Mechanism of Pain in Peptic Ulcer

Ruffin, Julian M.; Baylin, George J.; Legerton, Clarence W.; Texter, E. Clinton

doi:10.1016/s0016-5085(53)80036-3

Cited by 32 publications

(7 citation statements)

References 22 publications

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“…These experiments may be interpreted as showing either that the gastric mucosa is sensitive to HC1 or that the acid passes through the pylorus and then irritates the duodenal ulcer, having penetrated its covering slough (Bonney and Pickering, 1946). But one experiment with a mixture of barium and acid demonstrated pain reproduction without any barium leaving the stomach (Ruffin et al, 1953). It must be emphasized that most workers have found that the normal gastric mucosa is insensitive to HCI and that no pain is produced when acid is instilled into the stomach (Spira, 1956).…”

Section: Discussionmentioning

confidence: 99%

“…Pain from Abnormal Gastric Motility.-Increased frequency or amplitude of gastric contractions has been recorded during attacks of pain (Ruffin et al, 1953). If the stomach has previously been filled with acid then gastric contractions are more likely to cause pain.…”

Section: Discussionmentioning

confidence: 99%

“…If the stomach has previously been filled with acid then gastric contractions are more likely to cause pain. These contractions do not necessarily cause emptying of the stomach contents into the duodenum, because pain may occur with the pvlorus still closed (Ruffin et al, 1953). Inhibition of the contractions by nitrites (Beams, 1932) or Banthine (Hightower and Gambill, 1953) can cause the pain to disappear.…”

Section: Discussionmentioning

confidence: 99%

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Production of Epigastric Pain in Duodenal Ulcer by Lower Oesophageal Acid Perfusion

Earlam¹

1970

BMJ

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Summary: Thirty-six patients with duodenal ulceration were divided into group 1 (30), who had epigastric pain, and group 2 (6), who had pain in the upper abdomen but not in the epigastrium, and were studied by perfusing the lower oesophagus with dilute acid in an attempt to reproduce epigastric pain. In group 1, 25 suffered epigastric pain, indistinguishable from that which they normally had, after perfusion of 30 ml. of 041N HC1 in under four minutes (mean values), but none of group 2 had pain.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Production of Epigastric Pain in Duodenal Ulcer by Lower Oesophageal Acid Perfusion

Earlam¹

1970

BMJ

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“…Pain occurs with the onset of hypermotility and ceases when motor function returns to normal. Pain is absent or diminished in the absence of hypermotility even when the acidbarium meal is seen to fill the ulcer crater (Ruffin et al 1953). (c) Vagotomy results in gastric hypotonus and it is significant that pain is absent after vagotomy even though the ulcer may still be demonstrable by radiography.…”

Section: Painmentioning

confidence: 99%

President's Address. Muscle Spasm in the Etiology of Chronic Peptic Ulcer

Qvist

1974

Proceedings of the Royal Society of Medicine

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Motor activity and spasm were for many years regarded as factors of great importance in the genesis and symptomatology of chronic peptic ulcer. In recent times, however, the factor of myospasm has claimed far less attention, the emphasis being placed almost entirely on acidity as being of greatest significance in the etiology, symptomatology and therapy of peptic ulceration. There is little reference in current literature to the relief of muscle spasm as a factor of importance in the healing of peptic ulcer.It is suggested that motor activity is in fact an important element in the pathology and clinical features of chronic peptic ulcer. There are numerous conditions in which myospasm and peptic ulcer are associated and also some conditions of gastrointestinal hypotonia in which peptic ulcer is rarely found.

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“…Radiological and pressure studies have shown that the pain of duodenal ulcer occurred at the same time as increasing motility and contraction of the duodenal bulb (Wilson, 1928;Patterson and Sandweiss, 1942). Pain has also been related to increased gastric contractions (Ruffin et al, 1953).…”

Section: Relation Between Endoscopic and Symptomatic Assessmentsmentioning

confidence: 99%