Vasodilation induced by endothelin: role of EDRF and prostanoids in rat hindquarters

1990 ◽  
Vol 259 (6) ◽  
pp. H1835-H1841 ◽  
Author(s):  
E. H. Ohlstein ◽  
L. Vickery ◽  
C. Sauermelch ◽  
R. N. Willette
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Microvascular Perfusion ◽  
Hemodynamic Effects ◽  
Hemodynamic Responses ◽  
Pithed Rats ◽  
Dose Dependent

Hemodynamic responses to endothelin (ET-1) were studied in hindquarters of anesthetized rats and also in isolated buffer-perfused hindquarters of pithed rats. ET-1 (10-100 pmol ia) produced brief dose-related increases in hindquarter blood flow. Acetylcholine (ACh. 0.3-1 micrograms ia) produced similar vasodilator responses. Hemodynamic responses elicited by either ET-1 or ACh were not significantly altered by pretreatment with indomethacin. ET-1 produced dose-dependent increases in skeletal muscle microvascular perfusion, whereas ET-1 had no effect on cutaneous microvascular perfusion, suggesting that vasodilation in the skeletal muscle of the hindlimb contributes to the increase in hindquarter blood flow induced by ET-1. Hemodynamic effects of ET-1 and ACh were studied in the isolated in situ buffer-perfused hindquarters of pithed rats. ET-1 (0.01-300 pmol ia) produced only dose-dependent increases in hindquarter perfusion pressure under basal conditions or when the vascular preparation was precontracted with methoxamine. ET-1 induced vasorelaxation was not observed. ACh (3 microgram ia) produced a 64% reduction in hindquarter perfusion pressure; indicative of endothelium-dependent relaxation. ET-3 (0.1-300 pmol) produced only dose-dependent increases in hindquarter perfusion pressure. When hemodynamic effects of ET-1 were studied under conditions of constant pressure, results were similar to those obtained under constant flow. This study demonstrates that in the rat hindquarters endothelium-derived relaxing factors and prostanoids do not appear to be mediators of endothelin-induced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic control of swimbladder perfusion in the European eel Anguilla anguilla.

1994 ◽  
Vol 189 (1) ◽  
pp. 237-250 ◽  
Author(s):  
B Pelster
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Dorsal Aorta ◽  
Initial Increase ◽  
European Eel ◽  
Rete Mirabile ◽  
Adrenergic Control ◽  
Dose Dependent

Adrenergic control of swimbladder blood flow was analysed in blood-perfused preparations of the European eel as well as in situ by recording the changes in swimbladder blood flow and blood pressure following an injection of catecholamine into the dorsal artery. In blood-perfused swimbladder preparations, injection of the alpha-adrenergic agonist phenylephrine into the perfusion loop caused a marked dose-dependent increase in perfusion pressure at constant flow, while injection of the beta-agonist isoproterenol slightly decreased perfusion pressure. The beta-effect was not as pronounced as the alpha-adrenergic vasoconstriction and was observed only during the first application of catecholamine in each preparation. In situ injection of adrenaline (final concentration 10(-8)-10(-9) mol kg-1 body mass) into the dorsal aorta caused a dose-dependent transient increase in dorsal aortic blood pressure and in cardiac output which, after 5-10 min, returned to resting levels. Swimbladder perfusion also increased initially after an injection of adrenaline, but after about 1-2 min suddenly decreased and then slowly recovered to preinjection levels. Following the injection of adrenaline into the dorsal aorta, blood pressure changes in vessels at the swimbladder pole of the rete mirabile revealed a similar biphasic pattern with an initial increase, a subsequent decrease and a slow return to preinjection levels, while pressure in the arterial influx vessel of the rete resembled dorsal aortic pressure. After injection of the beta-blocker propranolol, adrenaline evoked a smaller initial increase in blood flow, but the subsequent reduction in flow was even more pronounced. Injection, in addition, of the alpha-adrenergic blocker phentolamine abolished the sharp adrenaline-induced decrease in swimbladder perfusion. It is concluded that alpha- and beta-adrenergically controlled resistance vessels are located close to the rete mirabile, probably at the arterial entrance into the rete. These vessels control perfusion of the rete mirabile and of the swimbladder and are thus involved in the control of gas deposition into the swimbladder.

cGMP phosphodiesterase inhibition improves the vascular and metabolic actions of insulin in skeletal muscle

2011 ◽  
Vol 301 (2) ◽  
pp. E342-E350 ◽  
Author(s):  
A. J. Genders ◽  
E. A. Bradley ◽  
S. Rattigan ◽  
S. M. Richards
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Mrna Level ◽  
Microvascular Perfusion ◽  
Microvascular Blood Flow ◽  
Whole Body ◽  
Acute Administration ◽  
Dependent Inhibition ◽  
Promising Avenue

