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Ergot alkaloids have been associated with vasoconstriction in grazing livestock affected by the fescue toxicosis syndrome. Previous in vitro investigations studying how ergot alkaloids caused vasoconstriction have shown that ergovaline has a distinct receptor affinity and sustained contractile response. A similar contractile response has not been noted for lysergic acid. The objectives of this study were to determine if repetitive in vitro exposure of bovine lateral saphenous vein to lysergic acid or ergovaline would result in an increasing contractile response and if a measurable bioaccumulation of the alkaloids in the vascular tissue occurs over time. Segments of vein were surgically biopsied from healthy, Angus x Brangus cross-bred, fescuenaive yearling heifers (n = 16) or collected from healthy mixed breed and sex cattle immediately after slaughter (n = 12) at a local abattoir. Veins were trimmed of excess fat and connective tissue, sliced into cross-sections, and suspended in a myograph chamber containing 5 mL of oxygenated Krebs-Henseleit buffer (95% 02/5% CQ; pH - 7.4; 37[degrees]C). Contractile responses to repetitive additions of ergovaline (1 x [10.sup.-9] and 1 x [10.sup.-7] M) and lysergic acid (1 x [10.sup.-5] and 1 x [10.sup.-4] M) were evaluated using the biopsied veins. For the bioaccumulation experiments, veins collected at the abattoir underwent repetitive additions of 1 x [10.sup.-7] M ergovaline and 1 x [10.sup.-5] M lysergic acid and the segments were removed after every 2 additions and media rinses for alkaloid quantification via HPLC/mass spectrometry. Contractile data were normalized as a percentage of contractile response induced by a reference dose of norepinephrine (1 X [10.sup.-4] M). Repetitive additions of 1 x [10.sup.-9] M ergovaline and 1 x [10.sup.5] and 1 x [10.sup.-4] Mlysergic acid resulted in contractile response with a negative slope (P < 0.02). In contrast, repetitive addition of 1 x [10.sup.-7] M ergovaline resulted in a contractile response that increased with each addition (P < 0.01). Lysergic acid and ergovaline were detected at all 4 exposure levels (2x to 8x), but only the 1 x [10.sup.-7] M ergovaline treatmerit resulted in increased tissue content as the number of exposures increased (P < 0.05). These data indicate that ergovaline, but not lysergic acid, bioaccumulates with repetitive exposure in vitro. These results suggest that ergovaline may have a greater potential for inducing toxicosis in grazing animals than lysergic acid because of its potential to bioaccumulate at the cellular site of action. Key words: bovine, ergovaline, lysergic acid, tall fescue, vasoconstriction

Ergocryptine is an ergot alkaloid that affects dopaminergic activity principally by interacting with [D.sub.2]-type receptors. In this study the ability of ergocryptine and several other ergot alkaloids to release [3H]dopamine from isolated nerve endings was demonstrated using in vitro superfusion of rat striatal synaptosomes. Ergocryptine, ergocristine, and bromocryptine produced an elevation in baseline dopamine release of approximately 400% with effective concentrations ([EC.sub.50]) of approximately 30 [[micro]molar]. Ergotamine, ergonovine, ergovaline, and ergocornine were devoid of activity. The time-course of the ergocryptine-stimulated release was relatively slow compared with amphetamine, nicotine, or [K.sup.+]-stimulated [3H]dopamine release; the maximal increase in release required a 5-min treatment. A number of receptor antagonists were examined for their ability to block ergocryptine-stimulated release. Of the dopaminergic, adrenergic, serotonergic, GABA-ergic, and cholinergic antagonists examined, only phentolamine produced a moderate attenuation in evoked release. Omission of [Ca.sup.++] from the medium did not affect ergocryptine-evoked release. Following ergocryptine treatment, the synaptosomes were fully responsive to other stimulant. The results indicate that, in addition to interacting with dopamine receptors, several ergot alkaloids may produce dopaminergic effects by increasing the release of dopamine from central nerve endings. Several mechanisms to account for the evoked neurotransmitter release are discussed. Key Words: Ergot Alkaloids, Dopamine, Neurotransmitters, Rats, Receptors, Antagonists

Plasma samples from two experiments were processed to determine whether ergot alkaloids associated with endophyte-infected tall rescue altered peripheral thyroxine ([T.sub.4]), triiodothyronine ([T.sub.3]), or cortisol concentrations in cattle. In Exp. 1, seven Angus steers (294 kg) received i.v. bolus injections of saline (SAL), ergonovine maleate (7 mg; EM), or ergotamine tartrate (7 mg; ET) at weekly intervals, and they received all treatments during the study. Blood was sampled every 15 min for 5 h, and treatments were given after h 1. Mean ambient temperature was 34C. Treatment x time affected plasma concentrations of [T.sub.3] (P < .05) and of cortisol (P < .001) but not that of [T.sub.4] (P > .2). Plasma [T.sub.3] concentrations were not affected by SAL, whereas concentrations increased (P Key Words: Cattle, Festuca Poisoning, Ergot Alkaloids, Thyroxine, Triiodothyronine, Cortisol

The results from the neurogenic inflammation and c-fos expression studies have confirmed the neural transmission blockade mechanism of both sumatriptan and ergot alkaloids in relieving vascular headaches. The mitigating mechanism involves the mediation of a prejunctional 5-hydroxytryptamine-like receptor which constricts coronary artery and intra-cranial vascular smooth muscle. Furthermore, the neuronal mechanism of sumatriptan and ergot alkaloids makes them viable medications for migraines complicating meningeal inflammation.

Ergot alkaloids cause fescue toxicosis when livestock graze endophyte-infected tall fescue. It is generally accepted that ergovaline is the toxic component of endophyte-infected tall fescue, but there is no direct evidence to support this hypothesis. The objective of this study was to examine relative and potential transport of ergoline and ergopeptine alkaloids across isolated gastric tissues in vitro. Sheep ruminal and omasal tissues were surgically removed and placed in parabiotic chambers. Equimolar concentrations of lysergic acid, lysergol, ergonovine, ergotamine, and ergocryptine were added to a Kreb's Ringer phosphate (KRP) solution on the mucosal side of the tissue. Tissue was incubated in near-physiological conditions for 240 min. Samples were taken from KRP on the serosal side of the chambers at times 0, 30, 60, 120, 180, and 240 min and analyzed for ergot alkaloids by competitive ELISA. The serosal KRP remaining after incubation was freeze-dried and the alkaloid species quantified by HPLC. The area of ruminal and omasal tissues was measured and the potential transportable alkaloids calculated by multiplying the moles of transported alkaloids per square centimeter of each tissue type by the surface area of the tissue. Studies were conducted to compare alkaloid transport in reticular, ruminal, and omasal tissues and to determine whether transport was active or passive. Ruminal tissue had greater ergot alkaloid transport potential than omasal tissue (85 vs 60 mmol) because of a larger surface area. The ruminal posterior dorsal sac had the greatest potential for alkaloid transport, but the other ruminal tissues were not different from one another. Alkaloid transport was less among reticular tissues than among ruminal tissues. Transport of alkaloids seemed to be an active process. The alkaloids with greatest transport potential were lysergic acid and lysergol. Ergopeptine alkaloids tended to pass across omasal tissues in greater quantities than across ruminal tissues, but their transport was minimal compared to lysergic acid and lysergol. Key Words: Ergot Alkaloids, Festuca, Rumen Mucosa, Toxicity