Local Reflex in Microcirculation in Human Skeletal Muscle

The effect of venous stasis of 40 mmHg upon blood flow in human skeletal muscle was studied in four normal subjects and in two chronically sympathectomized patients. Blood flow in skeletal muscle was measured by the local ¹³³Xenon washout technique. Blood flow decreased about 30 per cent during venous stasis of 40 mmHg. In a “passive vascular bed” induced by means of histamine, blood flow decreased only by 16 per cent, indicating that the decrease in blood flow is due to a vasoconstrictor response to increase in vascular transmural pressure. The vasoconstrictor response was unaffected by a spinal sympathetic blockade, but was blocked in areas infiltrated with lidocaine or with phentolamine. The vasoconstrictor response was present in the nonoperated limbs used as a control, but abolished in the denervated arms in the two chronically sympathectomized patients. The findings strongly suggest that the vasoconstrictor response in skeletal muscle is due to a local nervous mechanism involving adrenergic fibres. Thus a local reflex mechanism, most likely a sympathetic axon reflex, seems to be present in human skeletal muscle as in cutaneous and subcutaneous tissue. This indicates that about 45 per cent of the change in total vascular conductance, when a person changes from supine to upright position, is due to this local reflex mechanism operating independently of the central nervous system.     

Local Reflex in Microcirculation in Human Cutaneous Tissue

Blood flow in cutaneous tissue measured by the local ¹³³Xenon washout technique decreased about 35 per cent during venous stasis of 40 mmHg in three normal subjects. The response was unaffected by block of the nerve three cm proximally to the labelled area. When the tissue was infiltrated with lidocaine or with phentolamine, blood flow remained constant, indicating that the decrease in blood flow is due to an arteriolar vasoconstrictor response to increase in venous transmural pressure. Local venous stasis elicited a vasoconstrictor response in an adjoining area not affected by the stasis. The response was blocked by lidocaine applied to the side of stasis. In 2 chronically sympathectomized patients, the vasoconstrictor response was abolished in the denervated limbs hut present on the non-operated side (1 patient with unilateral sympathectomy). The results indicate that the vasoconstrictor response to an increase in venous transmural pressure is due to a local nervous mechanism involving sympathetic adrenergic fibres, most likely a sympathetic axon reflex.     

Effect of orthostatic blood pressure changes upon capillary filtration-absorption rate in the human calf

The effect of postural changes upon fluid filtration rate in the calf was studied in 3 healthy subjects placed in supine position. Volume changes in the calf were measured by a water plethysmograph. Relative changes in blood flow in subcutaneous tissue and anterior tibial muscle were measured by the local ¹³³Xe washout technique. Lowering the calf from 5–25 cm caused a linear increase in filtration rate whereas blood flow in subcutaneous tissue of the segment studied and anterior tibial muscle remained constant. Based on this average CFC was about 0.0012 ml min^-1 100 g^-1 mmHg^-1 Further lowering of the calf caused a decrease in blood flow in subcutaneous tissue and skeletal muscle by about 50% corresponding to an increase in total vascular resistance by about 100%. During these circumstances the increase in filtration rate was reduced by about 33%. The results indicate that the local veno-arteriolar reflex responsible for the observed vasoconstriction in the tissue under study together with intrinsic vascular mechanisms reduces transcapillary fluid filtration in the lowered position. The mechanism appears to be mainly due to a reduction of the increase in mean capillary pressure whereas CFC seems to remain almost constant.     

Sympathetic reflex-induced vasoconstriction during renal venous stasis elicited from the capsule in the dog kidney

The study was performed in order to determine the effect of venous pressure elevation induced by unilateral partial renal venous ligation upon total renal blood flow and filtration fraction in the dog kidney. An anaesthesia with no known inhibitory effect on sympathetically mediated vasoconstriction was used. During control conditions instantaneous increase in renal venous pressure to 60 mmHg induced a decrease in renal blood flow (66 +/- 4%) corresponding to an ipsilateral vasoconstriction which was completely abolished following (1) surgical denervation of the kidney, (2) local alpha-receptor blockade of the kidney, and (3) application of lidocaine on the kidney surface. The most striking feature during step increase in renal venous pressure to 40 mmHg was an increase in renal vascular conductance. Renal venous pressure elevation of more than 40 mmHg induced a vasoconstriction, but the vasoconstrictor response was less pronounced as compared with that observed during instantaneous increase in renal venous pressure to the same level. The results strongly suggest that venous stasis of more than 40 mmHg activates an adrenergic sympathetic vasoconstrictor reflex comprising the spinal cord. The reflex is probably elicited from stretch receptors located in the renal capsule. Changes in filtration fraction at venous stasis during the experimental conditions indicate that renal venous pressure elevation activates mechanisms other than neural ones accounting for the reduction in the filtration fraction.     

