197619a0Nature1974867196302096196190028-0836196310.1038/197619a0ukNatureNatureNATUREnatureNature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions. Nature also provides rapid, authoritative, insightful and arresting news and interpretation of topical and coming trends affecting science, scientists and the wider public./nature/journal/v197/n4867issueJournal homeArchiveCurrent issueAdvance online publicationPrivacy policySubscribeNature Publishing GroupCurrent issue197619a0Grass Tetany and Histamine
AU  - FOWLER, H. D.The Agricultural Institute, Soils Division, Johnstown Castle Agricultural College, Wexford, Ireland.THE occurrence, distribution and aetiology of grass tetany in cattle and sheep have already been adequately described1,2. The most consistent symptom in all cases is a low serum magnesium-level, values below 1 mg per 100 ml. being common. The condition is sometimes accompanied by hypocalcaemia2. Nevertheless, severe hypomagnesaemia can be present in some cases without the appearance of clinical symptoms of tetany, which raises the question of the possible occurrence of other causative factors. The high incidence of grass tetany, for example, on young, rapidly growing pastures has given rise to views that some factor may be introduced by the herbage, and Seekles2 has even suggested the term /`nutrition-tetany/' for the condition. This factor may be independent of those which act by reducing availability of magnesium to the animal.Death in grass tetany is usually attributed to shock. A paper by Schayer3 would ascribe all shock phenomena to rapid histamine release into the blood. The histamine-levels in blood serum in cases of grass tetany have been shown by Seekles4 either to be abnormally high or abnormally low. Abnormally low values were attributed to the dilating action of histamine on blood capillaries causing increased permeability of the capillary walls. Among compounds known to cause histamine release on injection both aliphatic and substituted aromatic amines and the ammonium ion have been recorded5. Whether dietary factors could produce similar effects is not yet known but Parrot6 has been able to cause the death of guinea pigs by parenteral administration of histamine and has also shown that prior administration of putrescine reduces the minimum lethal dose to one-tenth of its formerly required level. The guinea pig is, however, known to bo abnormally sensitive to histamine. The presence of putrescine and cadaverine in spring grass has been reported by van der Horst7 and histamine also is present8.
The influence of low- and high-calcium diets in guinea pigs on death from histamine has been investigated9; low calcium diets reduce the minimum lethal dose administered into the stomach. Similarly, diets high in potassium lead to greater susceptibility to histamine when administered intravenously to mice10 and the influence of heavy potash fertilization in conditioning the production of tetany-prone swards has been frequently reported1.
The treatment of grass tetany by the use of antihista-minics in conjunction with magnesium-calcium therapy has been reported by Hendriks11 and some preliminary observations using 'Antiallergicum Vetag' (Veterinaria S.A. Zurich), both with and without magnesium?calcium injections have given results which justify further investigation.
It seems desirable, therefore, to widen the scope of investigations in grass tetany from the field of magnesi um availability alone to the manner in which magnesium deficiency, either alone or with other factors, causes tetany. In this wider investigation the relationship of magnesium deficiency to histamine metabolism may play an important part and deserves closer examination.Comm. Agric. Bur. Tech. Comm. No. 15, 136 (1956).Seminar on Control of Diseases in Cattle and Sheep at Pasture, O.E.E.C. European Productivity Agency, EPA/AG/Project, 204/2, Utrecht, 3 (Sept. 1957).Schayer, , R. W., Amer. J. Physiol., 198, 1187 (1960).PubMedISIChemPortSeekles, , L., Sixth Intern. Cong. Comparative Pathology, Madrid, 337 (1952).Neveu, , Therese, J. Physiologie (Paris), 52 (3), 47 (1960).Parrot, , J. L., Gabe, , M., and Herrault, , A., C.R. Soc. Biol., 141, 486 (1947).van der Horst, , C. J. G., Tijdschrift voor Diergeneeskunde, 85 (17), 1060 (1960).Fowler, , H. D., Nature, 193, 582 (1962).ArticlePubMedISIChemPortValette, , G., and Calderon, , C. E., C.R. Acad. Sci., Paris, 242, 1228 (1956).MacMillan, , W. H., and McHugo, , P. B., Amer. J. Physiol., 191, 583 (1957).Hendriks, , H. J., Thesis, Univ. Utrecht, 5 April, 1962.