GlucagonÀÌ êÖäûÝÂÝô¿¡ ¹ÌÄ¡´Â ç¯ú¿¡ μÇÏ¿©
Effect of Glucagon on Gastric Secretion
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KMID : 0351619730140020317
Abstract
GlucagonÀÌ histamine¿¡ ´ëÇÑ êÖäûÝÂÝôÚãëë¿¡ ¹ÌÄ¡´Â ç¯úÂÀ» κóÌÇϱâ À§ÇÏ¿© 13¸¶¸®ÀÇ íÚðúà÷̳À» Pavlov pouchÏØ(6¸¶¸®)°ú Heidenhain pouchÏØ(7¸¶¸®)À¸·Î ³ª´©¾î histamineÀ» ù«ù» ¶Ç´Â ò¥áÙð¡ñ¼ÇÏ¿© êÖäûÝÂÝô¸¦ í©Ð½ÇÑ ßÒ÷¾¿¡¼ glucagonÀ» ð¡ñ¼ÇÏ¿© êÖäûÝÂÝôÕá, ë´õá߫Ӹ, úìÓØ ¹× úìôè calciumö·¸¦ ö´ïÒÇÑ Ì¿Íý¸¦ é©å³ÇÏ¸é ´ÙÀ½°ú °°´Ù.
Histidine÷áæ¨·Î úéîÊÇÏ°Ô ñòÊ¥µÈ êÖäûÝÂÝôÕá°ú ë´õá߫Ӹ´Â glucagon÷áæ¨·Î¼ Êõá´ÇÏ´Â ÌËú¾ÀÌ ÀÖ¾úÀ¸³ª îïô÷îÜÀ¸·Î º¸¾Æ êóëòÇÑ °ÍÀº ¾Æ´Ï¿´À¸¸ç Paviov pouchÏØ°ú Heidenhain pouchÏØ°úÀÇ ó¬ì¶´Â º¼ ¼ö ¾ø¾ú´Ù.
Gulcagon÷áæ¨·Î¼ úìÓØÕáÀÌ ñòÊ¥ÇÏ¿´À» ¶§ êÖäûÝÂÝô°¡ Êõá´ÇÏ¿´À¸³ª úìÓØÕá ñòÊ¥¿Í êÖäûÝÂÝôÊõá´´Â ÝïÖÇÇÏÁö ¾Ê¾Ò´ø °ÍÀ¸·Î º¸¾Æ úìÓØÕá ñòÊ¥°¡ êÖäûÝÂÝôåäð¤ÀÇ òÁïÈîÜ é©ì×Àº ¾Æ´Ï¶ó°í ßæÊÆµÇ¸ç Paviov pouchÏØ°ú Heidenhain pouchÏØ »çÀÌ¿¡ ÷åܬÇÑ ó¬ì¶°¡ ¾ø¾úµç ÞÀãùÀº êÖäûÝÂÝôåä𤰡 Ú»ñËãêÌèíÂéÄ¿¡ ÑÃì×ÇÏ´Â °ÍÀÌ ¾Æ´ÔÀ» õÏö´ÄÉ ÇÏ¿´´Ù.
Glucagon÷áæ¨´Â úìôè calciumÒØÓø¿¡ ç¯úÂÀ» ÁÖÁö ¾Ê¾ÒÀ¸¸ç glucagon¿¡ ÀÇÇÑ êÖäûÝÂÝôåäð¤´Â úìôècalciumr°ú μÌõ°¡ ¾ø´Â °ÍÀ¸·Î ßæÊÆµÇ¾ú´Ù.
Glucagon, the hyperglycemic glycogenolytic hormone, has been shown to inhibit the basal secretion, acid output and secretion induced by meals, sham feeding, insulin, gastrin and distention of the pyloric antrum both in man and in the experimental animal. However, the precise mechanism of its inhibitory action on gastric secretion is unclear and the effect on histamine induced gastric secretion is controversial.
In addition, glucagon has been known to decrease the concentration of serum calcium and it might be speculated that lowered serum calcium level plays a role to suppress the gastric secretion.
This experiment was undertaken to observe the effects of glucagon on histamine stimulated gastric secretion and the concentration of serum calcium in the dog.
The experiments were performed on seven denervated Heidenain pouch and six innervated Pavlov pouch dogs.
In one experimental group, glucagon was given continuously intraveneously for an hour after subcutanous injection of histamine twice at 30 minutes interval In the other, same administration of glucagon was done two hours after the initiation of continuous infusion of histamine which was continued for three hours.
Gastric juice was collected for every 30 minutes and the gastric secretory rate and acid output were measured. Blood sugar and serum calcium were determined every half an hour.
The following results were obtained:
1. After the administeration of glucagon, marked hyperglycemia was observed and the gastric secretory rate and acid output were considerably reduced in both Heidenhain and Pavlov pouch dogs, however, there was no parallelism between the increase in blood sugar and the reduction of gastric secretion.
2. No significant difference between innervated and denervated pouch dogs in an inhibitory effect on gastric secretion was noted.
3. The concentration of serum calcium was not changed by glucagon.
4. As a result, it is suggested that hypergloycemia or serum calcium level is not a primary factor and vagal nerve is not involved in an inhibition of gastric secretion which was induced by glucagon.
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