Myogenic responses and compliance of mesenteric and splenic vasculature in the rat

2003 ◽  
Vol 284 (6) ◽  
pp. R1604-R1610 ◽  
Author(s):  
Zoë L. S. Brookes ◽  
Susan Kaufman
Keyword(s):  
Perfusion Pressure ◽  
Arterial Diameter ◽  
Venous Capacitance ◽  
Fluid Extravasation ◽  
Venous Diameter ◽  
Vascular Beds ◽  
Myogenic Responses ◽  
Splenic Vessels ◽  
Free Media ◽  
Blood Reservoir

In the rat, the spleen is a major site of fluid efflux out of the blood. By contrast, the mesenteric vasculature serves as a blood reservoir. We proposed that the compliance and myogenic responses of these vascular beds would reflect their different functional demands. Mesenteric and splenic arterioles (∼150–200 μm) and venules (<250 μm) from rats anesthetized with pentobarbital sodium were mounted in a pressurized myograph. Mesenteric arterial diameter decreased from 146 ± 6 to 133 ± 6 μm on raising intraluminal pressures from 80 to 120 mmHg. This response was enhanced in the presence of N ω-nitro-l-arginine methyl ester (l-NAME; 139 ± 6 to 112 ± 7 μm). There was no such myogenic response in the splenic arterioles, except in the presence of l-NAME (194 ± 4 to 164 ± 4.2 μm). We propose that, whereas mesenteric arterioles exhibit myogenic responses, this is normally masked by NO-mediated dilation in the splenic vessels. The mesenteric venules were highly distensible (active, 184 ± 15 to 320 ± 30.9 μm; passive in Ca2+-free media, 209 ± 31 to 344 ± 27 μm; 4–8 mmHg) compared with the splenic vessels (active, 169 ± 11 to 184 ± 16 μm; passive, 187 ± 12 to 207 ± 17 μm). We conclude that, in response to an increase in perfusion pressure, mesenteric arterial diameter would decrease to limit the changes in flow and microvascular pressure. In addition, mesenteric venous capacitance would increase. By contrast, splenic arterial diameter would increase, while there would be little change in venous diameter. This would enhance the increase in intrasplenic microvascular pressure and increase fluid extravasation.

Vasodilation contributes to the rapid hyperemia with rhythmic contractions in humans

1998 ◽  
Vol 76 (4) ◽  
pp. 418-427 ◽  
Author(s):  
J K Shoemaker ◽  
M E Tschakovsky ◽  
R L Hughson
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Perfusion Pressure ◽  
Blood Velocity ◽  
Pulsed Doppler ◽  
Contraction Rate ◽  
Handgrip Exercise ◽  
Arterial Diameter ◽  
Exercise Tests ◽  
Rhythmic Contractions

The hypothesis that the rapid increases in blood flow at the exercise onsetare exclusively due to the mechanical effects of the muscle pump was tested in six volunteersduring dynamic handgrip exercise. While supine, each subject completed a series of eightdifferent exercise tests in which brachial artery blood pressure (BP) was altered by25–30 mmHg (1 mmHg = 133.3 Pa) by positioning the arm above or below the heart.Two different weights, corresponding to 4.9 and 9.7% of maximal voluntary isometriccontraction, were raised and lowered at two different contraction rate schedules (1s:1s and 2s:2swork–rest) each with a 50% duty cycle. Beat-by-beat measures of mean blood velocity (MBV)(pulsed Doppler) were obtained at rest and for 5 min following step increases in work ratewith emphasis on the first 24 s. MBV was increased 50–100% above rest following the firstcontraction in both arm positions (p < 0.05). The increase in MBV from rest was greaterin the below position compared with above, and this effect was observed following the first andsubsequent contractions (p < 0.05). However, the positional effect on the increase inMBV could not be explained entirely by the ~40% greater BP in this position. Also, the greaterworkload resulted in greater increases in MBV as early as the first contraction, compared withthe light workload (p < 0.05) despite similar reductions in forearm volume followingsingle contractions. MBV was greater with faster contraction rate tests by 8 s of exercise. Itwas concluded that microvascular vasodilation must act in concert with a reduction in venouspressure to increase forearm blood flow within the initial 2–4 s of exercise.Key words: Doppler, mean blood velocity, arterial diameter,handgrip exercise, perfusion pressure.

