Owen H. Wangensteen
University of Minnesota
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Featured researches published by Owen H. Wangensteen.
Experimental Biology and Medicine | 1951
Frederick S. Cross; Owen H. Wangensteen
Conclusions (1) Digestion and destruction of the living esophageal mucosa in cats and dogs can be accomplished by bile, pancreatic juice, and mixtures of the two. (2) Bleeding from esophageal erosions attending the complete diversion of bile and pancreatic juice into the esophagus in the dog causes a severe secondary anemia. (3) The development of the esophagitis and anemia in the dog is not altered by total excision of the acid secreting portion of the stomach.
Experimental Biology and Medicine | 1945
Ivan D. Baronofsky; Owen H. Wangensteen
Conclusions 1. Partial obstruction to the venous outflow from the stomach increases its weight in rabbits and dogs. 2. Esophageal varices can be produced by portal or splenic vien obstruction and, when histamine-inbeeswax is given to such animals, esophageal and gastric erosions and bleeding are produced. 3. Portal or splenic vien obstruction abets the ulcer diathesis.
American Journal of Surgery | 1970
Richard F. Edlich; John W. Borner; John Kuphal; Owen H. Wangensteen
Summary The role of gastric distention in regulating blood flow and its distribution within the gastric microcirculation was determined by the radiorubidium clearance technic. Gastric distention produces a profound and selective reduction in blood flow to the mucosa and submucosa of the corpus without altering blood flow to the adjacent muscularis. It is suggested that these changes in gastric blood flow result from lengthening and narrowing of the submucosal vessels of the distended corpus.
Experimental Biology and Medicine | 1950
Robert W. Toon; Owen H. Wangensteen
Conclusions 1. Anemia, either macrocytic or normocytic in type, can be consistently produced in the rat by the formation of blind intestinal segments. 2. Aureomycin appears to be a potent agent in the prevention of this anemia. 3. Ulceration of the blind intestinal segment does not appear to be the major etiological factor in the causation of this anemia.
Experimental Biology and Medicine | 1955
Edwin L. Brackney; Alan P. Thal; Owen H. Wangensteen
Summary 1. The output of free HCI by isolated gastric pouches more than doubled following resection of the duodenum and proximal 20 to 30 cm of jejunum. 2. Interposing a segment of small bowel approximately 1.5 meters long between the stomach and duodenum also caused the output of free HCl from isolated gastric pouches to more than double. 3. The marked increase in HCI secretion following both operations was observed in every case and seemed to be independent of the pre-operative level of HCI secretion by the pouches.
Experimental Biology and Medicine | 1948
C. W. Lillehei; J. L. Dixon; Owen H. Wangensteen
Conclusions The factors of post-hemorrhagic anemia and shock are evaluated in relation to their effect on the histamine-provoked ulcer in dogs. Our evidence indicates that anemia and hemodilution occurring without shock is a mild ulcer abetting factor. However, post-hemoTrhagic shock, even of relatively brief duration aids and abets the ulcer susceptibility most likely through its vasoconstrictor effect on the small blood vessels with resultant localized anemic areas in the mucosa. The combined effects of post-hemorrhagic anemia and shock on the ulcer diathesis are synergistic in that together they give a higher incidence of histamine-provoked ulcer than does either alone.
Experimental Biology and Medicine | 1953
Francisco L. Raffucci; F. John Lewis; Owen H. Wangensteen
Summary When hypothermia is induced in dogs prior to the production of liver anoxia by completely occluding the afferent hepatic circulation, the mortality rate of the procedure is greatly reduced (27.2%) as compared to that previously reported in control animals (100%).
Experimental Biology and Medicine | 1948
C. W. Lillehei; Owen H. Wangensteen
Conclusions 1. Postganglionic sympathectomy of the gastrointestinal tract potentiates the susceptibility to the histamine-induced ulcer in dogs. 2. This increased susceptibility to ulcer formation has continued over the longest interval during which a dog was observed, in one instance for 499 days following celiac ganglionectomy.
Experimental Biology and Medicine | 1932
Horace G. Scott; Owen H. Wangensteen
Summary Data are submitted on 38 animals in which 4 types of strangulation obstruction were produced and followed until death ensued in 3 of the 4 groups. In Group 11, the strangulated loops were resected before death, at a time when the animals appeared moribund. In the first 2 groups in which the veins were occluded, the arteries were patent or only partially occluded. In these groups the animals apparently died from loss of blood into the bowel and peritoneal cavity. In the last 2 groups in which the arterial occlusion was complete the animals lived about 4 times as long, and undoubtedly died from factors other than the loss of whole blood. Just what caused death in these last 2 groups we are unable to say at this time.
Experimental Biology and Medicine | 1947
Stanley R. Friesen; Owen H. Wangensteen
Conclusions Evidence is presented to show that increased concentration of the blood following burns is an important factor in the occurrence of gastro-duodenal ulcer after experimental burns. (The occurrence of gastro-intestinal congestion, erosion and/or ulcer in burns is directly related to the occurrence of hemoconcentration). Moreover, gastro-intestinal abnormality following burns, even when accompanied by histamine administration, may be prevented by avoidance of the hemoconcentration of burns by proper therapy. The incidence of gastric and/or duodenal ulceration provoked by hemoconcentration in burns is markedly increased when histamine-in-beeswax administration accompanies the burn.