Local regulation of subcutaneous blood flow and capillary filtration in limbs with occlusive arterial disease. Studies before and after arterial reconstruction

The aim of the study was to examine the local blood flow regulation and the capillary filtration rate in patients with occlusive arterial disease before and after arterial reconstructive surgery. Fourty-seven normal subjects and 99 patients were studied. Subcutaneous blood flow was measured on the forefoot by the local 133Xenon method. Forefoot arterial blood pressure was measured indirectly by cuff and strain-gauge technique. Capillary filtration rate was measured by strain-gauge plethysmography on the forefoot. The arterial and venous pressures of the forefoot were changed by elevating or lowering the foot in relation to heart level. In normal limbs autoregulation was demonstrated during elevation of the limb when blood flow remained almost constant despite the reduction in arterial and perfusion pressures. The local vasoconstrictor response to increased venous transmural pressure was demonstrated when the limb was lowered and blood flow decreased about 30% despite a constant perfusion pressure. In limbs with occlusive arterial disease both local blood flow regulation mechanisms became progressively more abnormal the severe the symptoms and the lower the distal blood pressure. Estimations of the changes in local vascular resistance suggested that the abnormalities in blood flow regulation in all but the severest cases are the result of changes in local perfusion pressure rather than the result of inability of the arteriolar smooth muscle to dilate and constrict in response to changes in arterial and venous pressures. After arterial reconstruction the two mechanisms generally normalized within about a week. However, disturbances occurred in some cases in the early postoperative period, possibly as the result of postoperative pain and stress. Postreconstructive hyperaemia developed in most limbs despite the early normalization of local blood flow regulation. Compared with normal limbs, the forefoot capillary filtration rate was reduced in limbs with occlusive arterial disease. In the early postoperative period the filtration rate remained reduced, but it increased to normal values within three months. Postreconstructive oedema developed independently of the normalization of blood flow regulation, and almost exclusively after femoro-distal by-pass surgery. The study supports the hypothesis that the postreconstructive oedema is a lymphoedema due to surgical trauma, rather than the result of microvascular derangement.     

Changes in subcutaneous blood flow during locally applied negative pressure to the skin

The effect of locally applied subatmospheric pressure on subcutaneous blood flow was studied in 12 healthy subjects. Blood flow was measured on the forearm by the local ¹³³Xe wash-out technique. Air suction between 10 mmHg and 250 mmHg was applied to the skin. Subatmospheric pressure of 20 mmHg caused only a minor increase of estimated vascular resistance of 9 per cent. Increasing the suction to 40 mmHg caused a pronounced vasoconstriction corresponding to an increase in vascular resistance of about 90%. Further increase in local suction beyond 40 mmHg caused no additional increase in vascular resistance. The vasoconstriction induced by local suction was abolished by local nervous blockade induced by lidocaine in low doses which do not affect myogenic activity of the vascular smooth muscle cells. This finding confirms previous studies that the vasoconstriction mainly is due to a local sympathetic veno-arteriolar axon reflex mechanism. The results suggest that the dominant part of the vasoconstriction induced by the local axon reflex occurs when vascular transmural pressure increases from 20 mmHg to 40 mmHg.     

