Hormonal and neurogenic adrenergic control of the fluid transfer from skeletal muscle to blood during hemorrhage

During hemorrhage net transcapillary absorption of interstitial fluid from skeletal muscle into the intravascular space compensates effectively for the blood loss. This absorption of fluid is mainly linked to decrease of the capillary hydrostatic pressure (Pc), as caused by reflex adrenergic re-adjustment of the ratio of pre-to postcapillary resistance (ra/rv). The present study demonstrates the existence of both a neurogenic and a humoral component in the adrenergic control of the fluid transfer from skeletal muscle to blood. In the early period of bleeding (<5 min) reflex activation of the vasomotor fibres contributed significantly to the fluid absorption. The subsequent, main part of the fluid gain from the extra-to the intravascular space was due to the action of the blood-borne catecholamines. Both the neurogenic and the hormonal control of the fluid absorption process was mainly linked to β-adrenergic inhibition of vascular smooth muscle tone. This control was effected via two mechanisms, viz. by a relatively larger β-adrenergic dilatation of post-than precapillary resistance vessels, leading to adjustment of ra/rv and thereby to decrease of Pc, and via β-adrenergic dilatation of ‘precapillary sphincters’ leading to increased capillary surface area available for fluid exchange.     

Model of interstitial pressure as a result of cyclical changes in the capillary wall fluid transport.

Reported interstitial pressures range from -8 to +6 mm Hg in different tissues and from <-20 mm Hg in burned tissue or more than +30 mm Hg in tumors. We have tried to link interstitial pressure to the here proposed cyclical changes in the fluid transport across the capillary wall.In the presented model interstitial pressure is considered as an average of pressures in numerous pericapillary spaces. A single pericapillary pressure is a dynamic difference between the net outward (hydraulic pressure+interstitial colloid osmotic pressure) and inward (plasma colloid oncotic pressure) forces. Hence, dominating net outward forces would result in a positive pericapillary interstitial pressure, while stronger inward forces would produce negative pressures in the pericapillary space. All interruptions of blood flow leave some blood in capillaries with a normal oncotic pressure and no hydrostatic pressure that might act as a strong absorber of interstitial fluid until the blood flow is reestablished.Model assumptions for the systemic circulation capillaries include (a) precapillary sphincters can almost entirely stop the capillary flow, (b) only a minority of sphincters are normally open in the tissue, and (c) hydrostatic pressures in unperfused capillaries are similar to the pressures at their venous ends.The key proposal is that capillaries with closed precapillary sphincters along their entire length have low hydrostatic pressure of 10 to 15 mm Hg. This pressure cannot force filtration, so these capillaries reabsorb interstitial fluid from the pericapillary space along their entire length. In the open capillaries, hydrostatic pressure filtrates fluid to the pericapillary space along most of their length. Fluid enters, moves some 20 or 30 micrometers away and back to be reabsorbed at the same point. Closed periods are periods of intense fluid reabsorption, while the short open periods refill the space with fresh fluid. It can be calculated that subcutaneous tissue interstitial pressure values might develop if the closed periods are 1.14 to 2.66 times longer than the open periods. Positive interstitial pressures observed in some organs might develop if open periods are longer than the closed periods.High interstitial colloid pressure in lungs makes both perfused and unperfused capillaries absorptive, resulting in more negative values of lung interstitial pressure. The same model is used to explain interstitial pressure values in tumors, burned tissue and intestinal villi.     

Magnetic field-like fluid circulation of a porous orifice tube and its relevance to the capillary-interstitial fluid circulation: preliminary report

In 1886, Starling proposed a hypothesis for the capillary-interstitial fluid transfer in which capillary filtration is attributed to arterial pressure, based on Poiseuille's work in long uniform tubes. In 1967-8, the precapillary sphincter, pores and negative interstitial pressure were reported. In 1984, clinical observations inconsistent with Starling's hypothesis prompted a physical study to verify pressure dynamics in a porous orifice (G) tubes. Results demonstrate that, unlike in Poiseuille's tube, a fluid passing inside the lumen of the G tube exerts a negative energy pressure gradient on its wall; most negative over its proximal part causing inflow of fluid by suction and positive over its distal part causing fluid outflow. A net negative pressure gradient also occurs in a surrounding chamber C, causing fluid to flow in an opposite direction to lumen flow. An autonomous dynamic magnetic field-like G-C circulation occurred between lumen and surrounding fluid compartments. Reviewed literature support the contention that this sole phenomenon adequately explains the capillary-interstitial fluid transfer under both physiological and pathological haemodynamic conditions.     

