Effects of metabolic blockade on distribution of blood flow to respiratory muscles

1988 ◽  
Vol 64 (1) ◽  
pp. 174-180 ◽  
Author(s):  
R. L. Johnson ◽  
M. B. Reid
Keyword(s):  
Blood Flow ◽  
Respiratory Muscles ◽  
Tca Cycle ◽  
Triceps Brachii ◽  
Active Muscle ◽  
Citrate Metabolism ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Inhibition Of Glycolysis ◽  
Increased Blood Flow

Sublethal inhibition of citrate metabolism in the tricarboxylic acid (TCA) cycle with monofluoroacetate (MFA) has been shown to cause a fivefold increase in myocardial blood flow without any change in cardiac output, blood pressure, or O2 consumption (C. Liang, J. Clin. Invest. 60: 61-69, 1977); however, blood flow did not increase to any organs examined other than the heart, including resting limb skeletal muscle. Preferential inhibition of glycolysis with iodoacetate (IA) failed to cause similar changes in distribution of blood flow. This unique response of myocardium to TCA cycle inhibition suggested a unique metabolic control of cardiac vasodilation. An alternate explanation is that MFA is preferentially concentrated in active muscle. After MFA, tissue citrate accumulates behind the block and the highest levels are reported in the heart and diaphragm, suggesting enhanced blockade or enhanced compensation in these two continuously active muscles. To test the hypothesis that vasodilation in the heart after MFA is not unique and that similar vasodilation will be evoked in active respiratory muscles, we measured blood flow to the myocardium, kidney, diaphragm, intercostals, transverse abdominals, and triceps brachii in anesthetized dogs using radionuclide-labeled microspheres, before and after MFA, and in another set of dogs before and after IA. Before MFA or IA, inspiratory loading significantly increased blood flow to active muscles of breathing in proportion to the added load. After MFA, blood flow to active muscles of breathing as well as to the heart became abnormally elevated with respect to mechanical work, and loading evoked no further increase in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular responses of dura mater

1989 ◽  
Vol 257 (1) ◽  
pp. H157-H161 ◽  
Author(s):  
F. M. Faraci ◽  
K. A. Kadel ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Substance P ◽  
Dura Mater ◽  
Sympathetic Nerves ◽  
Vascular Headache ◽  
Vascular Responses ◽  
Anesthetized Dogs ◽  
High Level ◽  
The Brain ◽  
Increased Blood Flow

The goal of this study was to examine vascular responses of the dura mater. Microspheres were used to measure blood flow to the dura and brain in anesthetized dogs. Under control conditions, blood flow to the dura was 38 +/- 3 (SE) ml.min-1.100 g-1. Values for blood flow to the dura obtained with simultaneous injection of 15- and 50-microns microspheres were similar, which suggests that shunting of 15-microns spheres was minimal. Left atrial infusion of substance P (100 ng.kg-1.min-1) and serotonin (40 micrograms.kg-1.min-1), two agonists that have been reported to increase vascular permeability in the dura, increased blood flow to the dura two- to threefold. Adenosine (iv) produced vasodilatation in the dura. Adenosine and serotonin did not affect cerebral blood flow, but substance P increased blood flow to the brain by approximately 40%. Seizures, which produce pronounced dilatation of cerebral vessels despite activation of sympathetic nerves, produced vasoconstriction in the dura. Thus 1) the dura is perfused at a relatively high level of blood flow under normal conditions and is very responsive to vasoactive stimuli, and 2) substance P and serotonin, which have been implicated in the pathogenesis of vascular headache, produce pronounced vasodilator responses in the dura mater.