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

2004 ◽  
Vol 97 (2) ◽  
pp. 683-688 ◽  
Author(s):  
Roger De Moraes ◽  
Giovanni Gioseffi ◽  
Antonio C. L. Nóbrega ◽  
Eduardo Tibiriçá
Keyword(s):  
Exercise Training ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Rabbit Kidney ◽  
Constant Flow ◽  
Renal Circulation ◽  
New Zealand White Rabbits ◽  
Vascular Beds ◽  
Renal Vascular ◽  
Isolated Kidneys

Exercise training is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro- and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n = 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n = 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 ± 8% ( n = 6; P < 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 ± 6% ( n = 6; P < 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 ± 8 and 13 ± 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P > 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with Nω-nitro-l-arginine methyl ester (l-NAME; 300 μM), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 ± 6 and 38 ± 5% for ExT and l-NAME + ExT, respectively ( n = 6; P < 0.05)]. On the other hand, l-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 ± 7 and 45 ± 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P < 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO.

Contrasting Effects of Colloid and Crystalloid Resuscitation Fluids on Cardiac Vascular Permeability

2006 ◽  
Vol 104 (6) ◽  
pp. 1223-1231 ◽  
Author(s):  
Matthias Jacob ◽  
Dirk Bruegger ◽  
Markus Rehm ◽  
Ulrich Welsch ◽  
Peter Conzen ◽  
...  
Keyword(s):  
Hydroxyethyl Starch ◽  
Perfusion Pressure ◽  
Ex Vivo ◽  
Myocardial Edema ◽  
Endothelial Glycocalyx ◽  
Perfused Heart ◽  
Fluid Filtration ◽  
Fluid Extravasation ◽  
The Impact ◽  
Krebs Henseleit Buffer

Background Fluid extravasation may lead to myocardial edema and consequent reduction in ventricular function. Albumin is presumed to interact with the endothelial glycocalyx. The authors' objective was to compare the impact of different resuscitation fluids (human albumin, hydroxyethyl starch, saline) on vascular integrity. Methods In an isolated perfused heart model (guinea pig), Krebs-Henseleit buffer was augmented with colloids (one third volume 5% albumin or 6% hydroxyethyl starch 130/0.4) or crystalloid (0.9% saline). Perfusion pressure and vascular fluid filtration (epicardial transudate formation) were assessed at different flow rates. After global, stopped-flow ischemia (37 degrees C, 20 min), hearts were reperfused with the same resuscitation fluid additives. In a second series, the authors applied the respective perfusates after enzymatic digestion of the endothelial glycocalyx (heparinase, 10 U over 15 min). Results Both 5% albumin and 6% hydroxyethyl starch decreased fluid extravasation versus saline (68.4 +/- 5.9, 134.8 +/- 20.5, and 436.8 +/- 14.7 microl/min, respectively, at 60 cm H(2)O perfusion pressure; P &lt; 0.05), the corresponding colloid osmotic pressures being 2.95, 5.45, and 0.00 mmHg. Digestion of the endothelial glycocalyx decreased coronary integrity in both colloid groups. After ischemia, a transient increase in vascular leak occurred with Krebs-Henseleit buffer containing hydroxyethyl starch and saline, but not with albumin. The authors observed no difference between intravascular and bulk interstitial colloid concentration in the steady state. Notwithstanding, electron microscopy revealed an intact endothelial glycocalyx and no interstitial edema in the albumin group. Conclusion Ex vivo, albumin more effectively prevented fluid extravasation in the heart than crystalloid or artificial colloid. This effect was partly independent of colloid osmotic pressure and may be attributable to an interaction of albumin with the endothelial glycocalyx.

