Pathophysiological mechanisms of sudden death induced by platelet activating factor
1 Platelet activating factor (Paf) (15–40 μg−1) kills male rabbits within 3 to 5 min. Intravenous injection of Paf at a dose of 15 μg kg−1 is uniformly lethal, and the rabbits died within 4.5 ± 0.4 min. 2 The sudden death is characterized by cessation of respiration, a marked decrease in mean arteri...
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| Veröffentlicht in: | British journal of pharmacology 1984-09, Vol.83 (1), p.125-130 |
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| creator | Lefer, Allan M. Müller, Hugo F. Smith, J. Bryan |
| description | 1
Platelet activating factor (Paf) (15–40 μg−1) kills male rabbits within 3 to 5 min. Intravenous injection of Paf at a dose of 15 μg kg−1 is uniformly lethal, and the rabbits died within 4.5 ± 0.4 min.
2
The sudden death is characterized by cessation of respiration, a marked decrease in mean arterial blood pressure (M.A.B.P.), and 8 fold increases in plasma thromboxane B2 (TxB2) concentrations with only modest elevation in plasma 6 keto‐prostaglandin F1α (6‐keto PGF1α) concentrations.
3
Pretreatment with the cyclo‐oxygenase inhibitor, ibuprofen (6.25 mg kg−1), or with the thromboxane synthetase inhibitors dazoxiben (2.5 mg kg−1), CGS‐13080, or OKY‐046 1 mg kg−1) increased survival rates to 83–100%.
4
Protected rabbits showed only modest changes in M.A.B.P. and no significant increase in plasma TxB2 concentrations. The protective drugs showed a dose‐related action on M.A.B.P., plasma TxB2 concentration and mortality rate in Paf‐induced sudden death.
5
The mechanisms of the protection appeared to be prevention of platelet aggregation (leading to pulmonary thrombosis) and pulmonary and coronary vasoconstriction. However, Paf does not appear to exert direct vasoconstrictor effects in isolated coronary or pulmonary arteries.
6
The effects of Paf in vivo appear to be mediated by TxA2 released by activated platelets in the absence of the protective effects of prostacyclin. Inhibition of thromboxane synthesis effectively prevents the Paf‐induced sudden death. |
| doi_str_mv | 10.1111/j.1476-5381.1984.tb10126.x |
| format | Article |
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Platelet activating factor (Paf) (15–40 μg−1) kills male rabbits within 3 to 5 min. Intravenous injection of Paf at a dose of 15 μg kg−1 is uniformly lethal, and the rabbits died within 4.5 ± 0.4 min.
2
The sudden death is characterized by cessation of respiration, a marked decrease in mean arterial blood pressure (M.A.B.P.), and 8 fold increases in plasma thromboxane B2 (TxB2) concentrations with only modest elevation in plasma 6 keto‐prostaglandin F1α (6‐keto PGF1α) concentrations.
3
Pretreatment with the cyclo‐oxygenase inhibitor, ibuprofen (6.25 mg kg−1), or with the thromboxane synthetase inhibitors dazoxiben (2.5 mg kg−1), CGS‐13080, or OKY‐046 1 mg kg−1) increased survival rates to 83–100%.
4
Protected rabbits showed only modest changes in M.A.B.P. and no significant increase in plasma TxB2 concentrations. The protective drugs showed a dose‐related action on M.A.B.P., plasma TxB2 concentration and mortality rate in Paf‐induced sudden death.
5
The mechanisms of the protection appeared to be prevention of platelet aggregation (leading to pulmonary thrombosis) and pulmonary and coronary vasoconstriction. However, Paf does not appear to exert direct vasoconstrictor effects in isolated coronary or pulmonary arteries.