Role of adenosine in postprandial and reactive hyperemia in canine jejunum

1992 ◽  
Vol 263 (4) ◽  
pp. G487-G493 ◽  
Author(s):  
D. R. Sawmiller ◽  
C. C. Chou
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Concentration Difference ◽  
Adenosine Concentration ◽  
Anesthetized Dogs ◽  
Series Of Experiments ◽  
Increased Blood Flow

The role of adenosine in postprandial jejunal hyperemia was investigated by determining the effect of placement of predigested food into the jejunal lumen on blood flow and oxygen consumption before and during intra-arterial infusion of dipyridamole (1.5 microM arterial concn) or adenosine deaminase (9 U/ml arterial concn) in anesthetized dogs. Neither drug significantly altered resting jejunal blood flow and oxygen consumption. Before dipyridamole or deaminase, food placement increased blood flow by 30-36%, 26-42%, and 21-46%, and oxygen consumption by 13-22%, 21-22%, and 26-29%, during 0- to 3-, 4- to 7-, and 8- to 11-min placement periods, respectively. Adenosine deaminase abolished the entire 11-min hyperemia, whereas dipyridamole significantly enhanced the initial 7-min hyperemia (45-49%). Both drugs abolished the initial 7-min food-induced increase in oxygen consumption. Dipyridamole attenuated (14%), whereas deaminase did not alter (28%), the increased oxygen consumption that occurred at 8-11 min. Adenosine deaminase also prevented the food-induced increase in venoarterial adenosine concentration difference. In separate series of experiments, luminal placement of food significantly increased jejunal lymphatic adenosine concentration and release. Also, reactive hyperemia was accompanied by an increase in venous adenosine concentration and release. This study provides further evidence to support the thesis that adenosine plays a role in postprandial and reactive hyperemia in the canine jejunum.

Effect of inhaled and intravenous acetylcholine on bronchial blood flow in anesthetized sheep

1996 ◽  
Vol 80 (1) ◽  
pp. 341-344 ◽  
Author(s):  
M. Scuri ◽  
V. McCaskill ◽  
A. D. Chediak ◽  
W. M. Abraham ◽  
A. Wanner
Keyword(s):  
Blood Flow ◽  
Systemic Arterial Pressure ◽  
Bronchial Mucosa ◽  
Anatomic Site ◽  
Bronchial Wall ◽  
Mechanically Ventilated ◽  
Lung Resistance ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Increased Blood Flow

The reported effects of cholinergic agonists on bronchial blood flow (Qbr) have been inconsistent. The aim of the present study was to determine whether the inconsistency could be due to the mode of agonist administration (systemic vs. aerosol) or the anatomic site of blood flow in the bronchus (mucosal vs. deep wall). In 10 anesthetized mechanically ventilated adult sheep, we measured Qbr in main bronchi by color-coded microspheres, systemic and pulmonary arterial pressures, cardiac output, and lung resistance (RL) before and after acetylcholine (ACh) administered either as an aerosol (nebulized dose 100 micrograms) or as an intravenous bolus (2 micrograms/kg). Before drug administration, 72% of mean Qbr was distributed to the bronchial mucosa and the remainder was distributed to the deep bronchial wall. For a comparable increase in mean RL (150% for intravenous ACh and 205% for aerosol ACh), mean total Qbr normalized for systemic arterial pressure increased by 291% after intravenous ACh (P < 0.05) and decreased by 9% after aerosol ACh (not significant). Mucosal and deep wall Qbr increased proportionally. Atropine (0.2 microgram/kg) prevented the changes in Qbr and RL after intravenous ACh. Thus intravenous but not aerosol ACh increased blood flow in the mucosa and deep wall of extrapulmonary bronchi. This suggests that the muscarinic receptors mediating vasodilation are more accessible to intravascular than intrabronchial ACh.

