Prostaglandins mediate skeletal muscle arteriole dilation in hyperdynamic bacteremia

1990 ◽  
Vol 259 (3) ◽  
pp. H728-H734
Author(s):  
H. G. Cryer ◽  
R. N. Garrison ◽  
P. D. Harris ◽  
B. H. Greenwald ◽  
N. L. Alsip
Keyword(s):  
Skeletal Muscle ◽  
Topical Application ◽  
Serotonin Receptors ◽  
Cremaster Muscle ◽  
Synthesis Inhibitor ◽  
E Coli ◽  
Decerebrate Rat ◽  
Prostaglandin Synthesis Inhibitor ◽  
Baseline Values

Live Escherichia coli bacteremia during the high cardiac output (hyperdynamic) phase of sepsis causes constriction of large arterioles but dilation of small arterioles in skeletal muscle. This study examines the role of dilator prostaglandins, serotonin, and histamine in these differential microvascular responses in the decerebrate rat that avoids the effects of drug anesthesia. Topical application of meclofenamate, a prostaglandin synthesis inhibitor, to the cremaster muscle 60 min after induction of E. coli bacteremia enhanced the constriction of large arterioles from 20 +/- 8 to 46 +/- 9% less than baseline and blunted the dilation of small arterioles from 39 +/- 9 to 17 +/- 7% above baseline values in the cremaster microcirculation. Induction of E. coli bacteremia after pretreatment of the cremaster with meclofenamate constricted large arterioles to 40 +/- 4% less than baseline and small arterioles to 31 +/- 4% less than baseline. This indicates that prostaglandins initiate small arteriole dilation in response to E. coli, but some other dilator factor is activated by prostaglandins to maintain small arteriole dilation during E. coli bacteremia. Topical application of cyproheptadine, an antagonist of both histamine and serotonin receptors, to the cremaster muscle did not alter the E. coli-induced constriction of large arterioles or the dilation of small arterioles in the cremaster microcirculation.

Prostaglandin modulation of adrenergic vascular control during hemorrhagic shock

1981 ◽  
Vol 241 (1) ◽  
pp. H85-H90 ◽  
Author(s):  
R. F. Bond ◽  
C. H. Bond ◽  
L. C. Peissner ◽  
E. S. Manning
Keyword(s):  
Skeletal Muscle ◽  
Hemorrhagic Shock ◽  
Vascular Control ◽  
Synthesis Inhibitor ◽  
Muscle Perfusion ◽  
System A ◽  
In Series ◽  
Adrenergic Nervous System ◽  
Prostaglandin Synthesis Inhibitor ◽  
Denervated Muscles

This study was designed to evaluate 1) whether the initial compensatory skeletal muscle vascular constriction induced by hemorrhagic hypotension is primarily the result of increased adrenergic neural tone rather than circulating vasoconstrictor agents, and 2) whether the secondary skeletal muscle decompensatory vasodilation is caused by inhibitory action of prostaglandins on peripheral adrenergic nervous system. A constant-flow vascularly isolated double canine gracilis muscle preparation in which one muscle served as innervated control for the contralateral muscle was used. Dogs were subjected to standard stepwise hemorrhagic shock protocol. In series 1, perfusion pressures of control muscles were compared to denervated muscles with the result that innervated muscle perfusion pressures increased initially from 105 to 175 mmHg but subsequently fell significantly (P less than 0.05) to 147 mmHg. Only modest increases in perfusion pressures with no significant secondary fall were noted in denervated muscles. Series 2 compared innervated control perfusion pressures to pressures perfusing muscles pretreated with prostaglandin-synthesis inhibitor sodium meclofenamate (MCF). The MCF-treated muscle perfusion pressures rose to 260 mmHg where they remained without the secondary fall noted in control muscles. These data support the two hypotheses tested.

Early onset of parturition induced by acute alcohol exposure in C57BL/6J mice: role of uterine PGE and PGF2a

1997 ◽  
Vol 9 (8) ◽  
pp. 815 ◽  
Author(s):  
J. L. Cook ◽  
C. L. Randall
Keyword(s):  
Fetal Growth ◽  
Early Onset ◽  
Growth And Development ◽  
Alcohol Treatment ◽  
Alcohol Exposure ◽  
Prostaglandin Synthesis ◽  
Gestational Length ◽  
Synthesis Inhibitor ◽  
Prostaglandin Synthesis Inhibitor

These studies were designed to determine the effect of acute alcohol treatment on gestational length and to probe for a mechanism underlying alcohol-induced early onset of parturition (EOP) in mice. Experiment 1: alcohol increases the incidence of EOP. Pregnant C57BL/6J mice were given alcohol (0, 4, 5 or 6 g kg -1 , i.g.) on Gestational Day (GD) 10, 15, 16, 17 or 18. Deliveries were monitored every 6 h from GD 18. Results indicated that 6 g kg -1 alcohol treatment on GD 17 or 18 increased the incidence of EOP. Experiment 2: prostaglandins (PGs) play roles in parturition. The purpose of Experiment 2 was to determine whether PGs mediate alcohol-induced EOP in mice. The results indicated that pretreatment on GD 17 with aspirin, a prostaglandin synthesis inhibitor, prevented alcohol-induced EOP. These data suggest that alcohol-induced EOP in mice may be mediated by PGs. Experiment 3: PGs are influenced by alcohol and are triggers of labour. Experiment3 measured uterine PGs associated with the onset of alcohol-induced EOP in mice. Alcohol increased uterine PGE and PGF2a , with PGE levels higher than control before labour, and elevated PGF2a levels correlating with labour. Changes in gestational length have important implications for pregnancy outcome, as well as for normal fetal growth and development.

