1have clinical significance which is being evaluated currently. Other efforts are being directed toward isolation and identification of the diffusible substance and the plaque material which it produces and an elucidation of the specific substrates involved.The diffusible substance that activates production of the red band differs from the substance that produces the plaque material. This is demonstrated by the fact that whereas all the bloods used for preparation of the media were able to act as substrate for the red band, a few did not act as substrate for production of plaques.Summary. Macroscopically visible lipid plaques were produced on the surface of human blood agar plates and on 10% plasma agar plates when they were inoculated centrally with certain strains of coagulase-positive S. aureus or exposed to active sterile agar segments ( ASA) . Similar lipid plaques covered the surface of liquid media containing plasma when activated sterile agar segments were suspended in the media. Staphylococ-cus antitoxin prevented the appearance of the lipid plaques. The lipid plaques consist primarily of octadecenoic acid, both free and in triglycerides. Lesser amounts of stearic, palmitic and various shorter chain acids are also present. The most likely explanation for the phenomenon is that a lipase released by certain strains of staphylococci acts upon the lipids in human plasma.

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Each of 12 patients undergoing routine diagnostic upper gastrointestinal endoscopy received a single iv infusion of clindamycin phosphate 300 mg over 10 min. During the endoscopy, mucosal biopsies of the gastric antrum and fundus were obtained at varying times following the infusion. The clindamycin concentrations in the biopsies and in serum samples also taken after the infusion were determined. In addition, six healthy volunteers participated in a cross-over study on two different days. On both days, each subject received a single iv infusion of clindamycin phosphate 300 mg, immediately after which, gastric secretion was stimulated by iv pentagastrin (2 micrograms/kg/h) which was infused continuously over 150 min. On one of the study days, acid secretion by the stomach was inhibited by a slow iv infusion of ranitidine 50 mg. Clindamycin concentrations in gastric aspirates and serum samples collected after the infusion were determined. Concentrations of clindamycin in the fundal mucosa were significantly higher than the simultaneous serum concentrations (median ratio of tissue concentration to serum concentration, 2.0; P < 0.005) while concentrations in the antral mucosa were similar to those in serum (median ratio, 1.2; P = 0.65). Ranitidine significantly inhibited pentagastrin-stimulated acid secretion as demonstrated by a decrease in the volume of gastric aspirate when ranitidine was administered compared with when it was not administered (P < 0.01). Clindamycin concentrations in gastric juice were approximately one and one-half times higher than those in serum samples obtained simultaneously, both during stimulation of gastric acid secretion with pentagastrin and during inhibition of pentagastrin-stimulated acid secretion with ranitidine. Gastric juice concentrations of clindamycin were significantly higher following administration of ranitidine than after stimulation of gastric secretion by pentagastrin alone. Fundal mucosal and gastric juice concentrations of clindamycin exceeded the hypothetical maximum serum concentrations, indicating that accumulation in the stomach occurred against a concentration gradient.

The majority of upper gastrointestinal bleeds stop spontaneously despite the low pH and proteolytic activity of gastric juice which inhibit coagulation and platelet aggregation. In order to investigate this paradox six healthy male volunteers received intragastric infusions of 160 ml autologous venous blood or 160 ml egg white acting as control in random order on separate days. Basal acid output was calculated before infusion, net acid secretion and gastric volume emptied were calculated after intragastric infusions. Serum gastrin concentrations were also measured before and after intragastric infusions and expressed as the integrated gastrin response. Basal acid output (mmol/h) was 4*7 (1.9) (mean (SEM)) before egg white infusion and 5 9 (2.6) before venous blood infusion. After egg white infusion net acid secretion (mmol/20 min) increased to 5*6 (3.1) compared with 2-3 (1.3) after venous blood infusion (p<005). The gastric volume emptied (ml/20 min) was less after venous blood infusion at 105 (28) compared with 321 (66) after egg white infusion (p<0 03). Integrated gastrin response was similar after venous blood and egg white infusion. When compared with an equivalent protein meal intragastric blood stimulates less acid secretion and delays gastric emptying. This effect may facilitate haemostasis after gastric bleeding.