Effects of forearm bier block with bretylium on the hemodynamic and metabolic responses to handgrip

2000 ◽  
Vol 279 (2) ◽  
pp. H586-H593 ◽  
Author(s):  
Frank Lee ◽  
J. Kevin Shoemaker ◽  
Patrick M. McQuillan ◽  
Allen R. Kunselman ◽  
Michael B. Smith ◽  
...  
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Muscle Blood Flow ◽  
Reflex Responses ◽  
Muscle Ph ◽  
Before And After ◽  
Autonomic Reflex ◽  
Bier Block ◽  
Forearm Muscle ◽  
Increased Blood Flow

We tested the hypothesis that a reduction in sympathetic tone to exercising forearm muscle would increase blood flow, reduce muscle acidosis, and attenuate reflex responses. Subjects performed a progressive, four-stage rhythmic handgrip protocol before and after forearm bier block with bretylium as forearm blood flow (Doppler) and metabolic (venous effluent metabolite concentration and 31P-NMR indexes) and autonomic reflex responses (heart rate, blood pressure, and sympathetic nerve traffic) were measured. Bretylium inhibits the release of norepinephrine at the neurovascular junction. Bier block increased blood flow as well as oxygen consumption in the exercising forearm ( P < 0.03 and P < 0.02, respectively). However, despite this increase in flow, venous K+ release and H+release were both increased during exercise ( P < 0.002 for both indexes). Additionally, minimal muscle pH measured during the first minute of recovery with NMR was lower after bier block (6.41 ± 0.08 vs. 6.20 ± 0.06; P < 0.036, simple effects). Meanwhile, reflex effects were unaffected by the bretylium bier block. The results support the conclusion that sympathetic stimulation to muscle during exercise not only limits muscle blood flow but also appears to limit anaerobiosis and H+ release, presumably through a preferential recruitment of oxidative fibers.

Alpha-adrenergic-mediated reflex responses to induced muscular contraction are changed with age in dogs

1993 ◽  
Vol 265 (6) ◽  
pp. H1899-H1908 ◽  
Author(s):  
G. C. Haidet
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Muscular Contraction ◽  
Related Difference ◽  
Abdominal Organs ◽  
Age Related ◽  
Before And After ◽  
Alpha Blockade ◽  
Anesthetized Dogs ◽  
Age Related Changes

Aging significantly affects reflex cardiovascular (CV) responses to induced muscular contraction in anesthetized dogs. To further investigate whether age-related changes in alpha-adrenergic-mediated responses to muscular contraction contribute to these previously reported age-related changes in CV responses associated with advanced age, hemodynamic and regional blood flow (BF) responses at baseline and during hindlimb contraction (HLC) were evaluated both before and after alpha-blockade (alpha-AB) in older (8-14 yr old) and in younger (2-3 yr old) beagles during alpha-chloralose anesthesia. alpha-AB with phentolamine resulted in significant (P < 0.05) reductions in mean arterial pressure before and during HLC, regardless of age. However, age-related differences in the systemic vascular resistance, cardiac output, and stroke volume responses to HLC, observed before alpha-AB, were eliminated after phentolamine as the result of an age-related difference in each of these responses to alpha-AB. Baseline BF (microspheres) was unchanged after alpha-AB in seven of eight abdominal organs, regardless of age. However, reductions in BF during HLC were attenuated in seven of eight abdominal organs in the younger dogs after alpha-AB, but in none of these organs in the older dogs, indicative of diminished alpha-mediated vasoconstriction in these organs in the older dogs during HLC. Furthermore, the age-related difference in the combined BF reduction to all eight abdominal organs before alpha-AB was eliminated after alpha-AB. Finally, BF increases to two of four contracting muscles, as well as the combined increase in blood flow to all four contracting muscles, were attenuated after alpha-AB, regardless of age. These results demonstrate that alpha-blockade eliminates many of the age-related differences in CV responses to HLC observed before alpha-AB and suggest that alpha-adrenergic-mediated responses to HLC change with age in beagles.

