After pretreatment with the selective monoamine oxidase B inhibitor, (-)-deprenyl, in doses sufficient for complete inhibition of the platelet enzyme, 4 normal and 6 parkinsoniam volunteers (2 receiving levodopa and 2 levodopa plus carbidopa) suffered no adverse pressor reaction ('cheese effect') after challenge with oral tyramine in amounts considerably greater than those likely to be encountered in a normal diet. Nor did the levodopa-deprenyl combination itself result in a pressor response. Normal human intestinal mucosa was shown predominantly to contain the deprenyl-insensitive A form of the enzyme, which presumably degraded administered tyramine in the deprenyl-treated volunteers; even those receiving the drug for prolonged periods manifested no 'cheese effect', suggesting that the A form remained uninhibited. Intestinal monoamine oxidase A was able to oxidise dopamine, whereas in human platelet or striatum the amine is a monoamine oxidase B substrate. Like tyramine, oral phenylethylamine challenge with amounts greater than those known to be present in a normal diet similarly gave rise to no adverse reaction in (-)-deprenyl-treated subjects; the reasons for this remain to be determined.

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Actions of salbutamol, disodium cromoglycate, and placebo administered as aerosols in acute asthma 725Resistance to DSCG in acute asthma is greater therefore, than to salbutamol. However, clinical observation suggests that resistance to beta-2 stimulants does also increase with severity of the attack. It would appear probable that only when severity exceeds the point at which measurements can be made with a peak flow meter does resistance to salbutamol become pronounced. Although placebo effects are greater in the attack than between attacks, again no information is available about attacks severe enough to prevent measurement using a peak flow meter. pipette into a capillary tube (for this technique blood pH capillary tubes cut to the same length as standard glass capillary tubes were used). They were sealed at one end by a flame and centrifuged for 15 minutes at 12 000 g, using a haematocrit centrifuge (Hawksley, London).After centrifugation the tubes were removed immediately and placed vertically. The length of the fat layer at the top and that of the solid layer at the bottom was measured with vernier callipers to the nearest 0 05 mm. Stool fat content was expressed as a percentage (steatocrit) of the total length of the solid column in the tube (that is fat layer + solid layer) (Fig. 1). The steatocrit was measured in duplicate. The stool fat content was also measured by Sobel's method2 which requires 3 g of stool.

No abstract