimental heart failure. Experiments were performed on 11 purebred beagles. Experimental heart failure was induced by rapid ventricular pacing for approximately 30 days. Femoral artery diameter was measured by sonomicrometry, and dose-response relationships to ACh, norepinephrine (NE), and nitroglycerin (NTG) were done before and after inhibition of cyclooxygenase by indomethacin. Heart failure resulted in a significant depression of ACh relaxation at all concentrations. In dogs with heart failure, indomethacin enhanced the dilation response to low concentrations of ACh. Constriction to NE and dilation to NTG were unchanged by heart failure. These data demonstrate that in the canine femoral artery endothelium-dependent dilation to ACh is depressed in experimental heart failure. Depression of endothelium-dependent vasodilation represents one local mechanism for abnormal control of the vasculature in congestive heart failure.

Factors involved in delaying the rise in peripheral resistance in developing heart failure

1994 ◽  
Vol 267 (1) ◽  
pp. H211-H216 ◽  
Author(s):  
K. Kiuchi ◽  
R. P. Shannon ◽  
N. Sato ◽  
M. Bigaud ◽  
C. Lajoie ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Peripheral Vascular ◽  
Vascular Control ◽  
Developing Heart

The development of heart failure (HF) on peripheral vascular control was studied in 10 conscious dogs with measurements of cardiac output (CO) and left ventricular (LV), arterial, and right atrial pressures. At 3 wk after pacing-induced HF, CO was not decreased from 2.5 +/- 0.2 l/min, whereas LV dP/dt fell (from 2,858 +/- 71 to 1,409 +/- 69 mmHg/s) and LV end-diastolic pressure increased (from 4.8 +/- 0.4 to 27.3 +/- 1.1 mmHg) (P < 0.05). At 4–7 wk after pacing, CO was significantly decreased (to 1.6 +/- 0.1 l/min; P < 0.05), but total peripheral resistance (TPR) did not rise, despite increases in plasma norepinephrine and renin activity (P < 0.05). In the presence of ganglionic blockade, TPR was still not increased in HF. In vitro studies in isolated femoral artery segments demonstrated reduced intrinsic tone (0.028 +/- 0.007 g/mg; P < 0.05) as compared with vessels from sham-operated controls (0.124 +/- 0.023 g/mg), whereas the intracellular calcium level was not altered in HF. Thus, during the development of HF, severe contractile dysfunction precedes the fall in CO, which, in turn, precedes the rise in TPR. The delayed rise in TPR appears to involve a reduction in intrinsic peripheral vascular tone, despite neurohumoral activation.

Acute plasma volume expansion alters cardiovascular but not thermal function during moderate intensity prolonged exercise

2000 ◽  
Vol 78 (3) ◽  
pp. 244-250 ◽  
Author(s):  
B D Roy ◽  
H J Green ◽  
S M Grant ◽  
M A Tarnopolsky
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Prolonged Exercise ◽  
Peripheral Resistance ◽  
Moderate Intensity ◽  
Thermoregulatory Response ◽  
Plasma Volume Expansion ◽  
Cardiovascular Performance ◽  
Before And After ◽  
Similar Decrease

To investigate the hypothesis that the increase in plasma volume (PV) that typically occurs with training results in improved cardiovascular and thermal regulation during prolonged exercise, eight untrained males (Vo2peak = 3.52 ± 0.12 L·min-1) performed 90 min of cycle ergometry at 62% Vo2peak before and after acute PV expansion. Subjects were infused with a PV-expanding solution (dextran (6%) or Pentaspan (10%)) equivalent to 6.7 mL·kg-1 body mass (PVX) or acted as their own control (CON) in a randomized order. PVX resulted in a calculated 15.8% increase in resting PV, which relative to CON, was maintained throughout the exercise (P < 0.05). During PVX, heart rate was lower (P < 0.05) and stroke volume and cardiac output were higher (P < 0.05) during the exercise. Mean arterial pressure and total peripheral resistance, although altered by exercise (P < 0.05), were not different between the two conditions. Core temperature, which was progressively increased by the exercise (P < 0.01), was not affected by PVX. A similar decrease in body weight was observed between the conditions as a result of the exercise (P < 0.01). These results indicate that acute PVX alters cardiovascular performance without affecting the thermoregulatory response to prolonged cycle exercise.Key words: cardiovascular, prolonged exercise, acute plasma volume expansion, thermoregulation, hypervolemia.

Effects of Prizidilol (SKF 92657) on Blood Pressure, Haemodynamics, Sympathetic Nervous System Activity and Plasma Volume in Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 465s-468s ◽  
Author(s):  
R. Fariello ◽  
C. L. Alicandri ◽  
E. Agabiti-Rosei ◽  
G. Romanelli ◽  
M. Castellano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Volume ◽  
Antihypertensive Effect ◽  
Blood Pressure Reduction ◽  
Cardiac Performance ◽  
Plasma Aldosterone ◽  
Nervous System Activity ◽  
Peripheral Vasodilatation ◽  
Noradrenaline And Adrenaline

1. The antihypertensive effect of 4 weeks' treatment with prizidilol (SKF 92657) (mean dosage 520 mg once or twice daily) was studied in ten essential hypertensive patients. 2. Both systolic and diastolic blood pressure were significantly reduced in all cases. Supine heart rate did not change, and in the erect position heart rate was significantly lowered. 3. Blood pressure reduction was due to peripheral vasodilatation, as the cardiac index increased after 4 weeks of prizidilol treatment. 4. After prizidilol plasma noradrenaline and adrenaline increased significantly, and PRA and plasma aldosterone were reduced. Although plasma volume increased, body weight did not change. 5. Cardiac performance, as evaluated by the PEP/LVET ratio, improved after treatment with prizidilol.