Nitric oxide as a regulator of adrenal blood flow

1993 ◽  
Vol 264 (2) ◽  
pp. H464-H469 ◽  
Author(s):  
M. J. Breslow ◽  
J. R. Tobin ◽  
D. S. Bredt ◽  
C. D. Ferris ◽  
S. H. Snyder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Neural Control ◽  
Splanchnic Nerve ◽  
No Synthase ◽  
Catecholamine Secretion ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Synthase Inhibitor ◽  
Splanchnic Nerve Stimulation

To determine whether nitric oxide (NO) is involved in adrenal medullary vasodilation during splanchnic nerve stimulation (NS)-induced catecholamine secretion, blood flow (Q) and secretory responses were measured in pentobarbital-anesthetized dogs before and after administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). L-NAME (40 mg/kg iv over 5 min, followed by 40 mg.kg-1.h-1) reduced NO synthase activity of medullary and cortical homogenates from 5.2 +/- 0.3 to 0.7 +/- 0.1 pmol.min-1.mg protein-1 and from 1.2 +/- 0.2 pmol.min-1.mg protein-1 to undetectable levels, respectively. L-NAME reduced resting medullary and cortical Q by 42 and 60%, respectively. NS before L-NAME increased medullary Q from 181 +/- 16 to 937 +/- 159 ml.min-1.100 g-1 and epinephrine secretion from 1.9 +/- 0.8 to 781 +/- 331 ng/min. NS after L-NAME had no effect on medullary Q (103 +/- 14 vs. 188 +/- 34 ml.min-1.100 g-1), while epinephrine secretion increased to the same extent as in control animals (1.9 +/- 0.7 vs. 576 +/- 250 ng/min). L-NAME also unmasked NS-induced cortical vasoconstriction; cortical Q decreased from 96 +/- 8 to 50 +/- 5 ml.min-1.100 g-1. Administration of hexamethonium (30 mg/kg iv), a nicotinic receptor antagonist, reduced NS-induced epinephrine secretion by 90%. These data suggest independent neural control of medullary Q and catecholamine secretion, the former by NO and the latter by acetylcholine.

Vasodilator reserve in respiratory muscles during maximal exertion in ponies

1986 ◽  
Vol 60 (5) ◽  
pp. 1571-1577 ◽  
Author(s):  
M. Manohar
Keyword(s):  
Blood Flow ◽  
Maximal Exercise ◽  
Respiratory Muscles ◽  
Aortic Pressure ◽  
Whole Body ◽  
Adenosine Infusion ◽  
Base Line ◽  
Triceps Brachii ◽  
Vasodilator Reserve ◽  
Mean Aortic Pressure

Eight healthy adult grade ponies were studied at rest as well as during maximal exertion carried out with and without adenosine infusion (3 microM X kg-1 X min-1 into the pulmonary artery) on a treadmill to compare levels of blood flow in respiratory muscles with those in other vigorously working muscles and to ascertain whether there remained any unutilized vasodilator reserve in respiratory muscles of maximally exercising ponies. Radionuclide-labeled 15-micron-diam microspheres, injected into the left ventricle, were used to study tissue blood flows. During maximal exertion, there were increases above base-line values in heart rate (336%), mean aortic pressure (41%), cardiac output (722%), and arterial O2 content (56%). The whole-body O2 consumption was 123 +/- 11 ml X min-1 X kg-1, and the stride/respiratory frequency of the galloping ponies was 138 +/- 4/min. With adenosine infusion during maximal exertion, mean aortic pressure decreased (P less than 0.05), but none of the above variables was different from maximal exercise alone. During maximal exertion, blood flow in the adrenal glands, myocardium, respiratory, and limb muscles increased, whereas that in the kidneys decreased and the cerebral perfusion remained unaltered. With adenosine infusion during maximal exercise, renal vasoconstriction intensified, whereas adrenal and coronary beds exhibited further vasodilatation. During maximal exertion, blood flow in the equine diaphragm (265 +/- 36 ml X min-1 X 100 g-1) was not different from that in the gluteus medius (253 +/- 36) and biceps femoris (233 +/- 29); both are principal muscles of propulsion in the equine subjects) or the triceps brachii (227 +/- 26) muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma dopamine in regulation of canine renal blood flow

1988 ◽  
Vol 255 (3) ◽  
pp. R379-R387 ◽  
Author(s):  
D. R. Kapusta ◽  
N. W. Robie
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sch 23390 ◽  
Renal Perfusion ◽  
Receptor Activation ◽  
Renal Autoregulation ◽  
Alpha Adrenoceptor ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Control Infusion