Fluid transfer from skeletal muscle to blood during hemorrhage. Importance of beta adrenergic vascular mechanisms.

Vascular reactions in the cat lower leg in response to short-term (10 min) hemorrhagic hypotension (approximately 80 mmHg) were studied before and after regional blockade of the beta-adrenoceptors. In the muscle region with intact beta-adrenoceptors, hemorrhage raised vascular resistance by about 80% and caused a dilatation of the precapillary sphincters, the latter effect evidenced in terms of a 35% increase of the capillary filtration coefficient. Concomitantly, an absorption of extravascular fluid to the blood stream occurred, a process tending to compensate for the reduction of intravascular fluid volume. After regional beta-blockade there was quite a marked augmentation of the hemorrhage induced increase of vascular resistance whereas the inhibition of precapillary sphincter tone and the transcapillary fluid absorption were almost abolished. These observations indicate that bleeding is associated with a significant beta-adrenergic dilator influence in both the resistance vessels and precapillary sphincters of skeletal muscle and that the beta-dilator mechanism may be essential for the important, compensatory fluid gain from the extravascular to the intravascular space during hemorrhage. The observed beta-adrenergic mediation of the net transcapillary fluid absorption could be ascribed to resetting of the pre-/postcapillary resistance ratio, leading to decreased capillary hydrostatic pressure, and to the dilator influence in the precapillary sphincters, leading to an increased number of the patent capillaries available for the transcapillary fluid exchange.     

Fluid transfer from skeletal muscle to blood during hemorrhage Importance of beta adrenergic vascular mechanisms

Vascular reactions in the cat lower leg muscles in response to short-term (10 min) hemorrhagic hypotension (?80 mmHg) were studied before and after regional blockade of the β-adrenoceptors. In the muscle region with intact β-adrenoceptors, hemorrhage raised vascular resistance by about 80% and caused a dilatation of the precapillary sphincters, the latter effect evidenced in terms of a 35% increase of the capillary filtration coefficient. Concomitantly, an absorption of extravascular fluid to the blood stream occurred, a process tending to compensate for the reduction of intravascular fluid volume. After regional β-blockade there was quite a marked augmentation of the hemorrhage induced increase of vascular resistance whereas the inhibition of precapillary sphincter tone and the transcapillary fluid absorption were almost abolished. These observations indicate that bleeding is associated with a significant β-adrenergic dilator influence in both the resistance vessels and precapillary sphincters of skeletal muscle and that the β-dilator mechanism may be essential for the important, compensatory fluid gain from the extravascular to the intravascular space during hemorrhage. The observed β-adrenergic mediation of the net transcapillary fluid absorption could be ascribed to resetting of the pre-/postcapillary resistance ratio, leading to decreased capillary hydrostatic pressure, and to the dilator influence in the precapillary sphincters, leading to an increased number of the patent capillaries available for the transcapillary fluid exchange.     

The influence of rheological and collapse factors on pre- and post-capillary flow resistances in the skeletal muscle vascular bed of the cat.

The importance of passive-elastic changes of vascular dimensions and shifts in regional effective viscosity for the pre-/postcapillary resistance ratio (RA/RV), and hence mean capillary pressure (PC), was analyzed in cat calf muscles. Reductions of mean venous distending pressure below 6-8 mm Hg induced marked RV increases due to escalating venous collapse. This mechanism tends to delimit the PC reductions and rate of transcapillary fluid absorption during intense precapillary vasoconstriction. Comparisons of RA/RV for erythrocyte suspensions (Hct 40-50) and cellfree perfusates at identical vascular dimensions showed that RA/RV was considerably higher, and PC correspondingly lower, for the erythrocyte suspension except at very low flows. This RA/RV difference increased with increasing flow and at very high flows PC was about 10 mm Hg lower during perfusion with the erythrocyte suspension. These findings apparently diverge from the known influence of the tube radius and linear flow velocity on effective in vitro viscosity of blood. Since distal precapillary and proximal capillary sections, both having smaller diameters than the erythrocytes, are located upstream to the point of filtration-absorption equilibrium, they contribute in this respect to RA. It is therefore suggested that the increasing RA/RV with erythrocyte perfusion, particularly at higher flows, is not due to genuine viscosity factors but to friction losses when cells in "bolus flow" are squeezed through the narrowest precapillary sections.     