6
The effects of Paf in vivo appear to be mediated by TxA2 released by activated platelets in the absence of the protective effects of prostacyclin. Inhibition of thromboxane synthesis effectively prevents the Paf‐induced sudden death.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.1984.tb10126.x</identifier><identifier>PMID: 6435705</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Blood Pressure - drug effects ; Cyclooxygenase Inhibitors ; Death, Sudden - etiology ; In Vitro Techniques ; Male ; Muscle, Smooth - drug effects ; Muscle, Smooth, Vascular - drug effects ; Platelet Activating Factor - antagonists & inhibitors ; Platelet Activating Factor - toxicity ; Pulmonary Artery - drug effects ; Rabbits ; Respiration - drug effects ; Thromboxane B2 - blood ; Thromboxane-A Synthase - antagonists & inhibitors</subject><ispartof>British journal of pharmacology, 1984-09, Vol.83 (1), p.125-130</ispartof><rights>1984 British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5096-d013b18a9eca61ad934a125aa60361465b2ce1bb7a92cbb945bfa6a10c8f4a833</citedby><cites>FETCH-LOGICAL-c5096-d013b18a9eca61ad934a125aa60361465b2ce1bb7a92cbb945bfa6a10c8f4a833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1987182/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1987182/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6435705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lefer, Allan M.</creatorcontrib><creatorcontrib>Müller, Hugo F.</creatorcontrib><creatorcontrib>Smith, J. Bryan</creatorcontrib><title>Pathophysiological mechanisms of sudden death induced by platelet activating factor</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
Platelet activating factor (Paf) (15–40 μg−1) kills male rabbits within 3 to 5 min. Intravenous injection of Paf at a dose of 15 μg kg−1 is uniformly lethal, and the rabbits died within 4.5 ± 0.4 min.
2
The sudden death is characterized by cessation of respiration, a marked decrease in mean arterial blood pressure (M.A.B.P.), and 8 fold increases in plasma thromboxane B2 (TxB2) concentrations with only modest elevation in plasma 6 keto‐prostaglandin F1α (6‐keto PGF1α) concentrations.
3
Pretreatment with the cyclo‐oxygenase inhibitor, ibuprofen (6.25 mg kg−1), or with the thromboxane synthetase inhibitors dazoxiben (2.5 mg kg−1), CGS‐13080, or OKY‐046 1 mg kg−1) increased survival rates to 83–100%.
4
Protected rabbits showed only modest changes in M.A.B.P. and no significant increase in plasma TxB2 concentrations. The protective drugs showed a dose‐related action on M.A.B.P., plasma TxB2 concentration and mortality rate in Paf‐induced sudden death.
5
The mechanisms of the protection appeared to be prevention of platelet aggregation (leading to pulmonary thrombosis) and pulmonary and coronary vasoconstriction. However, Paf does not appear to exert direct vasoconstrictor effects in isolated coronary or pulmonary arteries.
6
The effects of Paf in vivo appear to be mediated by TxA2 released by activated platelets in the absence of the protective effects of prostacyclin. Inhibition of thromboxane synthesis effectively prevents the Paf‐induced sudden death.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Blood Pressure - drug effects</subject><subject>Cyclooxygenase Inhibitors</subject><subject>Death, Sudden - etiology</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Muscle, Smooth - drug effects</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Platelet Activating Factor - antagonists & inhibitors</subject><subject>Platelet Activating Factor - toxicity</subject><subject>Pulmonary Artery - drug effects</subject><subject>Rabbits</subject><subject>Respiration - drug effects</subject><subject>Thromboxane B2 - blood</subject><subject>Thromboxane-A Synthase - antagonists & inhibitors</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkVGL1DAUhYMo67j6E4Tgg2-tuU2apj6I66KusOCC-hxu0nQmQ9qMTbvu_HszzjDoo3nJhXPul3AOIa-AlZDPm20JopFFzRWU0CpRzgYYVLJ8eERWZ-kxWTHGmgJAqafkWUpbxrLY1BfkQgpeN6xekW93OG_ibrNPPoa49hYDHZzd4OjTkGjsaVq6zo20c9lI_dgt1nXU7Oku4OyCmyna2d_j7Mc17fMcp-fkSY8huRen-5L8-PTx-_VNcfv185frq9vC1qyVRceAG1DYOosSsGu5QKhqRMm4BCFrU1kHxjTYVtaYVtSmR4nArOoFKs4vybsjd7eYwXXWjfOEQe8mP-C01xG9_lcZ_Uav473OmTWgqgx4fQJM8efi0qwHn6wLAUcXl6RBABeqhWx8ezTaKaY0uf78CDB9qERv9SF3fcj9gBf6VIl-yMsv__7mefXUQdbfH_VfPrj9f5D1h7ubPyP_Da7nnzQ</recordid><startdate>198409</startdate><enddate>198409</enddate><creator>Lefer, Allan M.