Comparative effects of vasodilator drugs on flow distribution and venous return

1985 ◽  
Vol 63 (11) ◽  
pp. 1345-1355 ◽  
Author(s):  
R. I. Ogilvie
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Time Constant ◽  
Venous Return ◽  
Flow Distribution ◽  
Fast Time ◽  
Central Blood Volume ◽  
Slow Time ◽  
Arterial Resistance ◽  
Slow Time Constant

Systemic vascular effects of hydralazine, prazosin, captopril, and nifedipine were studied in 115 anesthetized dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. At three dose levels producing comparable reductions in systemic arterial pressure (30–40% at the highest dose), these drugs had different effects on flow distribution and venous return. Hydralazine and prazosin had parallel and balanced effects on arterial resistance of the two vascular compartments, and flow distribution was unaltered. Captopril preferentially reduced arterial resistance of the compartment with a slow time constant for venous return (−26 ± 6%, −30 ± 6%, −50 ± 5% at 0.02, 0.10, and 0.50 mg∙kg−1∙h−1, respectively; [Formula: see text]) without altering arterial resistance of the fast time-constant compartment. Blood flow to the slow time-constant compartment was increased 43 ± 14% at the highest dose, and central blood volume was reduced 108 ± 15 mL. In contrast, nifedipine had a balanced effect on arterial resistance with the lowest dose (0.025 mg/kg) but caused a preferential reduction in arterial resistance of the fast time-constant compartment at higher doses (−38 ± 4% and −55 ± 2% at 0.05 and 0.10 mg/kg, respectively). Blood flow to the slow time-constant compartment was reduced 36 ± 5% at the highest dose of nifedipine, and central blood volume was increased 66 ± 12 mL. Total systemic venous compliance was unaltered or slightly reduced by each of the four drugs. These results add further evidence to the hypothesis that peripheral blood flow distribution is a major determinant of venous return to the heart.

Analysis of venous flow transients for estimation of vascular resistance, compliance, and blood flow distribution

1987 ◽  
Vol 65 (9) ◽  
pp. 1884-1890 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Time Constant ◽  
Venous Return ◽  
Fast Time ◽  
Slow Time ◽  
Venous Outflow ◽  
Venous Flow ◽  
Time Constants ◽  
Slow Time Constant ◽  
Over Time ◽  
Flow Transients

We analysed venous flow transients using a long venous circuit and right heart bypass in 17 dogs after a rapid decrease in atrial pressure. A biphase curve was obtained which we decomposed into a two-compartmental model, one with a fast time constant for venous return (0.069 min) and 52% of total circulating flow [Formula: see text], and one with a slower time constant (0.456 min) and 48% of [Formula: see text]. Subsequently, separate drainage from splanchnic and peripheral beds (with the renal venous return in the peripheral bed drainage) allowed comparison of time constants and venous outflow in these beds. The sum of the venous outflow volumes over time during separate drainage was indistinguishable from the single biphasic venous outflow volume curve over time observed with a long circuit and single reservoir. The fast time constant of the biphasic curve was not different from that determined by separate drainage from the peripheral circulation. The slow time constant of the single biphasic curve of 0.456 min was hybrid of two time constants, 0.216 min in the splanchnic bed and 0.862 min in the peripheral bed. Separate drainage from peripheral and splanchnic vascular beds demonstrated that the peripheral bed constituted 70% of venous outflow in the fast time constant compartment using Caldini's technique, whereas the splanchnic bed constituted 63% of venous outflow in the slow time constant compartment. It is concluded that, although Caldini's technique demonstrates biphasic venous flow transients, neither the fast nor the slow time constant compartments resolved from this analysis represent a particular anatomical region or vascular bed.

Effects of inotropic agents on arterial resistance and venous compliance in anesthetized dogs

1982 ◽  
Vol 60 (7) ◽  
pp. 968-976 ◽  
Author(s):  
R. I. Ogilvie
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Time Constant ◽  
Right Atrial ◽  
Fast Time ◽  
Vascular Effects ◽  
Venous Compliance ◽  
Peripheral Vasculature ◽  
Arterial Resistance ◽  
Flat Dose