scholarly journals Reduced Uterine Perfusion Pressure in Pregnant Rats Impairs Cerebral Vascular Myogenic Responses

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Michael J Ryan ◽  
Emily L Gilbert ◽  
Porter H Glover ◽  
Babbette D LaMarca ◽  
Joey P Granger
Keyword(s):  
Perfusion Pressure ◽  
Pregnant Rats ◽  
Myogenic Responses ◽  
Uterine Perfusion ◽  
Cerebral Vascular

Abstract P266: Thromboxane-prostanoid Receptors (tp-rs) Mediate Hypertension, H2o2 Generation and Impaired Renal Afferent Arteriolar Myogenic Responses Leading to Nephropathy in Doca/salt Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Christopher S Wilcox ◽  
Lingli Li ◽  
En Yin Lai ◽  
Adam Hosszu ◽  
William J Welch
Keyword(s):  
Blood Pressure ◽  
Perfusion Pressure ◽  
High Salt ◽  
Myogenic Tone ◽  
Prostanoid Receptors ◽  
Hypertensive Nephropathy ◽  
Sham Treatment ◽  
H2o2 Generation ◽  
Afferent Arterioles ◽  
Myogenic Responses

Background: DOCA/uninephrectomy/high salt (DOCA) is a model of hypertensive nephropathy. Afferent arteriolar myogenic responses prevent hypertensive renal barotrauma but myogenic tone is blocked by vascular generation of H 2 O 2 . Since thromboxane-prostanoid receptors (TP-Rs) generate H 2 O 2 , we tested the hypothesis that they mediate hypertensive nephropathy. Methods: DOCA and Sham TP-R +/+ and -/- mice (n=6/group) were studied at 2 weeks and myogenic responses recorded from the diameter of perfused single afferent arterioles studied in a bath preparation during increased perfusion pressure (40 to 80 mmHg). Results: DOCA treatment in TP-R +/+ mice increased (p<0.001) 24-hour excretion of H 2 O 2 (45 ± 3 vs 220 + 15 nmol) , TxB 2 (4 ± 2 vs 29 ± 4 pmol) and albumin (20 ± 5 vs 270 ± 20 mg) and increased MAP by 35 ± 5 mmHg. However, all effects of DOCA were prevented in TP-R -/- mice. Sham treatment had no effect in TPR +/+ or -/- mice. Myogenic responses were severely impaired in DOCA vs sham WT mice (Δ diameter: -4 ± 1 vs -8 ± 1%; p< 0.005). Myogenic responses also were reduced by incubation of arterioles with 10 -10 mol·l -1 of the TP-R mimetic, U-46,619 vs vehicle added to the bath for 10 minutes (Δ diameter: -7 ± 1 vs -10 ± 1%; p<0.01) and in WT mice infused for 3 days with U-46,619 (500 ng·kg -1 ·d -1 x 3) vs vehicle (Δ diameter: -3 ± 1 vs -10 ± 1%; p<0.005). Conclusion: Hypertensive nephropathy is dependent on TP-Rs that mediate the increase in H 2 O 2 and blood pressure and likely the impaired myogenic responses that expose the kidney to barotrauma

Sympathetic and Mesenteric Venous Responses to Baroreceptor or Chemoreceptor Stimulation during Epidural Anesthesia in Rabbits

1996 ◽  
Vol 85 (6) ◽  
pp. 1413-1421. ◽  
Author(s):  
Quinn H. Hogan ◽  
Alexander Kulier ◽  
Zeljko J. Bosnjak ◽  
John P. Kampine
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Epidural Anesthesia ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Venous Capacitance ◽  
Epidural Blockade ◽  
Mesenteric Veins ◽  
Bilateral Carotid ◽  
Venous Diameter

