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.

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.

Reactions of Arterial and Venous Vessels in the Human Forearm and Hand to Deep Breath or Mental Strain

1971 ◽  
Vol 40 (3) ◽  
pp. 271-282 ◽  
Author(s):  
W. Delius ◽  
E. Kellerová
Keyword(s):  
Time Course ◽  
Venous Occlusion ◽  
Mental Strain ◽  
Venous Tone ◽  
Similar Time ◽  
Deep Breath ◽  
Human Forearm ◽  
Capacitance Vessels ◽  
S Period ◽  
Cutaneous Vasoconstriction

1. Arterial and venous reactions in forearm and hand to a deep breath or to mental strain (a 50 s period of arithmetic) were measured in fourteen individuals. Blood flow and tissue volume change were measured by venous occlusion plethysmography, and venous tone by the occluded limb technique. 2. A deep breath caused cutaneous vasoconstriction which was short-lasting in resistance (arterial) vessels and long-lasting in capacitance vessels. 3. Mental strain caused cutaneous venous constriction and muscular arterial dilatation with a similar time-course, while the cutaneous arterial reaction was variable.

Vasodilators in critical illness

2016 ◽  
Author(s):  
A. B. J. Groeneveld ◽  
Alexandre Lima
Keyword(s):  
Smooth Muscles ◽  
Renin Angiotensin System ◽  
Phosphodiesterase Inhibitors ◽  
Peripheral Vessel ◽  
Venous Capacitance ◽  
Vasodilator Drugs ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Capacitance Vessels ◽  
The Right

Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.

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

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.

Effect of adenosine and glucagon on hepatic blood volume responses to sympathetic nerves

1991 ◽  
Vol 69 (1) ◽  
pp. 43-48 ◽  
Author(s):  
W. Wayne Lautt ◽  
Joshua Schafer ◽  
Dallas J. Legare
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Liver Weight ◽  
Maximal Response ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Hepatic blood volume responses were studied in cats using in vivo plethysmography. The maximal response (Rmax) to sympathetic nerve stimulation and to infusions of norepinephrine into the hepatic artery or portal vein was similar (12–14 mL expelled per liver in 2.9-kg cats; average liver weight, 76.8 ± 6.8 g). The ED50 for norepinephrine intraportal (0.44 ± 0.13) and intrahepatic arterial infusions (0.33 ± 0.08 μg∙kg−1∙min−1) were similar indicating equal access of both blood supplies to the capacitance vessels. Adenosine (2.0 mg∙kg−1∙min−1) did not cause significant volume changes but produced a mild (27%) suppression of Rmax due to nerve stimulation with no change in the frequency (3.4 Hz) needed to produce 50% of Rmax. Rmax tended (not statistically significant) to decrease during glucagon (1.0 μg∙kg−1∙min−1) infusion but the nerve frequency needed to produce 50% of Rmax rose to 5.6 Hz. Thus both adenosine and glucagon produced modulation of sympathetic nerve-induced capacitance responses without having significant effects on basal blood volume. Adenosine, by virtue of its marked effects on arterial resistance vessels (at substantially lower doses than those used here) and the relative lack of effect on venous capacitance vessels, may be useful for producing clinical afterload reduction without venous pooling.Key words: blood volume, capacitance, sympathetic nerves, adenosine, glucagon.

Enhanced vasodilation to acetylcholine in athletes is associated with lower plasma cholesterol

1996 ◽  
Vol 270 (6) ◽  
pp. H2008-H2013 ◽  
Author(s):  
B. A. Kingwell ◽  
B. Tran ◽  
J. D. Cameron ◽  
G. L. Jennings ◽  
A. M. Dart
Keyword(s):  
Sodium Nitroprusside ◽  
Vascular Resistance ◽  
Repeated Measures ◽  
Vascular Reactivity ◽  
Plasma Cholesterol ◽  
Total Cholesterol Level ◽  
Venous Occlusion ◽  
Ang Ii ◽  
Elevated Cholesterol ◽  
Forearm Vascular Resistance