Peritubular capillary control of proximal tubule reabsorption in the rat.

Changes in peritubular capillary hydrostatic and oncotic pressures, which probably affect net interstitial pressure and, thus, the force on fluid movement across the tubule basement membrane, can modulate absolute proximal reabsorption rate (APR). To examine the relationship between APR and net interstitial pressure, we measured peritubular capillary hydrostatic and oncotic pressure, single nephron filtration rate, APR, absolute distal reabsorption (ADR), and tubular hydrostatic pressure in hydropenic, saline-loaded, and plasma-loaded rats. Net interstitial pressure in saline loading was estimated from subcapsular hydrostatic pressure and lymph protein concentration measurements. The surface area-hydraulic conductivity product of the peritubular capillary network was estimated from these measurements with a model of capillary fluid exchange in which fluid uptake was defined to be APR plus ADR. The estimated value was assumed to remain constant in all three states, and was then used to estimate net interstitial pressure in hydropenic and plasma-loaded rats. APR and net interstitial pressure correlated strongly, a finding consistent with the hypothesized role for net interstitial pressure in regulating proximal reabsorption.     

Transcapillary Fluid Absorption and Other Vasular Reactions in the Human Forearm during Reduction of the Circulating Blood Volume

The responses of the human forearm vascular bed to a reduction of circulation blood volume, produced by pooling about 600 to 800 ml of blood in the legs, were followed by a plethysmographic technique. The pattern of vascular response was similar to that previously found in anesthetized animals after hemorrhage. It involved a reflex constriction of resistance and capacitance vessels and a net transcapillary absorption of extravascular fluid. The capillary filtration coefficient averaged 0.0061 ml/min × 100 g tissue × mm Hg , and did not change significantly during the pooling of blood, indicating no major change of precapillary sphincter tone. The absorption of extravascular fluid can be related to a fall in capillary hydrostatic pressure, which is, in turn, due to a reflex increase of the pre- to postcapillary resistance ratio. This process seems to aid greatly in the restoration of plasma volume. A reflex resetting of the pre-to postcapillary resistance ratio might therefore consitute an important component in the overalll cardiovascular compensatory adjustments to reduced circulating blood volume in man.     

'Sodium sensitivity' in man

Increased cell membrane permeability to sodium is proposed as the initial event leading to high blood pressure in susceptible subjects when sodium intake is increased. All cells, including circulating cells, would be affected, but a key role for endothelial cells in the pathophysiology of the diastolic blood pressure elevation is proposed. Involvement of capillary endothelium could increase capillary permeability to proteins, and thereby would contribute to the altered fluid distribution on the high sodium diet which has been observed. If movement of fluid into the interstitium raised interstitial fluid pressure, venous capacitance would fall and right atrial pressure would rise. Several mechanisms would cause vascular smooth muscle tone to increase. Altered fluid distribution correlates with the rise in diastolic blood pressure from reduced sodium to high sodium diet, but arteriolar constriction would reduce capillary flow so altered fluid distribution occurs first. Arteriolar constriction could serve as a negative feedback to the raised atrial filling pressure by reducing raised capillary flow, which would decrease both altered fluid distribution and interstitial fluid pressure rise. Consequently, diastolic blood pressure would be chronically raised in 'sodium sensitive' subjects taking increased amounts of sodium in the diet. The relationship of the findings to "essential" hypertension and to premorbid cardiovascular sequelae, and the key role of capillary endothelium in the development of "essential" hypertension is discussed.     

Central neural influence on precapillary microvessels and sphincter.