Background Baroreceptor and chemoreceptor reflexes maintain homeostasis through mechanisms that involve sympathetic activation. Because sympathetic control of the mesenteric veins plays a central role in hemodynamic responses to stress, the effects of epidural blockade on reflex responses to hypoxia and bilateral carotid occlusion (BCO) were examined by monitoring direct measures of splanchnic sympathetic neural traffic and mesenteric venous capacitance. Methods Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric venous diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Intraluminal venous pressure was monitored by a servo-null micropressure technique. Responses were recorded during repeated administration of three different stresses, F1O2 = 0% for 40 s, F1O2 = 11% for 2.5 min, and BCO for 60 s. Animals received either thoracolumbar epidural blockade (0.4 ml/kg lidocaine 1.5%; n = 7) or 15 mg/kg intramuscular lidocaine (n = 7). Results Hypoxia and BCO produced sympathetic stimulation and active constriction of mesenteric veins. Epidural anesthesia accentuated the mean arterial pressure decrease from F1O2 of 0%, caused the 11% response to F1O2 to become depressor instead of pressor, and decreased the pressor effect BCO. Sympathetic efferent nerve activity and venous diameter responses to hypoxia and BCO were attenuated or eliminated. Conclusions The hemodynamic effects of hypoxia result from a combination of direct depression and reflex activation. Thoracolumbar epidural anesthesia in rabbits impairs compensatory reflexes invoked by chemoreceptor stimulation and eliminates response to baroreceptor stimulation. Loss of splanchnic control of mesenteric capacitance contributes to the inhibition of the hemodynamic response to hypoxia or BCO during epidural anesthesia in rabbits.

scholarly journals Behavior of Vascular Beds In the Human Upper Limb at Low Perfusion Pressure

1967 ◽  
Vol 21 (3) ◽  
pp. 319-326 ◽  
Author(s):  
GEOFFREY M. COLLINS ◽  
JOHN LUDBROOK
Keyword(s):  
Upper Limb ◽  
Perfusion Pressure ◽  
Vascular Beds ◽  
Human Upper Limb

Dynamic changes in venous outflow by baroreflex and left ventricular distension

1988 ◽  
Vol 254 (2) ◽  
pp. R212-R221 ◽  
Author(s):  
S. Hoka ◽  
Z. J. Bosnjak ◽  
D. Siker ◽  
R. J. Luo ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Nerve Activity ◽  
Venous Outflow ◽  
Dynamic Changes ◽  
Venous Capacitance ◽  
Additional Group ◽  
Vascular Beds

We examined the dynamic changes in venous outflow from the splanchnic and extrasplanchnic vascular beds in response to carotid sinus (CS) baroreflex and left ventricular (LV) distension in 12 dogs anesthetized with pentobarbital sodium. Splenic sympathetic nerve activity was measured in an additional group of six dogs. A heart-lung bypass was used with constant cardiac output and constant venous pressure. LV distension was produced by inflating a balloon in the LV. LV distension and an increase in CS pressure from 50 to 200 mmHg decreased blood pressure by 26 +/- 5 and 30 +/- 6 mmHg and increased vascular capacitance by 5.5 +/- 0.9 and 4.5 +/- 1.2 ml/kg, respectively. Splanchnic venous outflow exhibited a transient decrease, whereas extrasplanchnic venous outflow showed a transient increase, in response to LV distension and increasing CS pressure, accompanied by a sustained decrease in splenic nerve activity. The results indicate important differences between splanchnic and extrasplanchnic components of the total venous system in terms of the regulation of venous capacitance. It is suggested that changes in venous capacitance produced by LV distension and CS baroreflex are primarily due to active changes in splanchnic venous tone.