Systemic vascular effects of dopamine, dobutamine, and prenalterol were studied in 45 anesthetized open-chest dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. Dopamine (2.5–10 μg∙kg−1∙min−1) was the most active drug with dose-related increases in heart rate 6–19%, arterial pressure (Pa) 3–36%, and venous compliance 2–25%. Small doses of dopamine (2.5 and 5 μg∙kg−1∙min−1) reduced arterial resistance of the slow time-constant compartment increasing [Formula: see text] distribution to that compartment 21–42%, whereas larger doses increased both arterial resistance and venous compliance in that compartment. Arterial resistance in the fast time-constant compartment increased with all doses of dopamine. Dobutamine (2.5–10 μg∙kg−1∙min−1) modestly increased heart rate 2–11% and Pa 9–12%) without altering [Formula: see text] distribution demonstrating a relatively flat dose response. Dobutamine 2.5–5 μg∙kg−1∙min−1 increased venous compliance 5–10% while 10 μg∙kg−1∙min−1 had no effect or decreased compliance of both compartments. Prenalterol 3 μg∙kg−1∙min−1 increased Pa 9% primarily by increasing arterial resistance in the fast time-constant compartment without altering heart rate or blood flow distribution. Doses of prenalterol 10–100 times greater caused dose-dependent reductions in Pa and vascular compliance. In this animal model of the circulation with a fixed cardiac output, dopamine had the greatest effect on the peripheral vasculature and chronotropy.

Time-constant histograms from the forced expired volume signal

1981 ◽  
Vol 51 (6) ◽  
pp. 1581-1593 ◽  
Author(s):  
R. L. Pimmel ◽  
T. K. Miller ◽  
J. M. Fouke ◽  
J. G. Eyles
Keyword(s):  
Time Constant ◽  
Vital Capacity ◽  
Compartment Model ◽  
Normal Subjects ◽  
Fast Time ◽  
Slow Time ◽  
Criterion Function ◽  
Time Constants ◽  
Nonnegativity Constraints ◽  
Slow Time Constant

The forced expired volume signal was analyzed using a parallel compartment model in which each compartment emptied exponentially. With this model the forced expired volume signal was represented by a histogram showing the fraction of the vital capacity as a functional of compartmental time constants. We developed an algorithm to compute this histogram from the volume signal. The algorithm used the least-squares criterion function with both smoothness and nonnegativity constraints. In a stimulation study reasonable histograms were obtained even in the presence of realistic random error. Three dependent forced expired volume signals from 16 subjects were analyzed, and the histograms were reproducible. Most histograms were bimodal with fast time constants of 0.12–0.55 s and slow time constants of 1.3–2.7 s. In all normal subjects and patients with restrictive disease more than 75% of the vital capacity was in the fast time-constant mode. Subjects with obstructive disease had more than 40% of the vital capacity in the slow time-constant mode.

Compartmental vascular changes in dogs after nephrectomy, DOCA, and saline: effect of nifedipine

1987 ◽  
Vol 65 (9) ◽  
pp. 1891-1897 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Time Constant ◽  
Venous Return ◽  
Flow Distribution ◽  
Filling Pressure ◽  
Fast Time ◽  
Mean Circulatory Filling Pressure ◽  
Hypertensive Group ◽  
Arteriolar Resistance ◽  
The Mean ◽  
Overall Resistance

Hypertension (mean arterial pressure, (MAP) 131 ± 3 mmHg) developed in 18 dogs 4 weeks after left nephrectomy, deoxycorticosterone acetate (DOCA), 5 mg/kg sc twice weekly), and 0.5% NaCl drinking solution. This can be compared with MAP (95 ± 7 mmHg) of 13 dogs with nephrectomy alone and MAP (86 ± 4 mmHg) of 25 dogs without nephrectomy. The two-compartment model of the circulation revealed no differences in systemic vascular compliance, compartmental compliance, or flow distribution to the compartments. However, the time constant for venous return for the compartment with the rapid time constant was increased from 0.05 ± 0.004 min in control animals to 0.07 ± 0.006 min in the nephrectomy alone group and 0.09 ± 0.008 min in the hypertensive group (p < 0.001), as a result of an increase in venous resistance. Arteriolar resistance in this compartment was also increased in the hypertensive animals, as was the mean circulatory filling pressure and overall resistance to venous return. Nifedipine (0.025–0.05 mg/kg) reduced MAP by 15% in the nephrectomy alone group and by 22% in the hypertensive group, with reduction in arteriolar resistance only in the fast time constant compartment. In the slow time constant compartment, arteriolar resistance was increased by more than 100% and flow decreased by more than 50% after nifedipine. Unilateral nephrectomy, DOCA, plus NaCl resulted in hypertension by increasing arteriolar resistance in a vascular compartment with a fast time constant for venous return. Nifedipine countered this effect by inducing arteriolar vasodilation in this compartment. In addition, nifedipine reduced the mean circulatory filling pressure and overall resistance to venous return.

