Alterations of endothelium-dependent digital vascular responses in horses given low-dose endotoxin.
Abstract: Low doses of endotoxin cause vasoconstriction and hypoperfusion of the digit, small intestine, and cecum in horses. To determine the potential cause of these vascular alterations, in vitro vascular responses of palmar digital arteries and veins were determined in 8 horses after intravenous (IV) infusion of 1 L 0.9% NaCl (control) and 0.1 microgram/kg Escherichia coli 055:B5 endotoxin in 1 L of 0.9% NaCl (endotoxin-treated). Vessels were surgically removed under general anesthesia, cut into 4-mm vascular rings, suspended in tissue baths, and attached to force displacement transducers for measurement of vascular tension. Cumulative concentration response curves to acetylcholine, bradykinin, nitroprusside, norepinephrine, 5-hydroxytryptamine (serotonin), and endothelin were determined. Maximal relaxation or contraction and the concentrations needed to produce 50% maximal relaxation or contraction were determined. Palmar digital arteries from endotoxin-treated horses relaxed significantly less in response to acetylcholine and bradykinin (endothelium-dependent), but not to nitroprusside (endothelium-independent) when compared with arteries from control horses. Digital arteries from endotoxin-treated horses also contracted significantly more with norepinephrine but less with serotonin. Digital veins responded less than digital arteries. In another study, vascular reactivity experiments documented that acetylcholine and bradykinin were endothelium-dependent vasodilators (endothelium-denuded vessels relaxed less than control vessels) in palmar digital vessels. Additionally, maximal relaxations for both vasodilators were significantly inhibited by N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide antagonist, suggesting that acetylcholine and bradykinin cause relaxation through the nitric oxide pathway. The data from these studies indicate that low dose endotoxin impairs endothelium-dependent relaxation and augments adrenergic contraction of palmar digital arteries in horses.
Publication Date: 1995-03-01 PubMed ID: 7778262DOI: 10.1111/j.1532-950x.1995.tb01301.xGoogle Scholar: Lookup
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- Journal Article
- Research Support
- U.S. Gov't
- Non-P.H.S.
Summary
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The research examines how low doses of endotoxin affect the blood vessels in a horse’s limb, specifically causing constriction and reduced blood flow. The study found that this endotoxin negatively impacts the relaxation and contraction functions of these vessels.
Study Design and Experiment
- The researchers performed a controlled experiment on eight horses, wherein each was given either a control (1L 0.9% NaCl) or an endotoxin treatment (0.1 microgram/kg Escherichia coli 055:B5 endotoxin in 1L of 0.9% NaCl).
- Vessels were removed from the horses under general anesthesia and organised into 4-mm vascular rings, which were subsequently suspended in tissue baths for tension readings using force displacement transducers.
- The researchers then studied responsiveness to various compounds that either induce contraction or relaxation in these vessels, including acetylcholine, bradykinin, norepinephrine, serotonin, and endothelin.
- There were measures of max relaxation or contraction and the concentrations needed to produce 50% max relaxation or contraction.
Findings and Conclusions
- The study found that arterial relaxation in response to acetylcholine and bradykinin (endothelium-dependent mechanisms) was markedly reduced in endotoxin-treated horses compared to controls.
- The researchers also discovered an increased contractile response to norepinephrine, but a decreased reaction to serotonin in these horses.
- In another part of the research, reactivity experiments established that acetylcholine and bradykinin were endothelium-dependent vasodilators. Furthermore, a nitric oxide antagonist, N-nitro-L-arginine methyl ester (L-NAME), significantly impeded the relaxing effects of these vasodilators, suggesting that they operate via the nitric oxide pathway.
- In conclusion, the data indicate that low doses of endotoxin hinder endothelium-dependent relaxation and enhance adrenergic contraction in the blood vessels of a horse’s limbs. The findings imply that endotoxin-induced vascular changes could contribute to clinical signs seen in conditions like laminitis and systemic inflammatory response syndrome in horses.
Cite This Article
APA
Baxter GM.
(1995).
Alterations of endothelium-dependent digital vascular responses in horses given low-dose endotoxin.
Vet Surg, 24(2), 87-96.
https://doi.org/10.1111/j.1532-950x.1995.tb01301.x Publication
Researcher Affiliations
- Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Ft Collins, USA.
MeSH Terms
- Acetylcholine / antagonists & inhibitors
- Acetylcholine / pharmacology
- Animals
- Arginine / analogs & derivatives
- Arginine / pharmacology
- Arteries / drug effects
- Arteries / metabolism
- Bradykinin / antagonists & inhibitors
- Bradykinin / pharmacology
- Endothelium, Vascular / drug effects
- Endothelium, Vascular / metabolism
- Endotoxins / administration & dosage
- Escherichia coli
- Female
- Forelimb / blood supply
- Horses / physiology
- Infusions, Intravenous
- Male
- Muscle Relaxation / drug effects
- Muscle Relaxation / physiology
- Muscle, Smooth, Vascular / drug effects
- Muscle, Smooth, Vascular / physiology
- NG-Nitroarginine Methyl Ester
- Nitric Oxide / antagonists & inhibitors
- Nitric Oxide / physiology
- Nitroprusside / pharmacology
- Vasodilation / drug effects
- Veins / drug effects
- Veins / metabolism
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