Adrenergic, purinergic, and endothelial mediators and modulators of norepinephrine-induced mesenteric autoregulatory escape

1994 ◽  
Vol 39 (8) ◽  
pp. 1655-1664 ◽  
Author(s):  
Geza Remak ◽  
Omar D. Hottenstein ◽  
Eugene D. Jacobson
Keyword(s):  
Autoregulatory Escape

Metabolic and circulatory responses of normoxic skeletal muscle to whole-body hypoxia

1988 ◽  
Vol 65 (5) ◽  
pp. 2063-2068 ◽  
Author(s):  
D. L. Bredle ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Autologous Blood ◽  
Whole Body ◽  
Membrane Oxygenator ◽  
O2 Uptake ◽  
Ici 118,551 ◽  
Autoregulatory Escape ◽  
Beta 2 ◽  
O2 Supply

Whole-body hypoxia may increase peripheral O2 demand because it increases catecholamine calorigenesis, an effect attributable to beta 2-adrenoceptors. We tested these possibilities by pump-perfusing innervated hindlimbs in eight dogs with autologous blood kept normoxic by a membrane oxygenator while ventilating the animals for 40 min with 9% O2 in N2 (NOB group). Similar periods of normoxic ventilation preceded and followed the hypoxic period. A second group (n = 8, beta B) was pretreated with the specific beta 2 blocker ICI 118,551. Hindlimb O2 uptake was elevated by 25 min of hypoxia in NOB, whereas whole-body O2 uptake was reduced. Limb O2 uptake remained elevated in recovery, but all effects on limb O2 uptake were absent in beta B. Hindlimb resistance and perfusion pressure increased in hypoxia in both groups, and there was little evidence of local escape from reflex vasoconstriction. These results clearly indicated that global hypoxia increased O2 demand in muscle when the local O2 supply was not limited and that beta 2-receptors were necessary for this response. Autoregulatory escape of limb muscle blood flow from centrally mediated vasoconstriction during whole-body hypoxia was also shown to be practically nil, if normoxia was maintained in the limb.

Autoregulatory escape from vasoconstriction of intestinal circulation in developing swine

1987 ◽  
Vol 252 (1) ◽  
pp. H118-H124 ◽  
Author(s):  
N. M. Buckley ◽  
M. Jarenwattananon ◽  
P. M. Gootman ◽  
I. D. Frasier
Keyword(s):  
Nerve Stimulation ◽  
Control Level ◽  
Splanchnic Nerve ◽  
Adrenergic Nerve ◽  
Vasoconstrictor Response ◽  
Mean Pressure ◽  
Functional Immaturity ◽  
Autoregulatory Escape ◽  
Infusion Of Norepinephrine ◽  
Intestinal Circulation

The capability of the developing intestinal circulation to maintain a vasoconstrictor response during postganglionic adrenergic nerve stimulation or norepinephrine infusion was examined in 34 swine aged 6 h to 2 mo anesthetized with pentobarbital sodium. Aortic and portal venous pressures, electrocardiogram (ECG), and blood flow (F) through the superior mesenteric artery were recorded, and intestinal vascular resistance (MVR) was calculated as mean pressure difference per mean F. Baroreceptor reflex inhibition by bilateral occlusion of the carotid arteries increased MVR, section of the splanchnic nerve and postganglionic fibers decreased MVR, and short-latency F decreases were obtained during mesenteric nerve stimulation (MNS). Latencies for the decreases in F shortened with age and with increasing MNS frequency (5–17 Hz) at any age. Prolonging MNS for 60 s at 10 or 12 Hz led to sustained high MVR in 6-h to 7-day-old animals; however, MVR decreased toward control before the end of the 60-s MNS period in animals 1 to 2 mo old. Intra-arterial infusion of norepinephrine (0.5 microgram X kg-1 X min-1) decreased F and increased MVR in all animals; but by 5 min of infusion, F was returning toward control level in all but the youngest. This demonstration that the least mature intestinal circulation was least capable of autoregulatory escape from vasoconstriction provides further evidence of its functional immaturity.

scholarly journals Autoregulatory Escape in the Gut

1971 ◽  
Vol 60 (1) ◽  
pp. 145-148 ◽  
Author(s):  
Linda L. Shanbour ◽  
Eugene D. Jacobson
Keyword(s):  
Autoregulatory Escape