Enhanced response of arterioles to oxygen during development of hypertension in SHR

1986 ◽  
Vol 250 (5) ◽  
pp. H761-H764 ◽  
Author(s):  
J. H. Lombard ◽  
M. E. Hess ◽  
W. J. Stekiel
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Local Control ◽  
Fourth Order ◽  
Spontaneously Hypertensive Rat ◽  
Control Mechanisms ◽  
Cremaster Muscle ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The goal of this study was to assess the possible role of O2-related local control mechanisms in contributing to an elevated skeletal muscle resistance during the development of hypertension in the spontaneously hypertensive rat (SHR). Diameters of first- (1A), second- (2A), third- (3A), and fourth-order (4A) arterioles were measured by television microscopy in the cremaster muscle of SHR in the early (4- to 6-wk-old) and rapidly developing (8- to 9-wk-old) stages of hypertension and in age-matched normotensive Wistar-Kyoto (WKY) controls. Active neurogenic tone was blocked by superfusing the tissue with 0.1 microgram/ml tetrodotoxin. When superfusion solution PO2 was elevated by changing the gas equilibration mixture from 0 to 5% O2, neurally blocked 3A and 4A of SHR exhibited a significantly greater constriction and a higher incidence of complete closure than those of their age-matched WKY controls. However, there were no significant differences in the constriction of larger arterioles (1A and 2A) in response to elevated superfusion solution PO2. The results suggest that O2-related local control mechanisms could contribute to constriction and closure of small arterioles and to an elevated skeletal muscle vascular resistance early in the development of hypertension in SHR

Role of tissue hypoxia as the mechanism of lactic acidosis during E. coli endotoxemia

1992 ◽  
Vol 72 (5) ◽  
pp. 1895-1901 ◽  
Author(s):  
F. J. Hurtado ◽  
A. M. Gutierrez ◽  
N. Silva ◽  
E. Fernandez ◽  
A. E. Khan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Lactate Concentration ◽  
High Energy ◽  
High Energy Phosphates ◽  
Arterial Lactate ◽  
E Coli ◽  
O2 Extraction ◽  
The Right

We compared the hemodynamic and metabolic alterations produced in rabbits by similar decreases in cardiac output created by inflating a balloon placed in the right ventricle (n = 6) with those produced by an intravenous bolus of Escherichia coli lipopolysaccharide (LPS; SEP group; n = 6). We measured O2 consumption (VO2), O2 transport (TO2), and O2 extraction ratio (ERO2) for the whole animal and also for the left hindlimb. Both groups experienced similar decreases in cardiac output, systemic TO2, and VO2 and similar increases in ERO2. For the hindlimb, TO2 was similar, but VO2 and ERO2 were lower for the SEP group 30 min after LPS administration (P less than 0.05); however, this difference disappeared during the remainder of the experiment. Arterial lactate concentration was greater (P less than 0.05) for the SEP group. There were no differences in skeletal muscle PO2, measured with a multiwire surface electrode, or in cardiac and skeletal muscle concentrations of high-energy phosphates. We hypothesize that a direct effect of LPS on cellular metabolism may have resulted in greater arterial lactate concentration for the SEP group.

Metyrapone restores the febrile response to Escherichia coli LPS in pregnant rats

2011 ◽  
Vol 300 (6) ◽  
pp. R1588-R1595 ◽  
Author(s):  
Brent N. Alexander ◽  
James E. Fewell
Keyword(s):  
Escherichia Coli ◽  
Immune Challenge ◽  
Febrile Response ◽  
Synthesis Inhibitor ◽  
Pregnant Rats ◽  
E Coli ◽  
Corticosterone Response ◽  
Near Term ◽  
Prior Administration

Fever, an important component of the host's defense response to immune challenge, is absent or attenuated in rats near the term of pregnancy. The present experiments were carried out to determine the role of endogenous glucocorticoids in mediating the altered core temperature (Tc) response to exogenous pyrogen (i.e., Escherichia coli LPS). For the experiments, metyrapone—a glucocorticoid synthesis inhibitor—was administered to near-term pregnant rats prior to an EC100 dose of E. coli LPS. Administration of LPS following vehicle elicited a significant corticosterone response and resulted in a decrease in Tc (i.e., hypothermia). Prior administration of metyrapone, however, which abolished the corticosterone response and altered the pyrogenic/cryogenic cytokine response to LPS, eliminated hypothermia and restored the febrile response. Our results provide evidence that endogenous glucocorticoids play a role in mediating the altered febrile response to immune stimuli observed in rats near the term of pregnancy.

