Richard P. Saik
University of California, San Diego
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Featured researches published by Richard P. Saik.
American Journal of Surgery | 1975
Richard P. Saik; A.Gerson Greenburg; Jack Matthews Farris; Gerald W. Peskin
Of 402 patients admitted with biliary disease over the last three years, cholangitis has been diagnosed in 36. This represents an 8.8 per cent overal incidence and a 33.8 per cent incidence among patients who have undergone operation or manipulation involving the common duct. Based on this experience, a program of prophylaxis and treatment of cholangitis has been devised with special emphasis on the management of elderly patients in the initial postoperative period.
American Journal of Surgery | 1976
Richard P. Saik; A.Gerson Greenburg; Jack M. Farrls; Gerald W. Peskln
The use of Congo Red testing for adequacy of vagotomy in a variety of clinical situations is described. Its intraoperative use is presented for the first time, thus allowing the surgeon immediate documentation of the completeness of his vagotomy and hopefully averting incomplete vagotomy, the single most common cause of ulcer recurrence after vagotomy-pyloroplasty.
Journal of Surgical Research | 1974
Richard P. Saik
Abstract Heidenhain pouches were constructed in five mongrel dogs weighing between 15 and 25 kg. Surgical anesthesia was accomplished by giving ketamine im and alphachloralose iv against a background of submaximal, maximal, and supermaximal histamine doses. Ketamine caused significant acid inhibition at all dose levels of histamine when compared to histamine alone. Chloralose caused no significant inhibition at the first dose of histamine in all animals tested and no significant inhibition in one dog at all four dose levels of histamine. At almost all doses of histamine, chloralose caused significantly less acid inhibition when compared to ketamine. Thus, chloralose anesthesia is suggested as a more suitable anesthetic in acutely studying gastric acid secretory changes, but still is not comparable to studying the awake unanesthetized animal.
Journal of Surgical Research | 1978
Richard P. Saik; Nathaniel Weisenfeld; A.Gerson Greenburg; Daniel Kripke; Gerald W. Peskin
Abstract A definite circadian rhythm in serum gastrin, as measured every 2 hr for 24 hr, exists in the normal fasted dog. This rhythm is abolished by removing acid and pH effects by explanting the innervated antrum onto the abdomen or stimulating by explanting onto the colon. Twofold variations in serum gastrin during a day occur in a cyclic nature and are presumably secondary to variations in intraluminal pH.
Journal of Surgical Research | 1976
Barry A. Levine; A.Gerson Greenburg; Gerald W. Peskin; Richard P. Saik
Abstract Experiments have been carried out in humans and animal subjects in an effort to further delineate antral mechanisms of gastrin release. Protein meals and variation of antral pH with buffered saline has been employed. Results show that: 1. 1. Fasting gastrin levels in duodenal ulcer patients and normals are the same. 2. 2. Antral G-cells of duodenal ulcer subjects respond more readily than normals to a protein meal stimulus. 3. 3. Variation in antral pH over the total range of clinical values does not significantly stimulate basal gastrin levels. Significant acid inhibition occurred in normal patients only. 4. 4. G-cell degranulation seems to occur in an alkaline milieu or be blocked by acidity, i.e., more G-cells are seen at an acid pH. 5. 5. The negative feedblock control over antral gastrin release appears to be less efficient in ulcer patients.
Journal of Surgical Research | 1975
Richard P. Saik; Nancy Anson; Gerald W. Peskin
Abstract Gastrin, CCK, and octapeptide all share the same C-terminal tetrapeptide amide. A Heidenhain pouch and gastric fistula were constructed in four mongrel dogs to ascertain the effect of CCK (16 Crick units/ kg/hr) and octapeptide (0.6 ug/kg/hr) on the HP acid output and serum gastrin response to a meal and calcium infusion (20 mg/kg). Basal acid output was stimulated by octapeptide alone, but not CCK. Resting gastrin was elevated by CCK (three of four dogs) and octapeptide (two of four dogs). Acid response to calcium infusion and a meal was stimulated by octapeptide, but again not significantly by CCK. CCK inhibited the acid response to a meal in one dog. Integrated gastrin output was potentiated by CCK significantly in three of four dogs to calcium and a meal, and by octapeptide in three out of four in response to a meal. CCK and octapeptide do not act as competitive inhibitors of acid output in this animal model at the doses utilized. Octapeptide was a more potent stimulant of acid suggesting contamination of CCK preparations with other inhibitors. CCK caused more significant potentiation of gastrin release in most cases without significant acid elevations. Acid elevation did not routinely correspond to elevated gastrin levels. Both octapeptide and CCK tended to cause elevated serum gastrin levels.
Digestive Surgery | 1987
Richard P. Saik; Candace Moore
Earlier reports have indicated increases in gastrin cell (G cell) mass in many disease states including hyperparathyroidism. This correlation has not been confirmed experimentally, nor has the influence of hypercalcemia separate from that of elevated parathormone been discerned. Sprague-Dawley rats (n = 16) were divided into experimental and control groups. The controls received biweekly intraperitoneal injections of 0.2 ml of propylene glycol and ethanol. Experimental rats received biweekly injections of cholecalciferol (125 µg/ml) in the above carrier and were then divided into 2 groups, group A with 5 weeks and group B with 8 weeks of treatment. Weekly blood was drawn for serum calcium (AA) and serum gastrin (RIA). At sacrifice, serum for parathormone assay (RIA) was drawn and the antral mucosa was stripped and digested. Total mucosa cells were counted and pelleted. Pellets were fixed and sectioned. Straining for G cells was performed using a double-antibody immunofiuorescence technique. Significant hypercalcemia was achieved by vitamin D treatment: mean serum calcium was 13.2 ± 1.2 and 13.5 ± 5.0 versus 10.7 ± 0.6 ml/dl in the controls (p 4 ± 10.97 × 104 to 5.22 × 104 ± 2.25 ± 104 in group A and 3.15 × 104 ± 1.38 × 104 in group B (p
Biotechnic & Histochemistry | 1985
Candace Moore; Richard P. Saik
A simple technique has been developed to quantitate the gastrin cells (G-cells) from the pyloric antrum of the rat. The antrum was digested in pronase to suspend the epithelial cells. This cell suspension was counted and pelleted. The pellet was embedded in paraffin, sectioned, then labeled using the indirect immunofluorescence technique specific for gastrin. The percentage of G-cells was determined from photographs of fluorescing sections and total G-cell numbers were determined by relating these data to total epithelial cell counts. In 14 rats the average G-cell population totaled 1.03 +/- 0.21 X 10(5) G-cells/antrum. The technique is simple, time-saving and avoids the uncertainties inherent in previous procedures for the estimation of G-cell numbers.
Journal of Surgical Research | 1978
Richard P. Saik; Diane Brown
Abstract Lithium and hydrogen flux was measured in three mongrel dogs via a gastric fistula both before and after injury with Nataurocholate (10m M ) and acetylsalicylic acid (20m M ). Both agents consistently caused back diffusion of hydrogen without a corresponding change in lithium. We conclude that lithium is not a sensitive indicator of mucosal disruption.
Journal of Lipid Research | 1976
Thomas E. Carew; Richard P. Saik; Kai H. Johansen; Charles A. Dennis; Daniel Steinberg