Escape from vasoconstriction in the gastric microcirculation

1975 ◽  
Vol 228 (6) ◽  
pp. 1893-1895 ◽  
Author(s):  
Paul H. Guth ◽  
Esther Smith
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
System Response ◽  
In Vivo Microscopy ◽  
Adrenergic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape ◽  
Splanchnic Nerve Stimulation ◽  
Gastric Microcirculation

Escape of splanchnic resistance vessels from vasoconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomoses (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splitting TV microscope recording system, response of gastric submucosal arterioles (13–33 µm) to 3 min of left splanchnic nerve stimulation, norepinephrine superfusion, and vasopressin superfusion was measured. All stimuli produced initial vasoconstriction. Escape occurred in all rats with nerve stimulation and norepinephrine, but in only one of five with vasopressin. No shunts were seen. The study demonstrates that the gastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchnic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

In vivo and in vitro vasoactive reactions of coronary arteriolar microvessels to nitroglycerin

1996 ◽  
Vol 271 (2) ◽  
pp. H461-H468 ◽  
Author(s):  
C. J. Jones ◽  
L. Kuo ◽  
M. J. Davis ◽  
W. M. Chilian
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Blood Velocity ◽  
Small Arteries ◽  
Intracoronary Infusion ◽  
Maximal Diameter ◽  
Autoregulatory Escape ◽  
Coronary Arterioles

The actions of nitroglycerin on the coronary microcirculation are controversial, with some laboratories reporting that coronary arterioles dilate to the drug and others reporting that they do not. Our goal was to reconcile these disparate observations. Specifically, we hypothesized that dilation of coronary arterioles by nitroglycerin is overwhelmed by intrinsic autoregulatory escape mechanisms. Accordingly, we projected that coronary arterioles would show transient, but not sustained, dilation to nitroglycerin in vivo. Furthermore, we hypothesized that isolated coronary arterioles would show sustained dilation to the drug, because intrinsic escape mechanisms would be absent under these conditions. To test these hypotheses, we measured diameter changes of canine coronary microvessels in vivo during continuous nitroglycerin administration (intracoronary infusion or epicardial suffusion) using intravital fluorescent microscopy (n = 17 dogs) at two time points: early (1-3 min), when coronary artery blood flow velocity was increased, and late (15-20 min), after blood flow velocity returned to control. Tb study responses of coronary arterioles in the absence of autoregulatory influences, we measured the diameter of isolated canine coronary arterioles to varying doses of nitroglycerin (n = 8 vessels, maximal diameter 81 +/- 4 microns). During the early phase of nitroglycerin infusion (1,3, and 10 micrograms.kg-1.min-1), coronary arterioles dilated by 4 +/- 1, 7 +/- 2, and 13 +/- 2% (all P < 0.05), whereas small arteries dilated by 1 +/- 2, 3 +/- 1, and 4 +/- 1%, respectively (P < 0.05 for the higher doses). Coronary artery blood velocity measured increased by 45 +/- 15% (3 micrograms.kg-1.min-1, P < 0.05). Suffusion of nitroglycerin (10(-5) M) dilated coronary arterioles, but not small arteries, by 17 +/- 5% (P < 0.05) between 1 and 3 min. After 15-20 min of nitroglycerin (3 micrograms.kg-1.min-1 by intracoronary infusion), diameters of coronary arterioles and coronary artery blood velocity returned to control, whereas dilation of small arteries remained significant at 4 +/- 1%. Coronary arteriolar dilation by epicardial suffusion of nitroglycerin also waned to control values by 15-20 min, whereas dilation of small arteries was observed: 5 +/- 2% (P < 0.05). In vitro, nitroglycerin caused dose-dependent dilation of coronary arterioles to their maximal diameter, which was sustained for 20 min. Thus nitroglycerin dilates coronary arterioles and small arteries. The dilation in vivo is transient for arterioles but sustained for arteries. In vitro, the dilation is sustained. Because microvessels in vitro are capable of sustaining dilation for 20 min, we conclude that the waning of arteriolar dilation in vivo is related to autoregulatory escape from dilation by nitroglycerin.