Role of endothelium in reactive dilation of skeletal muscle arterioles

1990 ◽  
Vol 259 (5) ◽  
pp. H1313-H1316 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cremaster Muscle ◽  
Anesthetized Rats ◽  
Vasoactive Factors ◽  
Peak Increase ◽  
Arteriolar Diameter

In cremaster muscle of pentobarbital-anesthetized rats, the role of endothelium in the reactive dilation of an arteriole (mean control diameter: 18.2 +/- 0.5 microns) during and after short (approximately 20 s) or long (approximately 80 s) occlusion of a parent arteriole was investigated. Distal to the occluder, arteriolar diameter increased during the occlusion (mean peak increase: 6.9 +/- 0.4 and 6.7 +/- 1.1 microns, respectively) and increased even further after the release of the occlusion as blood flow was reestablished (additional mean increase: 6.5 +/- 0.7 and 5.8 +/- 0.8 microns, respectively). The duration of arteriolar dilation after the release of the occlusion was dependent on the duration of occlusion (252.2 +/- 37 vs. 411.3 +/- 57 s; P less than 0.05). After impairment of the arteriolar endothelium by light/dye treatment, a dilation was still present during both the shorter and longer occlusions (mean increase: 4.73 +/- 1.4 and 4.73 +/- 1.3 microns, respectively); however, in both cases the additional dilation after release of the occlusion was greatly diminished. The duration of reactive arteriolar responses following impairment of the endothelium was significantly reduced only on release of the shorter occlusions. The results suggest that reactive dilation (hyperemia) of arterioles is the result of multiple, endothelium-dependent and endothelium-independent vasoactive factors.

Endogenous prostaglandins selectively mask large arteriole constriction to angiotensin II

1987 ◽  
Vol 253 (6) ◽  
pp. H1573-H1580 ◽  
Author(s):  
J. T. Fleming ◽  
P. D. Harris ◽  
I. G. Joshua
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin Synthesis ◽  
Second Order ◽  
Cremaster Muscle ◽  
Synthesis Inhibitor ◽  
Endogenous Prostaglandins ◽  
Specific Receptors ◽  
Prostaglandin Synthesis Inhibitor ◽  
Constrictor Response

Television microscopy was used to observe the responses of in vivo arterioles and venules of the rat cremaster muscle to the topical application of angiotensin II (10(-8) and 10(-6) M). Neither the first- (A1) or second-order arterioles (A2) nor the first- (V1) or second-order venules (V2) constricted significantly to angiotensin II. However, after the inhibition of local prostaglandin synthesis with either mefenamic acid or indomethacin, both A1 and A2, but not the venules, gave a significant constrictor response to angiotensin II (10(-6) M). Arterioles and venules, which were preconstricted with norepinephrine, dilated to their initial baseline diameters after angiotensin II (10(-6) M), a response not observed when the microvessels were pretreated with either an angiotensin antagonist or a prostaglandin synthesis inhibitor. These observations indicate that endogenous prostaglandins exert a significant dilator influence on the larger arterioles, that this dilator influence appears to oppose the constrictor effect of angiotensin II, and that angiotensin II acts on specific receptors to induce synthesis and/or release of dilator prostaglandins in large arterioles. However, prostaglandins cannot account for the absence of a venular constriction to angiotensin.

Prevention of Ethanol-induced Gastric Lesions in Rats by Wu-Bei-San

1998 ◽  
Vol 26 (01) ◽  
pp. 65-72 ◽  
Author(s):  
Wen-Chuan Lin
Keyword(s):  
Calcium Carbonate ◽  
Protective Action ◽  
Prostaglandin Synthesis ◽  
Simultaneous Administration ◽  
Acid Neutralization ◽  
Gastric Lesions ◽  
Synthesis Inhibitor ◽  
Experimental Conditions ◽  
Prostaglandin Synthesis Inhibitor

The effects of Wu-Bei-San (WBS) and its components Wu-Tsi-Ku (WTK) and Bei-Mu (BM) on gastric lesions induced by necrotizing agents were investigated in rats. Oral administration of WBS or WTK, but not BM, dose-dependently prevented gastric lesions induced by ethanol. Moreover, the gastric protective action of WTK was potentiated by simultaneous administration of BM under the same experimental conditions. Pretreatment with indomethacin, which is a prostaglandin synthesis inhibitor and idoacetamide, which is a sulfhydryl blocker did not influence the inhibited ethanol lesion of WBS. Gastric lesions induced by acidified aspirin were prevented by both WBS and calcium carbonate, which is a major constituents of WTK. However, pretreatment with calcium carbonate did not affect the gastric lesions induced by ethanol. These results indicate protective action of WBS on the gastric mucosa through both acid neutralization and cytoprotection, although more work is needed to clarify the role of WBS in cytoprotection.

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

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