</creator><creator>Müller, Hugo F.</creator><creator>Smith, J. Bryan</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>5PM</scope></search><sort><creationdate>198409</creationdate><title>Pathophysiological mechanisms of sudden death induced by platelet activating factor</title><author>Lefer, Allan M. ; Müller, Hugo F. ; Smith, J. Bryan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5096-d013b18a9eca61ad934a125aa60361465b2ce1bb7a92cbb945bfa6a10c8f4a833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Blood Pressure - drug effects</topic><topic>Cyclooxygenase Inhibitors</topic><topic>Death, Sudden - etiology</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Muscle, Smooth - drug effects</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Platelet Activating Factor - antagonists & inhibitors</topic><topic>Platelet Activating Factor - toxicity</topic><topic>Pulmonary Artery - drug effects</topic><topic>Rabbits</topic><topic>Respiration - drug effects</topic><topic>Thromboxane B2 - blood</topic><topic>Thromboxane-A Synthase - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lefer, Allan M.</creatorcontrib><creatorcontrib>Müller, Hugo F.</creatorcontrib><creatorcontrib>Smith, J. Bryan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lefer, Allan M.</au><au>Müller, Hugo F.</au><au>Smith, J. Bryan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathophysiological mechanisms of sudden death induced by platelet activating factor</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1984-09</date><risdate>1984</risdate><volume>83</volume><issue>1</issue><spage>125</spage><epage>130</epage><pages>125-130</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>1
Platelet activating factor (Paf) (15–40 μg−1) kills male rabbits within 3 to 5 min. Intravenous injection of Paf at a dose of 15 μg kg−1 is uniformly lethal, and the rabbits died within 4.5 ± 0.4 min.
2
The sudden death is characterized by cessation of respiration, a marked decrease in mean arterial blood pressure (M.A.B.P.), and 8 fold increases in plasma thromboxane B2 (TxB2) concentrations with only modest elevation in plasma 6 keto‐prostaglandin F1α (6‐keto PGF1α) concentrations.
3
Pretreatment with the cyclo‐oxygenase inhibitor, ibuprofen (6.25 mg kg−1), or with the thromboxane synthetase inhibitors dazoxiben (2.5 mg kg−1), CGS‐13080, or OKY‐046 1 mg kg−1) increased survival rates to 83–100%.
4
Protected rabbits showed only modest changes in M.A.B.P. and no significant increase in plasma TxB2 concentrations. The protective drugs showed a dose‐related action on M.A.B.P., plasma TxB2 concentration and mortality rate in Paf‐induced sudden death.
5
The mechanisms of the protection appeared to be prevention of platelet aggregation (leading to pulmonary thrombosis) and pulmonary and coronary vasoconstriction. However, Paf does not appear to exert direct vasoconstrictor effects in isolated coronary or pulmonary arteries.
6
The effects of Paf in vivo appear to be mediated by TxA2 released by activated platelets in the absence of the protective effects of prostacyclin. Inhibition of thromboxane synthesis effectively prevents the Paf‐induced sudden death.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>6435705</pmid><doi>10.1111/j.1476-5381.1984.tb10126.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Blood Pressure - drug effects Cyclooxygenase Inhibitors Death, Sudden - etiology In Vitro Techniques Male Muscle, Smooth - drug effects Muscle, Smooth, Vascular - drug effects Platelet Activating Factor - antagonists & inhibitors Platelet Activating Factor - toxicity Pulmonary Artery - drug effects Rabbits Respiration - drug effects Thromboxane B2 - blood Thromboxane-A Synthase - antagonists & inhibitors |
| title | Pathophysiological mechanisms of sudden death induced by platelet activating factor |
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