Abstract

Activation of trypsin and lipase from their precursors in the pancreas can cause digestion of blood vessels and parenchyma, leading to acute haemorrhagic pancreatitis. Trypsin activates kallikrein which in turn activates kinins: these lower the blood pressure by vasodilatation and increased capillary permeability and so cause ‘shock’. These mechanisms have been demonstrated in animals and seem likely to occur in human pancreatitis. Intravenous administration of Trasylol (FBA), a polypeptide extracted from bovine lungs, has been reported to halt experimental pancreatitis in animals by inactivating proteolytic enzymes, and to reduce the severity of the resulting shock by inactivating kallikrein.^1–4 Other reports^{5 6} did not confirm this. We have previously mentioned the thrombolytic properties of Trasylol.⁷