Endotoxin-induced alterations in contractility of isolated blood vessels from sheep

1991 ◽  
Vol 260 (6) ◽  
pp. H1790-H1794 ◽  
Author(s):  
S. Nelson ◽  
R. H. Steward ◽  
L. Traber ◽  
D. Traber
Keyword(s):  
Escherichia Coli ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Blood Vessels ◽  
Femoral Artery ◽  
Vascular Reactivity ◽  
Relaxing Factor ◽  
Tertiary Branch ◽  
Endothelium Derived Relaxing Factor ◽  
And Control

The present study examined reactivity to norepinephrine (NE) and KCl in isolated, suffused blood vessels from the systemic and pulmonary circulations of endotoxin-treated and control sheep. A possible mechanism underlying an endotoxin-induced alteration in vascular reactivity was also investigated. Chronically instrumented sheep were given Escherichia coli endotoxin (1.5 micrograms/kg). Eight to 12 h later these endotoxin-treated animals exhibited a significantly increased cardiac output and decreased systemic vascular pressure and resistance. The pulmonary vascular pressure and resistance were not changed. The isolated superficial femoral artery from the endotoxin sheep exhibited depressed contractions in response to KCl (75 mM) and to NE (10(-7)-10(-5) M), whereas the pulmonary artery (tertiary branch) did not exhibit altered reactivity. The decreased sensitivity to NE in the femoral artery from endotoxin sheep did not appear to involve an alteration of alpha- or beta-adrenoceptors, or an increased release of vasodilator prostanoids, or endothelium-derived relaxing factor.

Acute compensation to abrupt occlusion of rat femoral artery is prevented by NO synthase inhibitors

1994 ◽  
Vol 267 (6) ◽  
pp. H2523-H2530 ◽  
Author(s):  
J. L. Unthank ◽  
J. C. Nixon ◽  
M. C. Dalsing
Keyword(s):  
Femoral Artery ◽  
Arterial Occlusion ◽  
Artery Occlusion ◽  
No Synthase ◽  
Artery Blood Flow ◽  
Relaxing Factor ◽  
Femoral Artery Occlusion ◽  
Before And After ◽  
Endothelium Derived Relaxing Factor ◽  
Oxide Synthase

The hemodynamic significance of endothelium-derived relaxing factor (EDRF)-mediated mechanisms in vascular responses to abrupt rat femoral artery occlusion was investigated. Temporary arterial occlusion was produced before and after inhibition of nitric oxide synthase by N omega-nitro-L-arginine methyl ester (L-NAME) or NG-monomethyl-L-arginine (L-NMMA). Iliac artery blood flow and arterial pressures proximal and distal to the occlusion were measured. Normal vascular compensation included a return of resistance to preocclusion levels and a rise in distal pressure to a plateau within 5 min postocclusion. After treatment with L-NAME and L-NMMA, postocclusion resistance remained elevated by 53 and 36%, respectively. Collateral dilation after occlusion, as indicated by the rise in distal pressure, was prevented by L-NAME but not L-NMMA. Increases in adrenergic tone and mean arterial pressure by phenylephrine did not prevent compensation, suggesting the effects of L-NAME and L-NMMA did not result from elevated sympathetic activation or pressure. The results are consistent with the hypothesis that the stimulated release of endothelium-derived relaxing factor mediates the acute vascular compensation to abrupt arterial occlusion.

Enhanced release of endothelium-derived factor(s) by chronic increases in blood flow

1988 ◽  
Vol 255 (3) ◽  
pp. H446-H451 ◽  
Author(s):  
V. M. Miller ◽  
P. M. Vanhoutte
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Arteriovenous Fistula ◽  
Muscarinic Receptors ◽  
Femoral Artery ◽  
Response Curves ◽  
Femoral Arteries ◽  
Relaxing Factor ◽  
Bioassay System ◽  
Endothelium Derived Relaxing Factor

Chronic increases in blood flow caused by an arteriovenous fistula augment endothelium-dependent relaxations to acetylcholine. To determine whether endothelial muscarinic receptors are altered, concentration-response curves to acetylcholine were obtained in the presence of pirenzepine in fistula- and sham-operated canine femoral arteries. Pirenzepine inhibited the response to acetylcholine in both arteries. The pA2 (log Kb) for the antagonist was the same. A bioassay system was used to assess release of endothelium-derived relaxing factor. Rings of femoral artery (without endothelium) from unoperated dogs relaxed more when superfused with perfusate derived from endothelium of fistula-operated arteries during acetylcholine stimulation. Rings without endothelium of sham- and fistula-operated arteries relaxed to the same extent when superfused with perfusate derived from the endothelium of unoperated femoral arteries. These results suggest that augmented relaxations to acetylcholine in canine arteries where blood flow is chronically elevated do not result from changes in the subtype of endothelial muscarinic receptors or in the sensitivity of the underlying smooth muscle to endothelium-derived relaxing factor(s). They are likely due to increased release of endothelium-derived relaxing factor(s) on muscarinic activation.

