Effect of local exercise of forearm muscles on forearm capacitance vessels

1965 ◽  
Vol 20 (5) ◽  
pp. 968-974 ◽  
Author(s):  
B. Sture Bevegård ◽  
John T. Shepherd
Keyword(s):  
Venous Pressure ◽  
Normal Subjects ◽  
Venous Occlusion ◽  
Filling Rate ◽  
Forearm Muscles ◽  
Local Mechanism ◽  
Resistance Vessels ◽  
Venous Filling ◽  
Arterial Inflow ◽  
Capacitance Vessels

Normal subjects were studied to determine whether exercise of the muscles of one forearm causes changes in venous tone in that forearm by some local mechanism. Forearm venous pressure-volume relationships and the pressure in “isolated” vein segments were unchanged after exercise of forearm muscles. Following venous occlusion, the forearm volume increases and reaches a plateau later than forearm venous pressure. This delayed volume change increased with increasing venous filling rate regardless of whether this was accomplished by exercise or by other means. Thus, the local mechanism which dilates resistance vessels in active muscles does not seem to change the contractile state of the muscle in the capacity vessels. The viscous properties of the venous wall, however, act to damp the volume oscillations in intervals between muscular contractions when arterial inflow and venous filling rate are high. The ratio between initial rate of rise in forearm venous pressure and volume following venous occlusion could not be used as an index of active changes in tension of the smooth muscle of the capacitance vessels. strain-gauge plethysmography; isolated vein segments; venous response to varying filling rates; venous response to local exercise; veins and exercise Submitted on November 16, 1964

Criteria for analysis of arterial and venous occlusion

1991 ◽  
Vol 70 (2) ◽  
pp. 665-675 ◽  
Author(s):  
T. S. Hakim
Keyword(s):  
Autologous Blood ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Pressure Gradients ◽  
Experimental Conditions ◽  
Pressure System ◽  
Arterial Inflow ◽  
Outflow Rate ◽  
Set Up

To provide a better understanding of analysis of arterial (AO) and venous occlusion (VO) tracings, using a constant and nonpulsatile perfusion pressure system, we set up an isolated in situ dog lobe preparation perfused with autologous blood. Four signals were recorded: arterial pressure, arterial inflow rate, venous pressure, and venous outflow rate. The four signals were recorded into the memory of a computer. When flow into the lobe was abruptly stopped (AO), flow out of the lung continued unchanged for approximately 150 ms and then decreased slowly to zero. Likewise, when flow out of the lung was abruptly stopped (VO), the flow into the lung continued unchanged for approximately 130 ms and then decreased slowly to zero. A monoexponential curve was fitted to different stretches of data between 0.1 and 5 s postocclusion and extrapolated to the instant of occlusion (defined here as the instant when flow at the site of occlusion becomes zero). The results indicate that 1) the first 150 ms postocclusion should be avoided because of the oscillatory artifacts generated by the occlusion maneuver, 2) use of a long segment of postocclusion data (5 s) tends to underestimate the middle pressure gradient and overestimate the arterial and venous pressure gradients, and 3) the changes in segmental vascular resistance under different experimental conditions were found to be unaffected by the criteria of analysis. Analysis of the postocclusion (AO and VO) tracings was found to be most compatible with the double-occlusion capillary pressure by fitting a stretch of data between 0.2 and 2.5 s postocclusion and extrapolating back to the instant when flow becomes zero at the site of occlusion but no earlier.

Doppler Characterization of the Immediate Blood Flow Velocity Pattern after Release of Prolonged Venous Occlusion of the Forearm

1989 ◽  
Vol 77 (1) ◽  
pp. 11-12 ◽  
Author(s):  
J. N. W. West ◽  
M. S. Salih ◽  
W. A. Littler
Keyword(s):  
Blood Flow ◽  
Venous Occlusion ◽  
Short Term ◽  
Velocity Pattern ◽  
Flow Response ◽  
Resistance Vessels ◽  
Capacitance Vessels ◽  
Doppler Techniques ◽  
Flow Through