Circulation of sympathectomized dogs under pentobarbital anesthesia

1965 ◽  
Vol 208 (4) ◽  
pp. 790-794
Author(s):  
Shu Chien ◽  
Shunichi Usami
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Volume ◽  
Total Blood Volume ◽  
Central Blood Volume ◽  
Total Blood ◽  
Pentobarbital Anesthesia ◽  
Blood Flows ◽  
The Mean ◽  
Mean Circulation

In sympathectomized-splenectomized dogs under pentobarbital anesthesia, the total blood volume averaged 78 ml/kg, with 20% in the splanchnic circulation and 28% in the central blood volume. These values are almost the same as those found in the splenectomized (control) dogs with the sympathetic system intact. The over-all and the splanchnic Fcells factors are also not significantly different between these two groups. The sympathectomized animals had lower arterial pressure, cardiac output, and splanchnic blood flow, but the resistances calculated for the total and the splanchnic circulations were not significantly different from those of the control dogs. The mean circulation times for the total, the central, and the splanchnic circulations were all longer in the sympathectomized dogs. The data indicate that, under pentobarbital anesthesia, sympathectomized dogs are characterized by slower blood flows without any significant changes in either the blood volume or vascular resistance.

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.

Central blood volume and blood pressure in conscious primates

1988 ◽  
Vol 254 (4) ◽  
pp. H693-H701 ◽  
Author(s):  
K. G. Cornish ◽  
J. P. Gilmore ◽  
T. McCulloch
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood

Conscious intact (I) and sinoaortic-denervated monkeys (SAD) were studied to determine the extent to which high-pressure receptors contribute to the maintenance of arterial blood pressure (BP) when venous return is decreased by hemorrhage (H) or lower body negative pressure (LBNP). In the I animals, mean BP did not decrease significantly until 5% of the estimated blood volume (EBV) was removed, whereas, with sinoaortic denervation, mean BP decreased significantly when less than 2% of EBV was removed. Left atrial pressure (LAP) decreased similarly in both groups of animals. In the I group during LBNP, mean BP did not change significantly, whereas pulse pressure decreased significantly when LBNP was decreased to -5 cmH2O. In the SAD animals, mean BP decreased significantly at an LBNP of -2 cmH2O, and at -5 cmH2O mean BP declined from 134.1 +/- 4 to 102.7 +/- 7 mmHg. LAP decreased similarly in both groups of animals. The data support the view that a nonhypotensive reduction in venous return unloads arterial baroreceptors sufficiently to activate the arterial baroreflex, probably through reductions in pulse pressure. In addition, low-pressure receptors by themselves do not appear to contribute importantly to blood pressure maintenance when venous return is decreased by either LBNP or a nonhypotensive hemorrhage.

scholarly journals Splanchnic hyperemia and hypervolemia during Valsalva maneuver in postural tachycardia syndrome

2005 ◽  
Vol 289 (5) ◽  
pp. H1951-H1959 ◽  
Author(s):  
Julian M. Stewart ◽  
Marvin S. Medow ◽  
Leslie D. Montgomery ◽  
June L. Glover ◽  
Mark M. Millonas
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Volume ◽  
Phase Ii ◽  
Valsalva Maneuver ◽  
Postural Tachycardia Syndrome ◽  
Peripheral Blood Flow ◽  
Control Subjects ◽  
Arterial Resistance ◽  
Postural Tachycardia

Prior work demonstrated dependence of the change in blood pressure during the Valsalva maneuver (VM) on the extent of thoracic hypovolemia and splanchnic hypervolemia. Thoracic hypovolemia and splanchnic hypervolemia characterize certain patients with postural tachycardia syndrome (POTS) during orthostatic stress. These patients also experience abnormal phase II hypotension and phase IV hypertension during VM. We hypothesize that reduced splanchnic arterial resistance explains aberrant VM results in these patients. We studied 17 POTS patients aged 15–23 yr with normal resting peripheral blood flow by strain gauge plethysmography and 10 comparably aged healthy volunteers. All had normal blood volumes by dye dilution. We assessed changes in estimated thoracic, splanchnic, pelvic-thigh, and lower leg blood volume and blood flow by impedance plethysmography throughout VM performed in the supine position. Baseline splanchnic blood flow was increased and calculated arterial resistance was decreased in POTS compared with control subjects. Splanchnic resistance decreased and flow increased in POTS subjects, whereas splanchnic resistance increased and flow decreased in control subjects during stage II of VM. This was associated with increased splanchnic blood volume, decreased thoracic blood volume, increased heart rate, and decreased blood pressure in POTS. Pelvic and leg resistances were increased above control and remained so during stage IV of VM, accounting for the increased blood pressure overshoot in POTS. Thus splanchnic hyperemia and hypervolemia are related to excessive phase II blood pressure reduction in POTS despite intense peripheral vasoconstriction. Factors other than autonomic dysfunction may play a role in POTS.

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