Studies were performed in pentobarbital-anesthetized dogs to determine whether circulating plasma dopamine (DA) is involved in renal blood flow (RBF) regulation. During graded reductions in renal perfusion pressure (RPP), total renal venous (RV) DA content significantly increased at RPPs below the autoregulatory range. The RBF response to decrements in RPP was also examined during control, infusion of DA (1.2 micrograms.kg(-1).min(-1)ia), and after DA receptor blockade by SCH 23390 (30 micrograms/kg iv). During DA infusion, autoregulation was still evident over the same RPPs, although at higher flow rates. At pressures below the autoregulatory range, RBF decreased linearly and the autoregulatory curve merged with control at 50 mmHg. After SCH 23390, autoregulation ceased at a higher RPP than during control, and RBF was significantly less than control rates at pressures of 80 mmHg and below. To elucidate reasons for this latter response, reductions in RPP were repeated before and after administration of both prazosin (0.1 mg/kg iv) and SCH 23390. The results indicated that RBF rates were not different from control at any RPP. Further, prazosin alone did not alter renal autoregulation but significantly increased RBF at RPP below the autoregulatory range. Thus these results indicate that dopamine does not participate in RBF control at pressures above the inflection point for the lowest limit of RBF autoregulation but may be released at lower RPP to act as a vasodilator agent to oppose alpha-adrenoceptor-mediated reductions in RBF. Moreover, tonic DA receptor activation may influence the setting of the lower limit of canine RBF autoregulation.

Maintenance of renal autoregulation during infusion of aminophylline or adenosine

1985 ◽  
Vol 248 (3) ◽  
pp. F366-F373 ◽  
Author(s):  
A. J. Premen ◽  
J. E. Hall ◽  
H. L. Mizelle ◽  
J. E. Cornell
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Receptor Blockade ◽  
Renal Metabolism ◽  
Renal Autoregulation ◽  
Before And After ◽  
Anesthetized Dogs

Adenosine has been postulated to link control of glomerular filtration rate (GFR) and renal blood flow (RBF) with changes in renal metabolism. In the present study, we examined the role of adenosine in renal autoregulation by comparing the responses of normal anesthetized dogs to step decreases in renal artery pressure (RAP) to the response obtained after receptor blockade of adenosine with aminophylline or by flooding the kidney with exogenous adenosine. In six dogs at normal RAP, intrarenal infusion of aminophylline (10 mumol/min) did not alter renal hemodynamics. GFR and RBF were well autoregulated (greater than 90% of control) at RAP values equal to or greater than 85 mmHg before and after aminophylline. At RAP equal to 75 mmHg, GFR and RBF decreased by 27 +/- 10 and 20 +/- 8%, respectively, before aminophylline and by 25 +/- 7 and 13 +/- 6% after aminophylline. In a different group of six dogs, intrarenal infusion of adenosine (6 mumol/min) significantly increased RBF (32 +/- 9%) and decreased GFR (38 +/- 10%) at normal RAP. However, GFR and RBF were both well autoregulated (greater than 90% of control) at RAP values equal to or greater than 85 mmHg before and after adenosine. At RAP equal to 75 mmHg, GFR and RBF decreased by 10 +/- 5 and 7 +/- 3%, respectively, before adenosine and by 12 +/- 6 and 17 +/- 5% after adenosine. Neither aminophylline nor adenosine attenuated the elevations in plasma renin activity associated with reductions in RAP. These data fail to provide evidence that adenosine is an important factor in autoregulation of GFR and RBF during acute reductions in RAP within the autoregulatory range.

Renal effects of prostaglandin inhibition during increases in renal venous pressure

1991 ◽  
Vol 260 (4) ◽  
pp. F525-F529 ◽  
Author(s):  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Venous Pressure ◽  
Interstitial Pressure ◽  
Pentobarbital Sodium ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Changes

The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.

Sign in / Sign up

Export Citation Format

Share Document