Using a classic paper by Robin Fåhraeus and Torsten Lindqvist to teach basic hemorheology

2013 ◽  
Vol 37 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Linea Natalie Toksvang ◽  
Ronan M. G. Berg
Keyword(s):  
Apparent Viscosity ◽  
Peripheral Resistance ◽  
Tissue Perfusion ◽  
Vessel Diameter ◽  
Glass Capillary ◽  
Capillary Tubes ◽  
Cell Deformability ◽  
Blood Flows ◽  
Classic Paper

“The viscosity of the blood in narrow capillary tubes” by Robin Fåhraeus and Torsten Lindqvist ( Am J Physiol 96: 562–568, 1931) can be a valuable opportunity for teaching basic hemorheological principles in undergraduate cardiovascular physiology. This classic paper demonstrates that a progressive decline in apparent viscosity occurs when blood flows through glass capillary tubes of diminishing radius, which was later designated as the “Fåhraeus-Lindqvist effect.” Subsequent studies have shown that apparent viscosity continues to decline at diameters that correspond to the arteriolar segments of the systemic vascular tree, where the majority of the total peripheral resistance resides and is actively regulated in vivo. The Fåhraeus-Lindqvist effect thus reduces microvascular resistance, thereby maintaining local tissue perfusion at a relatively lower blood pressure. The paper by Fåhraeus and Lindqvist can be used as a platform for a plenary discussion of these concepts as well as of the relationships among hematocrit, vessel diameter, red blood cell deformability, and resistance to blood flow and how these factors may affect the work of the heart.

Pathogenesis of Arterial Hypertension after the Constriction of the Renal Artery Leaving the opposite Kidney Intact Both in the Anaesthetized and in the Conscious Dog

1972 ◽  
Vol 42 (6) ◽  
pp. 651-664 ◽  
Author(s):  
G. Bianchi ◽  
E. Baldoli ◽  
R. Lucca ◽  
P. Barbin
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Plasma Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Plasma Renin Concentration ◽  
Renal Artery Constriction

1. The renal artery was constricted leaving the opposite kidney intact in ten conscious and seven anaesthetized dogs. Intravenous infusion of exogenous renin was done in seven conscious dogs; in four of these the renal artery was constricted 15–17 days later. The following variables were measured in all animals before and after renal artery constriction: plasma renin concentration, blood pressure, cumulative sodium balance, plasma volume, extracellular fluid volume and plasma non-protein nitrogen. Before and after renal artery constriction in the conscious dogs cardiac output, stroke volume, total peripheral resistance and cardiac rate were also measured. In a few dogs angiotensin responsiveness and plasma concentration of renin substrate were also measured. 2. There was no significant difference between the regression of change in blood pressure on change in plasma renin concentration within 2 h from renal artery constriction in the conscious dogs and that observed during intravenous infusion of renin. Comparing the changes of these variables with the ones previously obtained with renal artery constriction to the lone remaining kidney, for a given increase of plasma renin concentration the rise of blood pressure was lower when the contralateral kidney was untouched. The changes of the other variables in the conscious dogs may be divided into three phases: a first phase lasting hours, in which, besides the changes described above, there was an increase of total peripheral resistance while the other variables remain unchanged: a second phase, 24 h after constriction, in which blood pressure, total peripheral resistance and plasma renin clearance decreased while plasma volume, cardiac output and extracellular fluid volume slightly increased; however, only the plasma volume change was statistically significant: and a third phase 6–7 days after constriction, when all the variables returned towards normal values, except that the blood pressure and total peripheral resistance remained significantly higher. Sodium balance remained at equilibrium throughout the study period. It is suggested that these results are compatible with the ‘autoregulation theory’ of renal hypertension. 3. Renal artery constriction in the anaesthetized animals caused a slight but significant sodium retention that very likely influenced the sequence of the events. On the second day after constriction, the plasma renin concentration was significantly increased, whereas the highest values of blood pressure, plasma volume and extracellular fluid volume occurred on the seventh day after constriction.

Hemodynamic and regional circulatory alterations in dog during anaphylactic challenge

1985 ◽  
Vol 249 (2) ◽  
pp. H430-H437 ◽  
Author(s):  
M. A. Kapin ◽  
J. L. Ferguson
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Anaphylactic Shock ◽  
Peripheral Resistance ◽  
Cardiac Performance ◽  
Severe Hypotension ◽  
Pressure Compensation ◽  
Arteriovenous Difference ◽  
The Brain ◽  
Arterial Glucose

Microspheres were employed to measure the cardiac output (CO), percent distribution of CO (%CO), and blood flow (BF) to various tissues in the dog during anaphylactic shock. Five minutes after challenge there was a 66 and 83% drop from control for mean arterial pressure and CO, respectively. Arterial glucose and lactic acid rose 62 and 537%, respectively. Furthermore, there was a narrowing of the systemic arteriovenous difference for PO2 and a widening of the venoarterial difference for PCO2. Pressure compensation toward control values began 5 min postchallenge and continued through 180 min. Circulatory perturbations during severe hypotension (less than mmHg) included depressed %CO and BF to the pancreas and spleen and elevated %CO to the brain and adrenals. Cerebral and adrenal BF remained unchanged at this period. BF to the kidneys, liver (hepatic artery), and gastrointestinal tract dropped markedly as a function of increased peripheral resistance and decreased CO. As cardiac performance improved, blood flow to the pancreas, spleen, liver, diaphragm, and gastrointestinal tissues returned toward control but was elevated to the adrenals and decreased to the brain.

Sign in / Sign up

Export Citation Format

Share Document