Escape from vasoconstriction in the gastric microcirculation

1975 ◽  
Vol 228 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
PH Guth ◽  
E Smith
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
System Response ◽  
In Vivo Microscopy ◽  
Adrenergic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape ◽  
Splanchnic Nerve Stimulation ◽  
Gastric Microcirculation

Escape of splanchic resistance vessels from vasconstriction due to adrenergic stimulation has been attributed to increasing submucosal blood flow due to dilation of submucosal arteriovenous anastomes (shunts). This postulate, as applied to the rat gastric microcirculation, was studied by in vivo microscopy. Using an image-splittingTV microscope recording system, response of gastric submucosal arterioles (13-33 mum)to 3 min of left splanchnic nerve stimulation, norepinephrine superfision, and vasopressin superfission was measured. All stimuli produced initial vasoconstriction.Escape occurred in all rats with nerve stimulation and norepinephrine, but in onlyone of five with vasopressin. No shunts were seen. The study demonstrates that thegastric submucosal arterioles exhibit an escape phenomenon, suggesting that "autoregulatory escape" in other splanchic beds also may be due to relaxation of constricted vessels and not to opening of shunts.

Gastric oxygen uptake during autoregulatory escape from sympathetic stimulation

1989 ◽  
Vol 257 (4) ◽  
pp. G633-G636
Author(s):  
J. W. Kiel ◽  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Sympathetic Stimulation ◽  
Oxygen Utilization ◽  
Total Blood ◽  
Perivascular Nerves ◽  
Gastric Corpus ◽  
Autoregulatory Escape ◽  
Total Blood Flow ◽  
Frequency Of Stimulation ◽  
Oxygen Difference

To assess the effects of sympathetic stimulation on gastric blood flow and oxygen utilization, the perivascular nerves were stimulated at 2, 4, 6, and 8 Hz in chambered segments of canine gastric corpus perfused at constant pressure. Spectrophotometric arteriovenous oxygen difference and electromagnetic blood flow were recorded continuously. Except at the lowest frequency of stimulation (2 Hz), total blood flow exhibited autoregulatory escape, i.e., blood flow decreased initially but then returned toward control. The fall in total blood flow at the onset of sympathetic stimulation was smaller at 2 Hz than at 4 Hz, but stimulation at 6 and 8 Hz caused no further reductions in total blood flow. However, at all frequencies, total blood flow escaped to the same steady-state value (approximately 17 ml.min-1.100 g-1). Although total blood flow was still less than control (approximately 25 ml.min-1.100 g-1), oxygen extraction increased proportionately so that oxygen consumption was not significantly less than control at any frequency of stimulation. We conclude that autoregulatory escape from sympathetic stimulation is mediated by local mechanisms acting to maintain tissue oxygenation in the stomach.

Norepinephrine release during autoregulatory escape: effects of alpha 2-receptor blockade

1991 ◽  
Vol 260 (2) ◽  
pp. H400-H408 ◽  
Author(s):  
L. Q. Chen ◽  
G. L. Riedel ◽  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Neural Control ◽  
Time Course ◽  
Venous Blood ◽  
Receptor Blockade ◽  
Control Mechanisms ◽  
Partial Recovery ◽  
Sympathetic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape

The partial recovery that intestinal blood flow undergoes during continued sympathetic nerve stimulation is termed autoregulatory escape. This study tested two hypotheses that might explain escape: 1) diminishing norepinephrine (NE) release during sustained stimulation and 2) an alpha 2-receptor-mediated competition between local and neural control mechanisms. The rates of NE release before and during stimulation of the perivascular sympathetic nerves were determined by measuring blood flow in isolated loops of canine small intestine and assaying the concentrations of NE in arterial and venous blood. The presence of functional alpha 2-receptors was demonstrated by clonidine injections, and the effects of alpha 2-receptor blockade were studied during yohimbine infusions. The time course of NE release was inconsistent with a cause-effect relationship; NE release was greatest during the phase when resistance had already escaped. Deliberately altering NE release by changing the stimulus duration did not affect escape. The study demonstrated 1) that diminished NE release during continued sympathetic stimulation does not occur and cannot account for escape, 2) that resistance vessels in the canine intestinal circulation possess functional alpha 2-receptors which are responsible for part of the vasoconstriction caused by sympathetic stimulation, 3) that blockade of presynaptic alpha 2-receptors significantly enhanced NE release during the initial 30-s period but not during the escape phase, and 4) that alpha 2-receptor blockade enhances autoregulatory escape. Altogether these findings indicate that the postsynaptic alpha 2-receptors on intestinal resistance vessels deserve further investigation as the possible site at which local and neural mechanisms compete to influence vascular resistance.

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