Bioassay of endothelium-derived relaxing factor(s): inactivation by catecholamines

1985 ◽  
Vol 249 (1) ◽  
pp. H95-H101 ◽  
Author(s):  
G. M. Rubanyi ◽  
R. R. Lorenz ◽  
P. M. Vanhoutte
Keyword(s):  
Endothelial Cells ◽  
Femoral Artery ◽  
Physiological Salt Solution ◽  
Second Phase ◽  
Partial Recovery ◽  
Rapid Phase ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Bioassay Technique ◽  
Endothelium Derived Relaxing Factor

A bioassay technique was developed to analyze the effect of vasoactive substance(s) released from endothelial cells. Canine femoral arteries with or without endothelium were perfused with physiological salt solution at 37 degrees C. The perfusate was bioassayed with a ring of coronary artery without endothelium. A substance(s) released by the endothelial cells under basal conditions caused relaxation of unstimulated coronary arteries or relaxation of those contracted with prostaglandin F2 alpha. The release of the relaxing substance(s) was augmented by acetylcholine. The relaxation induced by acetylcholine was biphasic: an initial rapid phase followed by a partial recovery and a slowly developing prolonged relaxation; the half-life of the substance(s) causing the initial phase averaged 6.3 s. Norepinephrine, epinephrine, and ascorbic acid, given downstream of the femoral artery, reversibly prevented the second phase but only attenuated the initial relaxation. These observations indicate that an endothelium-derived relaxing substance(s) is released into the lumen of the femoral artery under basal conditions and during stimulation with acetylcholine. Catecholamines can inactivate the relaxing substance(s) but do not prevent either its production by endothelial cells or its action on vascular smooth muscle.

Retinal venous oxygen saturation and cardiac output during controlled hemorrhage and resuscitation

2003 ◽  
Vol 94 (3) ◽  
pp. 891-896 ◽  
Author(s):  
Kurt R. Denninghoff ◽  
Matthew H. Smith ◽  
Art Lompado ◽  
Lloyd W. Hillman
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Oxygen Saturation ◽  
Femoral Artery ◽  
Mixed Venous Oxygen Saturation ◽  
Oxygen Level ◽  
Shed Blood ◽  
Venous Oxygen Saturation ◽  
Retinal Artery ◽  
Mixed Venous

The objective was to test calibration of an eye oximeter (EOX) in a vitiligo swine eye and correlate retinal venous oxygen saturation (SrvO2), mixed venous oxygen saturation (SvO2), and cardiac output (CO) during robust changes in blood volume. Ten anesthetized adult Sinclair swine with retinal vitiligo were placed on stepwise decreasing amounts of oxygen. At each oxygen level, femoral artery oxygen saturation (SaO2) and retinal artery oxygen saturation (SraO2) were obtained. After equilibration on 100% O2, subjects were bled at 1.4 ml · kg−1· min−1for 20 min. Subsequently, anticoagulated shed blood was reinfused at the same rate. During graded hypoxia, exsanguination, and reinfusion, SraO2and SrvO2were measured by using the EOX, and CO and SvO2were measured by using a pulmonary artery catheter. During graded hypoxia, SraO2correlated with SaO2( r = 0.92). SrvO2correlated with SvO2( r = 0.89) during exsanguination and reinfusion. SvO2and SrvO2correlated with CO during blood removal and resuscitation ( r = 0.92). Use of vitiligo retinas improved the calibration of EOX measurements. In this robust hemorrhage model, SrvO2correlates with CO and SvO2across the range of exsanguination and resuscitation.

scholarly journals Role of endothelium-derived relaxing factor during transition of pulmonary circulation at birth

1990 ◽  
Vol 259 (6) ◽  
pp. H1921-H1927 ◽  
Author(s):  
S. H. Abman ◽  
B. A. Chatfield ◽  
S. L. Hall ◽  
I. F. McMurtry
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Circulation ◽  
Atrial Natriuretic Factor ◽  
Pulmonary Blood Flow ◽  
Relaxing Factor ◽  
Natriuretic Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Atrial Natriuretic

To examine the potential role of endothelium-derived relaxing factor (EDRF) in regulation of the perinatal pulmonary circulation, we studied the hemodynamic effects of a selective inhibitor of EDRF production, nitro-L-arginine (L-NA), on pulmonary vascular tone and dilator reactivity in the late-gestation ovine fetus and on the pulmonary vasodilation that normally occurs at birth. L-NA infusion decreased pulmonary blood flow from 78 +/- 8 to 65 +/- 6 ml/min (P less than 0.01) and increased pulmonary artery pressure from 48 +/- 2 to 54 +/- 3 mmHg (P less than 0.002, n = 8 animals). To study the selectivity of L-NA on vasodilator responses to endothelium-dependent (acetylcholine) and -independent (atrial natriuretic factor) stimuli, we measured responses to brief infusions of each dilator before and after L-NA treatment. Acetylcholine increased pulmonary blood flow during the control period but not after L-NA treatment. In contrast, L-NA had little effect on the vasodilator response to atrial natriuretic factor. To study the role of EDRF in the transition of the pulmonary circulation from fetal to neonatal conditions, we infused L-NA into the left pulmonary artery immediately before cesarean-section delivery. In comparison with control animals, the rise in pulmonary blood flow at 1 h after delivery was reduced in the L-NA-treated animals (331 +/- 28 in control vs. 185 +/- 16 ml/min in treated, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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