1. There is a biphasic flow response measured plethysmographically after release of prolonged venous occlusion of the forearm. 2. The response consists of an early, vasodilatory, increase in flow and is followed by a decrease in flow relative to control, thought to be mediated by myogenic contraction of resistance vessels. 3. Methodological constraints with the technique of forearm plethysmography have to date precluded an individual beat-by-beat examination of this response, in particular for resolving the question of the immediate flow pattern after release of venous occlusion. It has been suggested by Caro, Foley & Sudlow [Journal of Physiology (London) (1970), 207, 257–269] that there is a delay of up to five systolic beats before vasodilatation takes place, leading to their suggestion that the vasodilatation is passive and secondary to an increased flow through emptied capacitance vessels. 4. The introduction of peripheral Doppler techniques has led us to re-examine this response in an attempt to define short-term resistance vessel behaviour on a beat-by-beat basis. 5. Our data confirmed the hypothesis of Caro, Foley & Sudlow [Journal of Physiology (London) (1970), 207, 257–269] that there is a constant and definite latency preceding the onset of vasodilatory flow, as reflected by changes in Doppler velocities.

Partitioning of pulmonary vascular resistance in dogs by arterial and venous occlusion

1982 ◽  
Vol 52 (3) ◽  
pp. 710-715 ◽  
Author(s):  
T. S. Hakim ◽  
R. P. Michel ◽  
H. K. Chang
Keyword(s):  
Flow Rate ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Pulmonary Vasculature ◽  
Pressure Drops ◽  
Lower Lung ◽  
Arterial Inflow ◽  
Arteries And Veins ◽  
Lung Lobes

We perfused in situ isolated left lower lung lobes at a steady flow rate in zone 3 condition. When the lobar arterial inflow was suddenly occluded, the arterial pressure (Pa) fell rapidly and then more slowly. When the lobar venous outflow was suddenly occluded, the venous pressure (Pv) rose rapidly and then continued to rise more slowly. The rapid changes in Pa and Pv with inflow and outflow occlusion, respectively, represent the pressure drops across the arterial (delta Pa) and venous (delta Pv) relatively indistensible vessels. The total arteriovenous pressure difference (delta Pt) minus delta Pa + delta Pv gives the pressure drop across the vessels in the middle (delta Pm) that are much more distensible. Serotonin and histamine infusion increased delta Pa and delta Pv, respectively, but left delta Pm unchanged. delta Pa and delta Pv, but not delta Pm, increased as flow rate was increased. The studies with varying flow rate and venous pressures suggested that the arteries and veins became resistant to distension when their transmural pressures exceeded 10--5 Torr, respectively. Under the conditions studied, the middle nonmuscular segment contributed a major fraction of the vascular compliance and less than 16% of the total resistance. The muscular arteries and veins contributed equally to the remaining resistance. We conclude that the arterial and venous occlusion method is a useful technique to describe the resistance and compliance of different segments of the pulmonary vasculature.

A new method for estimating skeletal muscle capillary pressure

1984 ◽  
Vol 246 (6) ◽  
pp. H880-H885
Author(s):  
R. J. Korthuis ◽  
D. N. Granger ◽  
A. E. Taylor
Keyword(s):  
Skeletal Muscle ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Fluid Filtration ◽  
Arterial Inflow ◽  
Capillary Pressures ◽  
Highly Correlated ◽  
Artificial Plasma

Venous (Pc,vo) and arterial occlusion capillary pressures were simultaneously compared with isogravimetric capillary pressure (Pci) in isolated rat hindquarters and canine gracilis muscles perfused with blood or an artificial plasma. Arterial or venous pressure transients following rapid occlusion of arterial inflow or venous outflow, respectively, were analyzed for the inflection point between rapid and slow components. This transition point was assumed to represent the beginning of discharge of blood stored in (arterial occlusion) or the addition of blood to (venous occlusion) skeletal muscle microvessels and was defined as the effective capillary pressure. In all preparations, Pc,vo was identical to Pci. Arterial occlusion pressures were the same as Pci and Pc,vo in artificial plasma-perfused preparations but were significantly greater (P less than 0.01) than Pci and Pc,vo obtained in blood-perfused preparations. This inequality between arterial occlusion pressure and Pci may be related to a critical closure of small precapillary vessels or the non-Newtonian behavior of blood. In addition, venous occlusion pressures were highly correlated (r = 0.95, P less than 0.01) to calculated capillary pressures obtained following simultaneous equivalent elevations of arterial and venous pressure. These results indicate that the primary sites of vascular compliance and fluid filtration reside at or very near one another in the skeletal muscle microcirculation and that the more easily determined venous occlusion capillary pressure is an adequate measure of the effective capillary pressure in skeletal muscle.

