<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Physiology and Pharmacology</title>
<title_fa></title_fa>
<short_title>Physiol Pharmacol</short_title>
<subject>Medical Sciences</subject>
<web_url>http://ppj.phypha.ir</web_url>
<journal_hbi_system_id>32</journal_hbi_system_id>
<journal_hbi_system_user>journal32</journal_hbi_system_user>
<journal_id_issn>24765236</journal_id_issn>
<journal_id_issn_online>24765244</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi>10.61882/phypha</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid>(previous ISSN: 17350581)</journal_id_sid>
<journal_id_nlai></journal_id_nlai>
<journal_id_science></journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1380</year>
	<month>1</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2001</year>
	<month>4</month>
	<day>1</day>
</pubdate>
<volume>5</volume>
<number>1</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa>بررسی اثر D - گلوکز داخل معدی بر هایپراسیدیتی ناشی از هیستامین و کرباکول در موش صحرایی نر</title_fa>
	<title>The effect of intragastric D-glucose on hyperacidity induced by histamine and carbachol in male rat</title>
	<subject_fa>Nervous system (others)</subject_fa>
	<subject>Others</subject>
	<content_type_fa>Experimental research article</content_type_fa>
	<content_type>Experimental research article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>It has been shown that enhanced acid secretion can be suppressed in the rat by systemic administration of glucose. We have recently reported that enhancement of acid secretion as a result of pentagastrin was diminished by intragastric administration of D-glucose. Present study was designed to investigate whether intragastric D-glucose influences gastric acid secretion associated with carbachol and histamine in rat, and then we compared these results with our previous results obtained by pentagastrin-induced hyperacidity. Intravenous infusion of carbachol (1 mg/100 g/h) and histamine (0.5 mg/100 g/h) caused an immediate increase in acid secretion with a peak starting after 40 and 60 min and then reached to a steady state respectively. 1ntragastric administration of D-glucose significantly reduced the hyperacidity induced by histamine and carbachol (p&lt;0.01). The effect of intragastric D-glucose on hyperacidity induced by pentagastrin or histamine when compared with carbachol-induced hyperacidity was significantly greater than carbachol group. In conclusion, it is suggested that the inhibitory effect of intragastric D-g1ucose observed in hyperacidity may be the result of glucose-induced modification of intragastric pathways in parietal cells that control gastric acid secretion. </abstract>
	<keyword_fa></keyword_fa>
	<keyword>lntragastric D-glucose; Carbachol; Histamine; Gastric acid</keyword>
	<start_page>35</start_page>
	<end_page>41</end_page>
	<web_url>http://ppj.phypha.ir/browse.php?a_code=A-10-123-2&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
</author_list>


	</article>
</articleset>
</journal>