Effect of “Vein Pump” Activation upon Venous Pressure and Blood Flow in Human Subcutaneous Tissue

The effect of “vein pump” activation upon superficial venous pressure and blood flow in human subcutaneous adipose tissue was studied in 6 normals and 2 patients with venous insufficiency. Blood flow in subcutaneous tissue was measured at the lateral malleolus by the local ¹³³Xenon washout technique. with the subject placed in a supine position. During passive lowering of the leg blood flow decreased 50 per cent and total vascular resistance increased 136 per cent. Activation of the vein pump by continuously tipping the foot up and down caused a decrease in venous pressure of 5 mmHg in horizontal position. Venous pressure increased only by 8 mmHg when the leg was lowered during exercise. In this situation blood flow remained constant corresponding to an increase in vascular resistance of 42 per cent. However increasing venous pressure to 28 mmHg by venous stasis in the lowered leg during exercise caused an additional increase in vascular resistance of 82 per cent. In the patients with venous insufficiency exercise did not prevent the decrease in blood flow during lowering of the leg. Hence venous pressure elevation of 25 mmHg or more caused an additional increase in vascular resistance in subcutaneous tissue, “vasoconstrictor response”. It is concluded that this “vasoconstrictor response” depends on a vasoconstrictor impulse transmission from veins to arterioles, veno-arteriolar reflex.     

Hemodynamic and functional changes during renal venous stasis in dog kidneys

The effect of renal venous pressure (RVP) elevation on renal hemodynamics and tubular function was studied in neurolept anaesthetized dogs. Renal blood flow (RBF) was measured electromagnetically. Clearance of 51Cr-EDTA was used as a measure of the rate of glomerular filtration (GFR). GFR, urinary excretion rates of sodium and water, and lithium clearance (CLi) were used for assessing the absolute and fractional reabsorption rates of sodium and water in the proximal as well as in more distal segments of the nephron. The vasoconstrictor response to RVP elevation was partly abolished by acute surgical denervation or by local application of lidocain on the renal capsule, suggesting that RVP elevation activates an adrenergic vasoconstrictor reflex comprising the spinal cord, and elicited from stretch receptors located in the renal capsule. Further studies in alpha-adrenoceptor blocked or chronic denervated kidneys and in decapsulated kidneys favour the view, that neurogenic and myogenic mechanisms significantly influence the vasoconstrictor response to RVP elevation: The neurogenic contribution to the vasoconstrictor response comprising intrarenal and extrarenal vasoconstrictor mechanisms evoked reflexly by RVP elevation; the myogenic contribution to the vasoconstrictor response comprising opposing vasodilator mechanisms due to increase in renal interstitial tissue pressure during RVP elevation. Studies carried out in intact kidneys, acutely surgically or chronically denervated kidneys or alpha-adrenoceptor blocked kidneys indicate that the increase in proximal reabsorption rates during moderate RVP elevation is due mainly to local intrarenal alpha-adrenergic reflex mechanisms, since the decrease in CLi (during constant filtered load) induced by RVP elevation was unaffected by acute surgical denervation, but completely abolished by chronic denervation of the kidney, or by local alpha-adrenoceptor blockade of the kidney.     

Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure.

Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [133Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at -10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 +/- 2% (mean +/- SEM) and in skeletal muscle by 16 +/- 1%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 +/- 3% in subcutaneous tissue and of 30 +/- 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.     

Effect of lower body negative pressure upon local regulation of blood flow in human subcutaneous tissue

Local regulation of subcutaneous blood flow in the forearm was studied during lower body negative pressure (LBNP) in 7 young healthy male subjects in supine position. Blood flow was measured on the forearm by the local ¹³³Xe washout technique. LBNP of -40 and -60 mmHg induced a decrease in the ¹³³Xe washout rate of 34 and 50% respectively. This response to LBNP could be blocked by proximal nervous blockade indicating that the vasoconstriction observed was due to a central sympathetic reflex mechanism. The vasoconstrictor response to increase in venous transmural pressure induced by lowering the arm (veno-arteriolar reflex mechanism) could not be demonstrated during 40 mmHg LBNP. The abolishment of this reflex is most likely due to centrally elicited increase in sympathetic activity as a normal veno-arteriolar reflex was elicited following proximal nervous blockade.     