The responses to central nervous system (CNS) stimulation of consecutive segments of arterioles down to the precapillary sphincter were measured in the mesoappendix and/or cremaster of nine male rats with indwelling electrodes. Under pentobarbital sodium anesthesia, vasoactive sites were stimulated at threshold for maximal constriction or lumen closure of the precapillary sphincter and/or immediately preceding precapillary arteriole (metarteriole). In all experiments, CNS stimulation induced blood pressure elevation and constriction of three consecutive segments of precapillary vessels and of the sphincter. A threefold increase in rate of vasomotion of precapillary sphincter and metarteriole was the rule, but this was noted infrequently in larger arterioles. In addition to an overall influence of the CNS on microcirculation, the data show a gradient of responses to stimulation, the slope of which is negatively related to the size of the vessels and sphincter, in both tissues studied. A complete lumen closure of the metarteriole and precapillary sphincter (when present) in response to CNS stimulation implies active participation in the regulation of local blood flow. No evidence was foun for central neural regulation of the precapillary sphincter independent of arteriolar control.     

Transcapillary fluid movement in human calf after drinking hypertonic saline

1. Transcapillary absorption of interstitial fluid was demonstrated with a pressure plethysmograph applied to the human calf after the ingestion of 200 ml. hypertonic (5.1%) saline. Capillary absorption began within 15 min after ingestion and lasted for about 2 hr. The maximum rate of absorption (0.019 ml./min. 100 ml. tissue) was attained 30-75 min after ingestion.2. The total amount of fluid absorbed into capillary blood vessels in the calf was 1.11 ml./100 ml. tissue. The amount of fluid thus absorbed in the whole body was estimated to be 677 ml.3. The capillary filtration coefficient (CFC) of the calf was also measured by the pressure plethysmograph. This was 0.0038 ml./min. mm Hg. 100 ml. tissue.4. The peak value of capillary absorption pressure was 5.2 mm Hg.5. The total osmotic pressure of the plasma rose by 12.6 m-osmole/kg H(2)O after ingestion. This rise was accompanied by transcapillary fluid absorption.6. The plasma protein concentration and packed cell volume were almost unchanged by ingestion, indicating that the plasma volume was unaltered.7. It was estimated that the net shift of fluid between intracellular and interstitial compartments during the period of transcapillary fluid absorption was very small.8. It is concluded that the volume of fluid moving from plasma into intestinal lumen is the same as that flowing from interstitial fluid into plasma, and that the transcapillary absorption is caused by a difference in osmotic pressure between the plasma and the interstitial fluid.     

Protective role of sympathetic nerve activity to exercising skeletal muscle in the regulation of capillary pressure and fluid filtration

This study describes the integrated sympathetic/metabolic control of capillary pressure (Pc) and filtration in cat skeletal muscle as studied during graded exercise and superimposed graded (2, 6 and 16 Hz) vasoconstrictor nerve excitation. The applied technique permitted simultaneous analysis of the underlying changes of resistance in the whole vascular bed (RT) and in its large-bore arterial resistance vessels (greater than 25 microns), small arterioles (less than 25 microns) and veins. Graded exercise per se caused graded increases in capillary pressure, which at heavy work exceeded the resting control value by 12.2 mmHg, in turn leading to marked loss of plasma fluid by filtration. Sympathetic nerve stimulation was much more efficient in lowering capillary pressure during exercise than at rest, in spite of an exercise-induced marked attenuation of the vasoconstrictor response (RT). The sympathetically evoked capillary pressure fall per unit resistance increase was larger the greater the degree of exercise vasodilation, implying a highly nonlinear relation between capillary pressure and RT and also between the more direct determinant of capillary pressure the post- to precapillary resistance ratio, and RT. Strenuous exercise in vivo is known to be associated with a markedly increased reflex sympathetic discharge to exercising muscle which has been a puzzling feature in view of its untoward restriction of the exercise hyperaemia response. To the extent the present results are representative for this in vivo situation, they suggest that sympathetic discharge to exercising muscle, in spite of some flow restricting effect, might serve a highly beneficial function, causing effective protection against excessive work-induced rise of capillary pressure and harmful plasma fluid loss into the extravascular space of working muscle.     