There is considerable support for the concept that insulin-mediated increases in microvascular blood flow to muscle impact significantly on muscle glucose uptake. Since the microvascular blood flow increases with insulin have been shown to be nitric oxide-dependent inhibition of cGMP-degrading phosphodiesterases (cGMP PDEs) is predicted to enhance insulin-mediated increases in microvascular perfusion and muscle glucose uptake. Therefore, we studied the effects of the pan-cGMP PDE inhibitor zaprinast on the metabolic and vascular actions of insulin in muscle. Hyperinsulinemic euglycemic clamps (3 mU·min−1·kg−1) were performed in anesthetized rats and changes in microvascular blood flow assessed from rates of 1-methylxanthine metabolism across the muscle bed by capillary xanthine oxidase in response to insulin and zaprinast. We also characterized cGMP PDE isoform expression in muscle by real-time PCR and immunostaining of frozen muscle sections. Zaprinast enhanced insulin-mediated microvascular perfusion by 29% and muscle glucose uptake by 89%, while whole body glucose infusion rate during insulin infusion was increased by 33% at 2 h. PDE2, -9, and -10 were the major isoforms expressed at the mRNA level in muscle, while PDE1B, -9A, -10A, and -11A proteins were expressed in blood vessels. Acute administration of the cGMP PDE inhibitor zaprinast enhances muscle microvascular blood flow and glucose uptake response to insulin. The expression of a number of cGMP PDE isoforms in skeletal muscle suggests that targeting specific cGMP PDE isoforms may provide a promising avenue for development of a novel class of therapeutics for enhancing muscle insulin sensitivity.

scholarly journals Role of Nebulin on Actomyosin Interaction Studied in situ in Demembranated Skeletal Muscle Fibers from Newborn Mice

2009 ◽  
Vol 96 (3) ◽  
pp. 127a
Author(s):  
M.L. Bang ◽  
M. Caremani ◽  
E. Brunello ◽  
R. Littlefield ◽  
R. Lieber ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Newborn Mice ◽  
Skeletal Muscle Fibers ◽  
Actomyosin Interaction

scholarly journals Role of Perfusion Pressure in Major Organ Blood Flow during Cardiopulmonary Bypass in Canines

2000 ◽  
Vol 39 (5) ◽  
pp. 748
Author(s):  
Young Lan Kwak ◽  
Young Hwan Park ◽  
Sang Beom Nam ◽  
Young Jun Oh ◽  
Seung Ho Kim ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Perfusion Pressure ◽  
Organ Blood Flow ◽  
Major Organ

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

1997 ◽  
Vol 272 (6) ◽  
pp. H2541-H2546 ◽  
Author(s):  
G. Dornyei ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Thromboxane A2 ◽  
No Synthase ◽  
Gracilis Muscle ◽  
Vasoactive Agents ◽  
Before And After ◽  
Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

Blood flow elevation increases VO2 maximum during repetitive tetanic contractions of dog muscle in situ

1993 ◽  
Vol 74 (4) ◽  
pp. 1499-1503 ◽  
Author(s):  
W. F. Brechue ◽  
B. T. Ameredes ◽  
G. M. Andrew ◽  
W. N. Stainsby
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Power Production ◽  
Arterial Supply ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Control Series ◽  
Flow Through ◽  
Series Of Experiments

Blood flow through the gastrocnemius-plantaris muscle of the dog in situ was increased by a pump in the arterial supply during a 30-min period of 1/s isotonic tetanic contractions. Compared with a control series of experiments with normoxemia and spontaneous flow, the pump increased flow 84%, from 1.51 +/- 0.08 to 2.78 +/- 0.15 ml.g-1.min-1. The perfusion pressure was increased from 125 to 196 mmHg. The pump hyperemia increased maximal O2 uptake (VO2) at 5 min of contractions by 31%, from 8.97 +/- 0.44 to 12.89 +/- 0.30 mumol.g-1.min-1. The extraction was decreased, and venous PO2 (PVO2) was increased. Fatigue, measured as a drop in power production from the highest level at 10 s to 30 min, was 49% during pump hyperemia and 54% in the control conditions. VO2 decreased 30% from the 5-min value to the 30-min value with pump hyperemia and 28% over the same time in the control conditions. At maximal VO2, the ratio VO2/PVO2 was increased by pump hyperemia compared with control conditions, suggesting an increased O2 diffusing conductance of the muscles. We conclude that the elevated perfusion pressure of pump hyperemia increased flow to raise maximal VO2 mainly in areas of the muscle that had restricted flow under control conditions.