Effects of venous pressure elevation on myogenic vasoconstrictive responses to static and dynamic arterial pressures

In order to establish the nature of the stretch-evoked dynamic properties of vascular smooth muscle in arterioles, we have examined the static and dynamic effects of both arterial pulse pressure and elevated venous pressure on the resistance vessels (arteries and arterioles) in an intestinal mesenteric preparation derived from dogs. The dynamic myogenic response to stretch stimuli was directly related to both the frequency of arterial pulse pressure (1-20 c/min) and the level of venous pressure (0-45 mmHg). Under elevated venous pressure (20 mmHg), the mean arterial flow decreased with an increase in the frequency of arterial pulse pressure. The arteriolar vascular tone (namely, vascular resistance) was seen to be enhanced. We found that elevated venous pressure promotes active constriction (9-53%) of arteriolar smooth muscle (myogenic mechanism). The elevation of venous pressure also caused a rhythmic constriction (vasomotion) in the site of both vein and artery, which was completely abolished by an alpha-blocker (phentolamine). The results suggest that during venous pressure elevation a very pronounced myogenic constriction in terminal arterioles is caused by either a local neural reflex or a propagated myogenic response in the arteriolar network.     

Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure

Jacobsen , T. N., Nielsen , H. V., Kassis , E. & Amtorp o S. 1992. Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure. Acta Physiol Scand 144 , 247–252. Received 8 March 1991, accepted 7 Novcmber 1991. ISSN 0001–6772. Department of Cardiology, Gentofte Hospital, University of Copenhagen, Denmark Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [¹³³Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at —10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 ± 2% (mean ± SEM) and in skeletal muscle by 16 ± l%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 ± 3% in subcutaneous tissue and of 30 ± 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.     

Effect of Chronic Sympathetic Denervation upon Local Regulation of Blood Flow in Human Subcutaneous Tissue

The effect of chronic sympathetic denervation upon the vasoconstrictor response to an increase of vascular transmural pressure in human subcutaneous adipose tissue was investigated in 6 patients suffering from manual hyperhidrosis. Changes in transmural pressure were obtained either by postural changes of a forearm or by venous stasis of 30 mmHg. Blood flow was measured in the distal part of the forearm or crus by means of the local ¹³³Xenon washout technique. 2 patients were studied before and after sympathectomy. When the area under study was lowered about 40 cm below the jugular notch, blood flow decreased about 50 per cent preoperatively, about 30 per cent 24 h after the operation, but remained constant 4 days after or later. Similar results were obtained during venous stasis. Hence about 4 days after sympathectomy, the vasoconstrictor response to an increase in vascular transmural pressure was abolished. In 3 chronically sympathectomized patients blood flow remained constant in the denervated limb, but decreased significantly in the control limb. In another patient studied 580 days after surgery blood flow remained constant during lowering of the denervated forearm as well as during venous stasis. These findings might indicate that the vasoconstrictor response to an increase in vascular transmural pressure in human subcutaneous adipose tissue is due to a local nervous mechanism involving symphathetic adrenergic nerves, but a myogenic mechanism cannot be definitively excluded.     

Local vascular responses to elevation of an organ above the heart

Elevation of an organ above the heart reduces the arterial and venous hydrostatic pressures in proportion to the height of elevation. Intact autoregulation protects organs, such as the brain and skeletal muscle, from significant alterations in blood flow and hydrostatic capillary pressure due to the decrease in arterial inflow pressure during such a manoeuvre. However, the consequences of the decreased hydrostatic pressure on the venous side are far from clarified. The present study analyses the local haemodynamic effects of the decrease in arterial and venous hydrostatic pressures that occur during vertical elevation of an organ above the heart at atmospheric and raised tissue pressures (0, 10 and 30 mmHg). A sympathectomized cat skeletal muscle enclosed in a plethysmograph and perfused from the animal was used as the experimental model. The results show that elevation of the muscle above the heart at atmospheric tissue pressure created a variable vascular resistance starting at the venous outlet of the organ, and related to the difference between tissue pressure and venous outflow pressure. This resistance completely protects the organ from the hydrostatic pressure alterations on the venous side. The results also show that arterial pressure variations will exert the same haemodynamic influences on the organ as tissue pressure variations, except for the formation of the venous outflow resistance at raised tissue pressure. The application of these results to normal and injured organs, e.g. normal and injured skeletal muscle and brain, with various tissue pressures, is discussed.     