We investigated a change in vascular reactivity as a potential adaptive mechanism to chronic exercise. The study consisted of 2 separate protocols with 10 male athletes and 10 age-matched sedentary male control subjects participating in each. Protocol 1 investigated forearm blood flow responses to intra-arterial infusions of acetylcholine and sodium nitroprusside by use of venous occlusion plethysmography. Protocol 2 used identical techniques to study responses to norepinephrine, angiotensin II (ANG II), and NG-monomethyl-L-arginine (L-NMMA). The percent reduction in forearm vascular resistance to acetylcholine was significantly greater in the athletic compared with the sedentary group (multivariate analysis of variance for repeated measures, P = 0.03). Covariance analysis suggested that the lower total cholesterol level of the athletic group (P = 0.03) may contribute to their enhanced responsiveness to acetylcholine. There were no differences between athletic and sedentary groups in the forearm vascular resistance responses to norepinephrine, ANG II, sodium nitroprusside, or L-NMMA. These data support the hypothesis that long-term endurance training is associated with enhanced endothelium-dependent dilator reserve due to altered lipoprotein levels in athletes. This finding may have therapeutic application in conditions of elevated cholesterol and impaired vasodilator capacity including hypertension, hypercholesterolemia, atherosclerosis, and cardiac failure.

Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion

1982 ◽  
Vol 53 (5) ◽  
pp. 1110-1115 ◽  
Author(s):  
T. S. Hakim ◽  
R. P. Michel ◽  
H. K. Chang
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Lung Inflation ◽  
Pressure Drops ◽  
Constant Flow Rate ◽  
Initial Decrease ◽  
Occlusion Technique ◽  
First Time

To explain the changes in pulmonary vascular resistance (PVR) with positive- and negative-pressure inflation (PPI and NPI, respectively), we studied their effects in isolated canine left lower lobes perfused at constant flow rate. The venous pressure was kept constant relative to atmospheric pressure during lung inflation. The total arteriovenous pressure drop (delta Pt) was partitioned with the arterial and venous occlusion technique into pressure drops across arterial and venous segments (large indistensible extra-alveolar vessels) and a middle segment (small distensible extra-alveolar and alveolar vessels). PPI caused a curvilinear increase in delta Pt due to a large Starling resistance effect in the alveolar vessels associated with a small volume-dependent increase in the resistance of alveolar and extra-alveolar vessels. NPI caused an initial decrease in delta Pt due to reduction in the resistance of extra-alveolar vessels followed by an increase in delta Pt due to a volume-dependent increase in the resistance of all vessels. In conclusion, we provided for the first time evidence that lung inflation results in a volume-dependent increase in the resistance of both alveolar and extra-alveolar vessels. The data suggest that while the volume-related changes in PVR are identical with PPI and NPI, there are pressure-related changes that can be different between the two modes of inflation.

PERIPHERAL CIRCULATORY RESPONSE TO FEEDING IN THE NEWBORN INFANT

PEDIATRICS ◽  
1971 ◽  
Vol 47 (2) ◽  
pp. 378-383
Author(s):  
Alice C. Yao ◽  
C. Göran Wallgren ◽  
Sachchida N. Sinha ◽  
John Lind
Keyword(s):  
Vascular Resistance ◽  
Venous Occlusion ◽  
Term Infants ◽  
Significant Drop ◽  
Circulatory Response ◽  
Control Value ◽  
Limb Perfusion ◽  
Normal Term ◽  
Regional Vascular Resistance ◽  
Umbilical Arterial Catheter

The peripheral circulatory response to feeding was studied in 39 normal term infants, age ranging from 24 hours to 9 days. Blood flow to calf of left leg was measured by the venous occlusion plethysmographic method before and half hourly after feeding for 3 to 3½ hours. Arterial pressure was monitored in nine infants via an umbilical arterial catheter simultaneously and regional vascular resistance to flow in the leg calculated. Changes in pulse rate, and skin and rectal temperatures were also monitored. A significant drop in the calf perfusion averaging 49% of the control value was observed at the 30 minutes postprandial recording. This was due to an increased regional vascular resistance and blood pressure remained unchanged during the time of study. As a rule, a superseding hyperperfusion of the limb overshooting the control value by 40 to 50% occurred 1½ to 3 hours after feeding. This was comparable to the hyperkinetic phase described in adult man and other species after meals. The early postprandial vasoconstriction in the leg seems unique to the newborn. It is suggested that having the early circulatory demand provoked by feeding is relatively bigger in the newborn than in the adult and is met partly at the expense of lower limb perfusion.

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