Blood reservoir function in patients with Fontan circulation and asplenia syndrome

2019 ◽  
Vol 29 (8) ◽  
pp. 1016-1019
Author(s):  
Michitaka Fuse ◽  
Kenji Sugamoto ◽  
Seiko Kuwata ◽  
Rika Sekiya ◽  
Kohei Kawada ◽  
...  
Keyword(s):  
Blood Volume ◽  
Filling Pressure ◽  
Fontan Circulation ◽  
Splanchnic Circulation ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Hepatic Congestion ◽  
The Mean ◽  
Asplenia Syndrome ◽  
Blood Reservoir

AbstractSplanchnic circulation constitutes a major portion of the vasculature capacitance and plays an important role in maintaining blood perfusion. Because patients with asplenia syndrome lack this vascular bed as a blood reservoir, they may have a unique blood volume and distribution, which may be related to their vulnerability to the haemodynamic changes often observed in clinical practice. During cardiac catheterisation, the mean circulatory filling pressure was calculated with the Valsalva manoeuvre in 19 patients with Fontan circulation, including 5 patients with asplenia syndrome. We also measured the cardiac output index and circulatory blood volume by using a dye dilution technique. The blood volume and the mean circulatory filling pressure and the venous capacitance in patients with asplenia syndrome were similar to those in the remaining patients with Fontan circulation (85 ± 14 versus 77 ± 18 ml/kg, p = 0.43, 31 ± 8 versus 27 ± 5 mmHg, p = 0.19, 2.8 ± 0.6 versus 2.9 ± 0.9 ml/kg/mmHg, p = 0.86). Unexpectedly, our data indicated that patients with asplenia syndrome, who lack splanchnic capacitance circulation, have blood volume and venous capacitance comparable to those in patients with splanchnic circulation. These data suggest that (1) there is a blood reservoir other than the spleen even in patients with asplenia; (2) considering the large blood pool of the spleen, the presence of a symmetrical liver may represent the possible organ functioning as a blood reservoir in asplenia syndrome; and (3) if this is indeed the case, there may be a higher risk of hepatic congestion in patients with Fontan circulation with asplenia syndrome than in those without.

Regional autoregulatory responses during infusion of vasoconstrictor agents in conscious dogs

1990 ◽  
Vol 259 (4) ◽  
pp. H1270-H1277 ◽  
Author(s):  
L. J. Hellebrekers ◽  
J. F. Liard ◽  
A. L. Laborde ◽  
A. S. Greene ◽  
A. W. Cowley
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Conscious Dogs ◽  
Flow Probe ◽  
Electromagnetic Flow ◽  
Vascular Bed ◽  
Vasoconstrictor Agents ◽  
Electromagnetic Flow Probe ◽  
Vascular Beds ◽  
Renal Vascular

We investigated pressure-dependent autoregulatory responses in mesenteric, iliac, and renal vascular beds of conscious dogs during intravenous infusion of angiotensin II, phenylephrine, or arginine vasopressin at rates which increased arterial pressure by 20-40 mmHg. The arteries supplying these beds were instrumented with an electromagnetic flow probe, a nonoccluding catheter, and an electromagnetic flow probe, a nonoccluding catheter, and an occluder cuff connected with a servo-amplifier, which enabled us to return perfusion pressure to control levels during infusion of the vasoconstrictor agents. We attempted to differentiate between the increase in vascular resistance due to the direct effect of the vasoconstrictor agent and the increase induced by an autoregulatory response induced by elevations of aortic perfusion pressure. We measured a strong degree of autoregulation in the renal vascular bed with a fractional compensation value close to 1. Moderate autoregulation occurred in the mesenteric vascular bed, where the compensation was 0.4-0.5 with angiotensin II and phenylephrine and between 0.74 and 0.94 with vasopressin. No autoregulatory capacity could be demonstrated in the hindlimb. The findings indicate that, under conditions of increased systemic blood pressure, both the renal and the mesenteric vascular beds contribute to the increase in total peripheral resistance by pressure-dependent vasoconstrictor responses.

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