Beta Adrenergic Dilator Component of the Sympathetic Vascular Response in Skeletal Muscle Influence on the micro-circulation and on transcapillary exchange

A neurogenic β-adrenergic vasodilatation in skeletal muscle has been indicated by some recent investigations. The present study describes the extent to which this neurogenic β-dilator mechanism contributes to the integrated vascular response in consecutive sections of the muscle vascular bed during sympathetic nerve activation. This was done by studying the vascular reactions to graded sympathetic stimulation (1–16 Hz) before and after β-adrenoceptor blockade, β-blockade did not influence significantly the sympathetically induced changes of total muscle vascular resistance or capacitance. Vascular tone in the “micro-vessels” during stimulation was, however, clearly more pronounced in the β-blocked than in the non-blocked region, as revealed by segmental resistance analysis and by determination of precapillary sphincter tone (CFC). In addition, β-blockade markedly reduced the net transcapillary absorption of extravascular fluid evoked by nerve activation. This effect could be ascribed to the mentioned influence on the precapillary sphincters, leading to a decrease of the number of capillaries available for transcapillary exchange, and to a limitation of the nerve induced fall of capillary hydrostatic pressure. The described effects of β-blockade were observed at all rates of sympathetic stimulation. — The conclusion was reached that the β-adrenergic dilator component of the sympathetic vascular response in skeletal muscle significantly modifies the α-adrenergic constriction in the micro-vessels. It is suggested that, in the intact organism, this neurogenic β-dilator mechanism is primarily aimed at improving the transcapillary exchange.     

Beta adrenergic dilator component of the sympathetic vascular response in skeletal muscle. Influence on the micro-circulation and on transcapillary exchange.

A neurogenic beta-adrenergic vasodilatation in skeletal muscle has been indicated by some recent investigations. The present study describes the extent to which this neurogenic beta-dilator mechanism contributes to the integrated vascular response in consecutive sections of the muscle vascular bed during sympathetic nerve activation. This was done by studying the vascular reactions to graded sympathetic stimulation (1-16 Hz) before and after beta-adrenoceptor blockade. Beta-blockade did not influence significantly the sympathetically induced changes of total muscle vascular resistance or capacitance. Vascular tone in the "micro-vessels" during stimulation was, however, clearly more pronounced in the beta-blocked than in the non-blocked region, as revealed by segmental resistance analysis and by determination of precapillary sphincter tone (CFC). In addition, beta-blockade markedly reduced the net transcapillary absorption of extravascular fluid evoked by nerve activation. This effect could be ascribed to the mentioned influence on the precapillary sphincters, leading to a decrease of the number of capillaries available for transcapillary exchange, and to a limitation of the nerve induced fall of capillary hydrostatic pressure. The described effects of alpha-blockade were observed at all rates of sympathetic stimulation.--The conclusion was reached that the beta-adrenergic dilator component of the sympathetic vascular response in skeletal muscle significantly modifies the alpha-adrenergic constriction in the micro-vessels. It is suggested that, in the intact organism, this neurogenic beta-dilator mechanism is primarily aimed at improving the transcapillary exchange.     

β2-adrenergic control of plasma volume in hemorrhage

Hemorrhage is associated with absorption of extravascular fluid from skeletal muscle to blood in order to compensate for the loss of intravascular volume. Our previous studies have shown that this fluid gain is mainly linked to β-adrenergic microvascular adjustments leading to decrease in capillary hydrostatic pressure and to precapillary ‘sphincter’ mediated increase in the capillary surface area available for fluid exchange. In the present study the importance of β-adrenergic control of plasma volume in bleeding was confirmed by measurement of changes in plasma volume after graded hemorrhage in animals with intact and blocked vascular β₂-adrenoceptors (i. v. administration of the ‘selective’β₂-blocking agent ICI 118, 551). With intact β₂-adrenoceptors plasma volume was gradually restored after bleeding so that about 50% of the shed plasma volume (about 35% of the shed blood volume) had been compensated for at two hours after exsanguination of 20% as well as 40% of the blood volume. The corresponding figures in animals with blocked β₂-adrenoceptors were only 14% of the shed plasma volume and 8% of the shed blood volume at both degrees of hemorrhage.     

Beta 2-adrenergic attenuation of capillary pressure autoregulation during haemorrhagic hypotension, a mechanism promoting transcapillary fluid absorption in skeletal muscle.