Changes in tone of limb veins during supine exercise

1965 ◽  
Vol 20 (1) ◽  
pp. 1-8 ◽  
Author(s):  
B. Sture Bevegård ◽  
John T. Shepherd
Keyword(s):  
Forearm Blood Flow ◽  
Sympathetic Nerves ◽  
Normal Subjects ◽  
Work Load ◽  
Volume Strain ◽  
Arm Exercise ◽  
Resistance Vessels ◽  
Leg Exercise ◽  
Capacitance Vessels ◽  
Adaptation To Exercise

Normal subjects have been studied to assess the response of the capacitance vessels in the forearm during supine leg exercise. Measurements were made of changes in forearm volume (strain-gauge and water-filled plethysmographs) at a given pressure in the large forearm veins, of changes in pressure in the forearm veins with the circulation to the forearm arrested and in “isolated” vein segments. The results were consistent and demonstrated that exercise with a work load of 270–810 kg/min caused constriction of forearm capacitance vessels via the sympathetic nerves proportional to the severity of the exercise. Venoconstriction also occurred in the hand, and in the calf during arm exercise. Local exercise of the forearm muscles during supine leg exercise, which increased forearm blood flow by dilating the resistance vessels, did not prevent the increase in venous tone in the forearm. Thus a reflex increase in tone in the limb veins, both in the exercising and in the nonexercising parts, contributes to the cardiovascular adaptation to exercise. venoconstriction in exercising and nonexercising limbs; reflex venoconstriction with exercise graded to severity of work; reflex venoconstriction with exercise mediated through sympathetic nerves Submitted on June 15, 1964

Effect of Morphine on Limb Capacitance and Resistance Vessels

1981 ◽  
Vol 60 (1) ◽  
pp. 5-9 ◽  
Author(s):  
R. A. Cohen ◽  
J. D. Coffman
Keyword(s):  
Vascular Resistance ◽  
Venous Occlusion ◽  
Important Change ◽  
Venous Tone ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Intravenous Morphine ◽  
Capacitance Vessels ◽  
Venous Volume ◽  
Cutaneous Vascular Resistance

1. The actions of 15 mg of intravenous morphine on hand and forearm capacitance and resistance vessels were studied with venous occlusion plethysmography. 2. In contrast to a 5% increase in forearm venous volume, intravenous morphine caused a 26% decrease in hand venous volume. This hand venoconstriction was confirmed by finding an increase in hand venous tone. The effects of morphine on hand veins were attenuated by intra-arterial phentolamine and blocked by intravenous naloxone. 3. Whereas morphine had no significant effect on forearm resistance vessels, it caused a 70% reduction in hand vascular resistance. 4. Intra-arterial morphine had no local action on hand capacitance or resistance vessels. 5. Though the contrasting actions of morphine on hand and forearm capacitance vessels resulted in no important change in limb venous capacitance, the large reduction of cutaneous vascular resistance may contribute to haemodynamic benefit in patients with pulmonary oedema.

scholarly journals Cardiovascular effects of vasopressin following V1 receptor blockade compared to effects of nitroglycerin

2001 ◽  
Vol 281 (3) ◽  
pp. R887-R893 ◽  
Author(s):  
C. R. Cooke ◽  
B. M. Wall ◽  
K. M. Huch ◽  
T. Mangold
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Normal Subjects ◽  
Receptor Blockade ◽  
Hemodynamic Effects ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Studies to more clearly determine the mechanisms associated with arginine vasopressin (AVP)-induced vasodilation were performed in normal subjects and in quadriplegic subjects with impaired efferent sympathetic responses. Studies to compare the effects of AVP with the hemodynamic effects of nitroglycerin, an agent that primarily affects venous capacitance vessels, were also performed in normal subjects. Incremental infusions of AVP following V1-receptor blockade resulted in equivalent reductions in systemic vascular resistance (SVRI) in normal and in quadriplegic subjects. However, there were major differences in the effect on mean arterial pressure (MAP), which was reduced in quadriplegic subjects but did not change in normal subjects. This difference in MAP can be attributed to a difference in the magnitude of increase in cardiac output (CI), which was twofold greater in normal than in quadriplegic subjects. These observations are consistent with AVP-induced vasodilation of arterial resistance vessels with reflex sympathetic enhancement of CI and are clearly different from the hemodynamic effects of nitroglycerin, i.e., reductions in MAP, CI, and indexes of cardiac preload, with only minor changes in SVRI.