Effect of vein pump activation upon muscle blood flow and venous pressure in the human leg

The effect of vein pump activation upon superficial venous pressure and blood flow in human skeletal muscle tissue was studied in 7 healthy subjects. Blood flow was measured in the anterior tibia muscle by the local ¹³³Xe washout technique. The subjects were placed on a steeply tilted couch in nearly erect position. The vein pump in gastroenemius-soleus muscles was activated by heel-raisings. and the anterior tibial muscle remained relaxed during this procedure. Blood flow in the resting anterior tibial muscle was constant before, during and after 20 heel-raisings per min. A more heavy exercise with 40 heel-raisings per min increased blood flow about 100%. This increase in blood flow was absent during venous stasis (40 mmHg), and in areas infiltrated with lidocaine. It is concluded, that intense dynamic exercise in gastrocnemius-soleus muscles, in erect humans, increased blood flow considerably in another crural muscle remaining in the resting state. The present study strongly suggests, that the observed increase in blood flow, was associated with a decrease in regional subfascial venous pressure to below the threshold level of the local sympathetic veno-arteriolar reflex.     

Forces involved in transcapillary fluid movement in exercising cat skeletal muscle

Average capillary pressure (Pc) close to the venous end (fluid equilibrium point) of the exchange vessels (denoted Pc,v), arterial (PA) and venous pressure, and the rate of net transcapillary fluid flux were continuously recorded in sympathectomized muscle during 30 min of graded exercise and for 30 min in the post-exercise period. Regional changes in colloid osmotic pressure (pi pl) and total osmolality in plasma, the latter reflecting work-induced interstitial hyperosmolality, were measured at intervals. In the control state at rest with a Starling fluid equilibrium, Pc,v averaged 17.6 +/- 0.8 mmHg. Exercise caused a rapid transcapillary plasma fluid loss, the net driving pressure for which in the initial phase of heavy work was 58 mmHg (transcapillary fluid flux divided by the capillary filtration coefficient). This comprised an increase in Pc,v of 16 mmHg, a nonprotein osmotic force (Posm) related to exercise-induced tissue hyperosmolality corresponding to 46 mmHg and an opposing force established by a raised pi pl of 4 mmHg. A theoretical analysis indicated that the main fraction of the osmotic fluid loss passed through transcellular ultrapores and only a minor part through conventional small pores. In spite of the fact that Pc remained high throughout the exercise period, the outward fluid flux gradually declined and a Starling equilibrium was re-established 23 min after the commencement of heavy exercise. This was explained by a gradual decline of Posm and apparently also by a secondary increase in tissue pressure (Pif) and/or a decrease in interstitial colloid osmotic pressure (pi if). Net fluid absorption occurred in the post-exercise period as a result of a gradual decrease in Pc, reversed transcapillary Posm and also maintained high Pif and/or low pi if. Exercise (even light) abolished normal Pc autoregulation, implying that the filtration component of net transcapillary fluid flux becomes distinctly modulated if PA is altered.     

Local regulation of subcutaneous blood flow in normal subjects and in migraine patients before and after single-dose ergotamine tartrate

Local blood flow regulation of the foot was studied in 15 normal subjects and in nine migraine patients. Changes in arterial and venous pressures were induced by lowering and elevation of the limb. Changes in blood flow were estimated from the changes in the wash-out rate of a subcutaneous 133-Xenon depot. The local vasoconstrictor response to increased venous pressure elicited during lowering was identical in the normal subjects and in the migraine patients. During elevation, however, an abnormality in the autoregulation of blood flow could be demonstrated, as a decrease in blood flow during elevation to +40 cm was more pronounced in the patients than in the normal subjects (P = 0.04). About 3 h after 0.5 mg ergotamine tartrate/70 kg body weight i.v. the local regulation of blood flow had markedly changed in normal subjects as well as in migraine patients. During elevation to +20 and to +40 cm, blood flow increased significantly (P = 0.01 and P = 0.02). In two subjects the isotope depot was infiltrated with lidocaine and the ergotamine-induced increase in blood flow during elevation was blocked. The results may indicate that the veno-receptor of the veno-arteriolar reflex underlying the local vasoconstrictor response is a tension receptor, which due to the veno-constrictor effect of ergotamine is triggered even at heart level.     