Postprandial intestinal hyperemia: role of bile salts in the ileum

1981 ◽  
Vol 241 (6) ◽  
pp. G469-G477 ◽  
Author(s):  
P. R. Kvietys ◽  
J. M. McLendon ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Bile Salt ◽  
Bile Salts ◽  
Dependent Manner ◽  
Salt Solutions ◽  
Dose Dependent ◽  
Oxygen Difference ◽  
Artificial Pressure

In an autoperfused dog ileum preparation, artificial pressure, venous outflow pressure, blood flow, and arteriovenous oxygen difference were measured while bile and bile salt solutions, at physiological concentrations, were placed in the lumen. Intraluminal placement of endogenous bile, synthetic bile, or bile salt solutions increased ileal blood flow (99 +/- 10, 94 +/- 20, and 104 +/- 17%, respectively) and oxygen uptake (30 +/- 5, 36 +/- 9, and 28 +/- 5%, respectively). Endogenous bile pretreated with cholestyramine, a bile salt-sequestering resin, did not alter ileal blood flow, yet increased ileal oxygen uptake by 11 +/- 3%, a response similar to that observed while Tyrode's solution (the vehicle) was in the lumen. Intra-arterial infusion of bile salts increased ileal blood flow in a dose-dependent manner, while not significantly altering ileal oxygen uptake. The results of the present study indicate that bile salts play an important role in the functional (postprandial) hyperemia in the ileum by 1) directly dilating the ileal vasculature and 2) enhancing ileal metabolism during their active absorption.

Mechanical factors and the regulation of perfusion through atelectatic lung in pigs

1982 ◽  
Vol 52 (3) ◽  
pp. 647-654 ◽  
Author(s):  
S. Enjeti ◽  
P. B. Terry ◽  
H. A. Menkes ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Vascular Conductance ◽  
Hemodynamic Responses ◽  
Closed Chest ◽  
Open Chest ◽  
Regional Hemodynamics ◽  
Mechanical Factors

The role of mechanical interdependence in the perfusion of atelectatic lung was studied in two ways: a) regional hemodynamics were compared before (control) and after the development of lobar and sublobar atelectasis, and b) the effect of thoracotomy on regional hemodynamics was assessed. With lobar atelectasis mean lobar blood flow and vascular conductance decreased to 60% of control. Sublobar atelectasis caused mean sublobar blood flow and vascular conductance to decrease to 6% of control. Opening the chest after production of lobar atelectasis caused blood flow to fall to 50% of control. When sublobar atelectasis was produced in the open chest, sublobar blood flow decreased to 25% of control measurements made prior to thoracotomy. We conclude that with a closed chest, sublobar vascular distortion mediated by mechanical interdependence may be an important mechanism responsible for the differences in hemodynamic responses to atelectasis between lobes and sublobar regions.

scholarly journals Role of convective O2 delivery in determiningV˙o 2 on-kinetics in canine muscle contracting at peak V˙o 2

2000 ◽  
Vol 89 (4) ◽  
pp. 1293-1301 ◽  
Author(s):  
Bruno Grassi ◽  
Michael C. Hogan ◽  
Kevin M. Kelley ◽  
William G. Aschenbach ◽  
Jason J. Hamann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Muscle Fatigue ◽  
Oxidative Metabolism ◽  
Muscle Blood Flow ◽  
Content Difference ◽  
O2 Delivery ◽  
Gastrocnemius Muscles

A previous study (Grassi B, Gladden LB, Samaja M, Stary CM, and Hogan MC, J Appl Physiol 85: 1394–1403, 1998) showed that convective O2 delivery to muscle did not limit O2 uptake (V˙o 2) on-kinetics during transitions from rest to contractions at ∼60% of peakV˙o 2. The present study aimed to determine whether this finding is also true for transitions involving contractions of higher metabolic intensities.V˙o 2 on-kinetics were determined in isolated canine gastrocnemius muscles in situ ( n = 5) during transitions from rest to 4 min of electrically stimulated isometric tetanic contractions corresponding to the muscle peakV˙o 2. Two conditions were compared: 1) spontaneous adjustment of muscle blood flow (Q˙) (Control) and 2) pump-perfused Q˙, adjusted ∼15–30 s before contractions at a constant level corresponding to the steady-state value during contractions in Control (Fast O2 Delivery). In Fast O2 Delivery, adenosine was infused intra-arterially. Q˙ was measured continuously in the popliteal vein; arterial and popliteal venous O2 contents were measured at rest and at 5- to 7-s intervals during the transition. Muscle V˙o 2 was determined as Q˙times the arteriovenous blood O2 content difference. The time to reach 63% of the V˙o 2 difference between resting baseline and steady-state values during contractions was 24.9 ± 1.6 (SE) s in Control and 18.5 ± 1.8 s in Fast O2 Delivery ( P < 0.05). FasterV˙o 2 on-kinetics in Fast O2Delivery was associated with an ∼30% reduction in the calculated O2 deficit and with less muscle fatigue. During transitions involving contractions at peak V˙o 2, convective O2 delivery to muscle, together with an inertia of oxidative metabolism, contributes in determining theV˙o 2 on-kinetics.

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