Systemic and pulmonary hemodynamic responses to intracranial hypertension

1984 ◽  
Vol 247 (5) ◽  
pp. H715-H721 ◽  
Author(s):  
H. I. Chen ◽  
D. J. Wang
Keyword(s):  
Intracranial Hypertension ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Resistance Response ◽  
Pulmonary Blood Volume ◽  
Control Value ◽  
Pulmonary Hemodynamic ◽  
Arterial Inflow ◽  
Capacitance Vessels

Experiments were conducted in anesthetized, vagotomized, and open-chest dogs. Total heart bypass was performed to perfuse the systemic and pulmonary circulations with constant flow. The venous outflows were diverted into reservoirs. We studied the simultaneous changes in systemic vascular resistance (SVR) and capacity (SVC) as well as pulmonary vascular resistance (PVR) and capacity (PVC) during a period of intracranial hypertension (ICH). In 20 dogs with an intracranial pressure of 164 +/- 12 mmHg, SVR increased by 110% and SVC decreased by 8.4 +/- 1.2 ml/kg. The increase in PVR reached 69%, and the decrease in PVC amounted to 1.24 +/- 0.40 ml/kg body wt or 9.7 +/- 3.9 ml/100 g lung wt. The results indicate that ICH exerts profound effects on both systemic and pulmonary resistance and capacitance vessels. An analysis from the pulmonary blood volume change suggested that the pulmonary vascular compliance was significantly reduced by ICH from a control value of 0.33 +/- 0.06 to 0.26 +/- 0.05 ml X mmHg-1 X kg-1. In the pulmonary circulation, an elevation of left atrial pressure with lung volume expansion attenuated the resistance response, while it increased the capacity reduction. When pulmonary blood volume was kept constant by a constant venous outflow equal to the arterial inflow, the response of capacitance vessels to ICH increased both pulmonary arterial and venous pressures associated with a slight change in PVR. These findings suggest that an increase in pulmonary venous pressure with a constant or increased blood volume reduced the ICH-induced change in resistance.

Mechanism of the postural vasoconstrictor response in the human foot

1988 ◽  
Vol 75 (4) ◽  
pp. 379-387 ◽  
Author(s):  
Ahmad A. K. Hassan ◽  
J. E. Tooke
Keyword(s):  
Diastolic Pressure ◽  
Venous Pressure ◽  
Systolic Pressure ◽  
Sympathetic Nerves ◽  
Venous Occlusion ◽  
Central Component ◽  
Small Contribution ◽  
Doppler Flowmetry ◽  
Human Foot ◽  
Local Mechanism

1. The mechanism of postural vasoconstriction in the skin of the foot was examined in 102 healthy subjects by using laser Doppler flowmetry. 2. In 45 subjects, when one foot was lowered 50 cm below heart level and the other foot kept horizontal, blood flow was progressively reduced in the dependent foot (by 79%) with a concomitant, but less pronounced, reduction in flow in the horizontal foot (by 18%), indicating that a central mechanism is involved. After lumbar sympathetic blockade (in 10 patients with epidural anaesthesia), the flow in the horizontal foot remained virtually constant, indicating that the central component is mainly mediated via efferent sympathetic nerves, whereas the postural fall in flow in the dependent foot, though partially attenuated, was preserved, indicating that a local mechanism is mainly involved. 3. On lowering one foot below heart level in 12 subjects, there was a small but significant reduction in systolic and mean arterial pressures during the first minute of dependency. During the fourth minute, systolic pressure decreased, diastolic pressure and heart rate increased, but the mean arterial pressure was maintained. 4. In 19 subjects postural vasoconstriction was nearly abolished during local nervous blockade (lignocaine 3.7 × 10−4–7.4 × 10−2 mol/l), indicating that the local mechanism mediating the vasoconstriction is mainly neurogenic in nature. However, there was still a small fall (19%) in flow in the dependent foot during blockade, probably indicating a minor contribution of a local myogenic mechanism. 5. In three subjects, application of venous occlusion of 40 mmHg with the foot at heart level reduced the flow by 63% at rest, and by only 12% during local nervous blockade, indicating that the increased venous pressure on dependency provides the main stimulus for postural vasoconstriction. However, a greater reduction in flow was observed in 13 subjects when the foot was lowered 50 cm below the heart (75%) than during venous occlusion of 40 mmHg (52%) with foot at heart level, indicating that not only the increase in venous pressure but also the increase in arterial transmural pressure is implicated in the postural increase in precapillary resistance. 6. It is concluded that postural vasoconstriction in the human foot is mainly produced by a local neurogenic mechanism with a small contribution from a local myogenic response, in addition to a centrally elicited sympathetic component.

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