Vascular recruitment in forearm muscles during exercise

Blood flow and filtration of water across the vascular bed in human forearm muscles were studied at rest and during graded exercise with a hand ergometer. Blood flow was measured by dye dilution and water filtration was determined after injection of hyperoncotic albumin solution (23%) in the brachial artery creating a tissue to blood ultrafiltration measureable as a dilution in the effluent blood. The filtration constants were expressed as a filtration coefficient Fc (ml water/ml plasma mmHg increase in oncotic pressure), and, multiplying by the plasma flow, as a filtration capacity Kf (ml water/100 ml tissue min mmHg increase in oncotic pressure). During the increase in plasma flow induced by exercise, Fc remained constant at about 0.0007, but Kf increased in parallel with the hyperaemia from 0.0031 to 0.038 when plasma flow increased from 4 to 48 ml (100 ml min)-1. The data suggest a more massive recruitment of exchange area during exercise (a factor 12) than suspected on the basis of ultrafiltration in animals made with the prolonged venous stasis technique (showing a factor 2-5). The estimated variability in exchange surface area indicates, that animal studies of muscle circulation, whether pertaining to capillary permeability or capillary filtration should gain by an independent estimate of the number of capillaries that are flowing during the particular experimental situation.     

Effect of renal venous pressure elevation on tubular sodium and water reabsorption in the dog kidney

This study was performed in order to quantify the effects of renal venous pressure (RVP) elevation on absolute and fractional reabsorption rates of sodium and water in proximal and distal segments of the nephron in dog kidneys. Renal blood flow (RBF) was measured electromagnetically. Clearance of [51Cr]EDTA was used as a measure of the rate of glomerular filtration (GFR). GFR, urinary excretion rates of sodium and water, and lithium clearance were used for assessing the absolute and fractional reabsorption rates of sodium and water in the proximal as well as in more distal segments of the nephron. In the kidneys with intact innervation RVP elevation to 19.9 +/- 0.1 mmHg caused significant increases in both absolute (APR) and fractional (FPR) proximal reabsorption rates from 33.4 +/- 4.2 to 38.7 +/- 2.0 ml min-1 and from 0.62 +/- 0.04 to 0.71 +/- 0.04, respectively. These responses were unaffected by acute surgical denervation of the kidneys. In contrast, chronic renal denervation or infusion of phentolamine (5 micrograms kg-1 min-1) into the renal artery eliminated the increase in APR and FPR during RVP elevation to 20 mmHg. Chronic, but not acute renal denervation depleted renal tissue content of adrenaline and noradrenaline. The results suggest that the increase in APR and FPR during RVP elevation is due mainly to local sympathetic reflex mechanisms.     

Vascular adjustment and fluid reabsorption in the human forearm during elevation

Summary Elevation of vascular hydrostatic pressure is known to increase capillary filtration causing, for example orthostatic plasma fluid losses. The present study investigated possible compensatory fluid intravasation in the human forearm during graded elevation, that is during hydrostatic venous collapse. Recordings were made of forearm fluid volume (impedance-plethysmography), forearm blood flow (venous-occlusion-technique), and finger arterial pressure (Finapres^tm). A group of 20 male subjects were seated upright and had their horizontal right forearm passively elevated to 0, 18, 36, and 54 cm above the heart (3rd intercostal space) after equilibration at a reference level 18 cm below the heart. All positions were maintained for 15 min and taken in random order. The vascular volume which drained or refilled within 1.5 min after change of position was found to increase with height. The slow linear volume reduction representing the transcapillary reabsorption rate was found to be almost identical in the three positions above the heart (0.0382, 0.0372, and 0.0398 ml·100 ml^–1·min^–1). Forearm blood flow reached its highest values at heart level and decreased with height. Calculated total vascular resistance increased with a progressive slope up to about 200% of the value at heart level. As a main finding similar reabsorption rates suggested good maintenance of capillary pressure in positions up to 54 cm above the heart thus contrasting with findings on the calf. The coincidence with increasing total vascular resistance led us to the conclusion that graded venous collapse indicated by grading in venous volume makes for a considerable decrease in pre- to postcapillary resistance ratio with elevation. A venous contribution to autoregulation of capillary pressure may thus limit disadvantageous local fluid losses.