Search

Locoweeds cause significant livestock poisoning and economic loss in the western United States. The toxicity of Embellisia sp. fungi isolated from locoweed was compared with locoweed toxicity using the rat as a model. Rats were fed diets containing locoweed, fungus and alfalfa, or alfalfa. Locoweed- and fungus-fed rats consumed swainsonine-containing food at approximately 1.3 mg*[kg.sup.-1]*[d.sup.-1], gained less weight (P = 0.001) and ate less than controls. Swainsonine is the principal agent responsible for inducing locoism in animals. The concentrations of alkaline phosphatase and aspartate aminotransferase enzymes were greater (P < 0.05) in serum of locoweed- and fungus-fed rats compared with control rats. Similar intracellular vacuolation was observed in renal, pancreatic, and hepatic tissues of rats that consumed either locoweed or fungus. Rats that ate locoweed or Embellisia fungi displayed indistinguishable toxicity symptoms. The Embellisia fungi from locoweed can induce toxicity without the plants. Locoism management strategies need to involve management of the Embellisia fungi. Key Words: Endophyte, Fungus, Locoweeds, Swainsonine

Vasoconstriction has been associated with several symptoms of fescue toxicosis thought to be alkaloid induced. Lysergic acid, an ergot alkaloid, has been proposed as a toxic component of endophyte-infected tall fescue. The objective of this study was to examine the vasoconstrictive potential of D-lysergic acid using a bovine lateral (cranial branch) saphenous vein bioassay. Before testing lysergic acid, validation of the bovine lateral saphenous vein bioassay for use with a multimyograph apparatus was conducted using a dose-response to norepinephrine to evaluate the effects of limb of origin (right vs. left) and overnight storage on vessel contractile response. Segments (2 to 3 cm) of the cranial branch of the lateral saphenous vein were collected from healthy mixed breed cattle (n = 12 and n = 7 for the lysergic acid and norepinephrine experiments, respectively) at local abattoirs. Tissue was placed in modified Krebs-Henseleit, oxygenated buffer and kept on ice or stored at 2 to 8°C until used. Veins were trimmed of excess fat and connective tissue, sliced into 2- to 3-mm sections, and suspended in a myograph chamber containing 5 mL of oxygenated Krebs-Henseleit buffer (95% O2, 5% CO2 pH = 7.4; 37°C). Tissue was allowed to equilibrate at 1 g of tension for 90 mm before initiation of treatment additions. Increasing doses of norepinephrine (1 × 10-8 to 5 × 10-4 M) or lysergic acid (1 × 10-11 to 1 × 10-4 M) were administered every 15 mm after buffer replacement. Data were normalized as a percentage of the contractile response induced by a reference dose of norepinephrine. Veins from both left and right limbs demonstrated contractions in a dose-dependent manner (P < 0.01) but did not differ between limbs. There were no differences in dose-response to norepinephrine between tissue tested the day of dissection and tissue tested 24 h later. Exposure of vein segments to increasing concentrations of lysergic acid did not result in an appreciable contractile response until the addition of 1 × 10-4 M lysergic acid (15.6 ± 2.3% of the 1 × 10-4 M norepinephrine response). These data indicate that only highly elevated concentrations of lysergic acid result in vasoconstriction. Thus, in relation to the symptoms associated with vasoconstriction, lysergic acid may only play a minor role in the manifestation of fescue toxicosis. [ABSTRACT FROM AUTHOR]

Vasoconstriction is associated with consumption of toxic endophyteinfected tall fescue. Because it is not known if endophyte-produced alkaloids act alone or in concert, the objective of this study was to examine the vasoconstrictive potentials of D-lysergic acid (LSA) and ergovaline (ERV) individually or in combination with N-acetyl loline (NAL) using bovine lateral saphenous veins biopsied from fescue naïve cattle. Segments (2-3 cm) of vein were surgically biopsied from healthy cross-bred yearling cattle (n=5; 360 ±20 kg). Veins were trimmed of excess fat and connective tissue, sliced into 2-3 mm sections and suspended in a myograph chamber containing 5 mL of oxygenated Krebs-Henseleit buffer (95% O2/5% CO2; pH = 7.4; 37°C). Tissue was allowed to equilibrate at 1 g of tension for 90 min prior to initiation of treatment additions. Increasing doses of ERV or LSA (1x10-11 to 1x10-4 M) with or with out NAL (1x10-5 M) were administered every 15 min following buffer replacement. Data were normalized as a percent of contractile response induced by a reference dose of norepinephrine (1x10-4 M). Increasing concentrations of LSA did not result in an appreciable contractile response until the addition of 1x10-4 M LSA (22.6 ± 4.1%). A vascular response to increasing concentrations of ERV was apparent at 1x10-8 M (4.7 ± 2.2%) and increased to a maximum of 104.2 ± 6.0% with the addition of 1x10-4 M ERV. The presence of NAL did not alter the onset or magnitude of vascular response to either LSA or ERV (maximum responses of 24.9 ± 4.5 and 101.5 ± 10.9%, respectively). These data indicate that ERV is a more potent vascular toxicant than lysergic acid. Further, the presence of NAL did not inhibit or potentiate the effects of the ergot alkaloids on vascular activity. If these data persist in additional physiological systems, then tall fescue forages containing LSA and/or NAL should be safer for animal consumption than those containing ERV. [ABSTRACT FROM AUTHOR]

Vasoconstriction has been associated with several symptoms of fescue toxicosis thought to be alkaloid induced. Lysergic acid, an ergot alkaloid, has been proposed as a toxic component of endophyte-infected tall fescue. The objective of this study was to examine the vasoconstrictive potential of D-lysergic acid using a bovine lateral (cranial branch) saphenous vein bioassay. Before testing lysergic acid, validation of the bovine lateral saphenous vein bioassay for use with a multimyograph apparatus was conducted using a dose-response to norepinephrine to evaluate the effects of limb of origin (right vs. left) and overnight storage on vessel contractile response. Segments (2 to 3 cm) of the cranial branch of the lateral saphenous vein were collected from healthy mixed breed cattle (n = 12 and n = 7 for the lysergic acid and norepinephrine experiments, respectively) at local abattoirs. Tissue was placed in modified Krebs-Henseleit, oxygenated buffer and kept on ice or stored at 2 to 8°C until used. Veins were trimmed of excess fat and connective tissue, sliced into 2- to 3-mm sections, and suspended in a myograph chamber containing 5 mL of oxygenated Krebs-Henseleit buffer (95% O2, 5% CO2 pH = 7.4; 37°C). Tissue was allowed to equilibrate at 1 g of tension for 90 mm before initiation of treatment additions. Increasing doses of norepinephrine (1 × 10-8 to 5 × 10-4 M) or lysergic acid (1 × 10-11 to 1 × 10-4 M) were administered every 15 mm after buffer replacement. Data were normalized as a percentage of the contractile response induced by a reference dose of norepinephrine. Veins from both left and right limbs demonstrated contractions in a dose-dependent manner (P < 0.01) but did not differ between limbs. There were no differences in dose-response to norepinephrine between tissue tested the day of dissection and tissue tested 24 h later. Exposure of vein segments to increasing concentrations of lysergic acid did not result in an appreciable contractile response until the addition of 1 × 10-4 M lysergic acid (15.6 ± 2.3% of the 1 × 10-4 M norepinephrine response). These data indicate that only highly elevated concentrations of lysergic acid result in vasoconstriction. Thus, in relation to the symptoms associated with vasoconstriction, lysergic acid may only play a minor role in the manifestation of fescue toxicosis. [ABSTRACT FROM AUTHOR]