The aim of this study was to evaluate a possible humoral beta 2-adrenergic effect on the capillary pressure autoregulation capacity in cat skeletal muscle during bleeding. For this purpose capillary pressure autoregulation in response to graded decrease in arterial pressure was studied in sympathectomized muscle in the control state, and during haemorrhagic hypovolaemia in the presence and absence of selective beta 2-adrenoceptor blockade (ICI 118,551). The study was performed with a technique that permits continuous recordings of average capillary pressure in absolute terms and of the regional pre- and postcapillary vascular resistance, from which the pre- to post capillary resistance ratio could be determined. In the pre-haemorrhagic control state, an experimental decrease in arterial pressure from 100 to 50 mmHg caused a fall of capillary pressure from 17.6 by only 1.7 mmHg (delta PA/delta Pc = 29), demonstrating an efficient capillary pressure autoregulation. This autoregulation was accomplished by a decrease in pre- to post capillary resistance ratio in turn being a result of active precapillary dilatation and a passive increase in post capillary vascular resistance. Haemorrhage per se, via a humoral alpha-adrenergic preferentially precapillary vasoconstriction, caused a decrease in capillary pressure to 16.8 mmHg at arterial pressure 100 mmHg. A superimposed decrease in arterial pressure to 50 mmHg resulted in a capillary pressure fall by 3.7 mmHg (delta PA/delta Pc = 14), indicating impaired auto-regulation capacity. This attenuation to a great extent could be ascribed to adrenaline-induced B2-adrenoceptor stimulation, since beta 2-blockade restored the delta arterial pressure/capillary pressure ratio to 20. Low-dose isoprenaline infusion in the control state similarly caused marked impairment of capillary pressure autoregulation. The beta 2-adrenergic attenuation of capillary pressure autoregulation appears to be a beneficial effect in haemorrhagic hypotension, since it lowers capillary pressure passively in relation to the arterial pressure fall, thereby reinforcing the alpha-adrenergic active capillary pressure decrease, leading to more effective transcapillary fluid absorption and, hence, improved replenishment of plasma volume.     

A method for in situ measurement of ionic concentration in picoliter samples of renal tubular fluid

A method permitting rapid and frequent determination of the total ionic concentration in renal tubular fluid samples, by measuring sample electrical impedance, is described. No special electrodes or sophisticated equipment are required. Since picoliter volumes are sufficient for measurement, tubular fluid dynamics are not significantly disturbed by the sampling procedure. The sample is aspirated into the tip of the standard glass micropipette and its ionic concentration, in the range of 100–1000 mmol/l, can be determined by any sensitive impedance-measuring device. In the present studies the Wheatstone bridge of the Wiederhielm apparatus for pressure measurement in micropuncture studies was used for the purpose. The obvious limitation of the method is that the measurements do not include nonelectrolytes and cannot differentiate between individual ion species.     

Orthostatic stress is necessary to maintain the dynamic range of cardiovascular control in space

In the upright position, gravity fills the low-pressure systems of human circulation with blood and interstitial fluid in the sections below the diaphragm. Without gravity one pressure component in the vessels disappears and the relationship between hydrostatic pressure and oncotic pressure, which regulates fluid passage across the capillary endothelium in the terminal vascular bed, shifts constantly. The visible consequences of this are a puffy face and "bird" legs. The plasma volume shrinks in space and the range of cardiovascular control is reduced. When they stand up for the first time after landing, 30-50% of astronauts suffer from orthostatic intolerance. It remains unclear whether microgravity impairs cardiovascular reflexes, or whether it is the altered volume status that causes the cardiovascular instability following space flight. Lower body negative pressure was used in several space missions to stimulate the cardiovascular reflexes before, during and after a space flight. The results show that cardiovascular reflexes are maintained in microgravity. However, the astronauts' volume status changed in space, towards a volume-retracted state, as measurements of fluid-regulating hormones have shown. It can be hypothesized that the control of circulation and body fluid homeostasis in humans is adapted to their upright posture in the Earth's gravitational field. Autonomic control regulates fluid distribution to maintain the blood pressure in that posture, which most of us have to cope with for two-thirds of the day. A determined amount of interstitial volume is necessary to maintain the dynamic range of cardiovascular control in the upright posture; otherwise orthostatic intolerance may occur more often.     

成年高原藏羊睾丸小叶内微血管分布和形态特征

目的 探讨成年高原藏羊睾丸小叶微血管构筑特征.方法 采用ABS树脂血管铸型技术、扫描电镜观察法、墨汁明胶石蜡切片及常规石蜡切片技术,观察30只成年高原藏羊睾丸小叶微血管的构筑特征.结果 睾丸小叶内由向心或离心动脉发出的管间微动脉及管间毛细血管穿行于相邻生精小管形成的结缔组织间隙内;管间毛细血管相互交通形成管周毛细血管围...