Endocrine and haemodynamic investigations of normal and laminitic horses.

The historical and evolutionary perspectives of equine laminitis were placed in a contemporary context of hippology. A survey revealed 3% of the equine population in the UK to be affected by laminitis. Physiological aspects affecting pedal blood flow, namely endocrine and haemodynamic relationships, were considered under controlled management. Pedal haemodynamics, investigated non-invasively using Near Infrared Spectroscopy, detected changes in concentrations of oxyhaemoglobin, deoxyhaemoglobin and cytochrome oxidase, indicating tissue utilisation of oxygen and hence perfusion. Responses of chronic larninitics suggested attenuated blood flow and local hypoxia. Haemostasis was shown to occur in acute larninitis The role of nitric oxide was investigated by assessment of the effects of concentrations of substrate, synthetic nitric oxide donors, and endogenous and exogenous, inhibitors of nitric oxide synthesis. Reperfusion of ischaernic laminal tissue during acute laminitis was initiated by iv administration of I-arginine, a substrate of nitric oxide (NO) synthesis; this also increased blood flow in laminal tissues of a normal horse, but had little effect on blood pressure. Grass induced acute laminitis was successfully treated with transdermal application of glyceryl trinitrate paste to the pasterns. A competitive inhibitor of I-arginine synthesis increased blood pressure of normal horses but did not induce acute laminitis. Plasma I-arginine increased when normal and chronically laminitic horses went to grass. Plasma asymmetric dimethyl-l-arginine (ADMA) was lower in chronic laminitics than normal ponies; ADMA decreased when at grass from 1.2 [tmol/L to 0.7 [tmol/L in normal horses and from 0.8 tLmol/L to 0.47 [tmol /L in chronically laminitic ponies. Radioimmunoassays for angiotensin II, atrial natriuretic peptide and endothelin were validated and basal values for the horse established as 24 ±2 pg/ml, 34 ±2 pg/ml and 1.78 ± 0.2 pg/ml respectively. Seasonal differences in AII and ANP were observed. Endocrine changes, observed during acute laminitis, were neither large nor sustained. Blood pressures and heart rate were significantly raised at the acute stage but otherwise unremarkable. Although transient hypertension occurs during acute laminitis, chronic laminitics are not hypertensive. Moderate hypertension accompanies refractory laminitis but this does not appear to be mediated by angiotensin II or endothelin. Electrolyte concentrations were largely unaffected but slight seasonal differences were seen alongside sodium retention in refractory and some chronic cases. Digestive disturbances of acute laminitis were reflected in decreased urinary contents of hippuric: acid. Seasonal changes in ingested electrolytes and water soluble carbohydrates are part of the complex pathogenesis of acute laminitis. An hypothesis outlines potential and actual relationships between dietary factors, endotoxaemia and the vasoactive hormones whose interplay may adversely influence pedal haemodynamics in developmental and acute equine laminitis