Advances in shock research最新文献

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Hematologic disturbances during sepsis: platelets and leukocytes. 败血症期间的血液学紊乱:血小板和白细胞。
Advances in shock research Pub Date : 1982-01-01
L B Hinshaw, L T Archer, B K Beller-Todd
{"title":"Hematologic disturbances during sepsis: platelets and leukocytes.","authors":"L B Hinshaw,&nbsp;L T Archer,&nbsp;B K Beller-Todd","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This brief review summarizes recent observations about leukocyte and platelet involvements during sepsis and septic shock. Endotoxins are known to exert significant effects on leukocytes and platelets as well as monocytes, macrophages, endothelial, and mast cells. The presence of endotoxin itself is reported to enhance the phagocytic and killing capacity of neutrophils. Transfusion of additional white blood cells has been shown to increase the probability of recovery from sepsis. Defects in neutrophil function, impaired opsonization, sequestration of neutrophils in pulmonary capillaries, and depressed metabolic states adversely affecting neutrophils may significantly contribute to the lethal outcome of septic shock. Platelet responses in septic shock are reported to include aggregation accompanied by release of several agents, including vasoactive amines, ADP, and platelet factor 3. In summary, leukocytes and platelets are known to perform significant roles in sepsis and septic shock although the precise mechanisms of their involvement remain to be clearly defined.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Thromboxane and prostacyclin production during septic shock. 感染性休克时血栓素和前列环素的产生。
Advances in shock research Pub Date : 1982-01-01
R R Butler, W C Wise, P V Halushka, J A Cook
{"title":"Thromboxane and prostacyclin production during septic shock.","authors":"R R Butler,&nbsp;W C Wise,&nbsp;P V Halushka,&nbsp;J A Cook","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We investigated a rat fecal peritonitis model of acute intraabdominal sepsis in order to evaluate the potential role of arachidonic acid metabolites in septic shock. Immunoreactive TxB2, the stable metabolite of thromboxane A2, and i6-keto-PGF1 alpha, the stable metabolite of prostacyclin, were measured by radioimmunoassay. Plasma levels of iTxB2 rapidly increased from nondetectable (ND less than 200 pg/ml) to 1,052 +/- 208 pg/ml, one hour after feces injection. iTxB2 then increased to 1,681 +/- 248 pg/ml at four hours and remained unchanged through six hours. Plasma i6-keto-PGF1 alpha increased from ND to 3,848 +/- 489 pg/ml a one hour. Four hours after feces, i6-keto-PGF1 alpha levels rose to 7, 450 +/- 933 pg/ml then continued to rise to 9,465 +/- 792 pg/ml at six hours. Either essential fatty acid deficiency (arachidonic acid depletion) or indomethacin treatment (cyclo-oxygenase inhibition) significantly decreased (P less than 0.01) the elevation of plasma iTxB2 and i6-keto-PGF1 alpha associated with fecal peritonitis. Thrombocytopenia occurred within six hours after injection of feces and was significantly improved (P less than 0.05) by indomethacin. Elevated fibrin degradation products at six hours (18 +/- 3 micrograms/ml) were significantly reduced in essential fatty acid-deficient (7 +/- 2 micrograms/ml; P less than 0.05) and indomethacin-treated (4 +/- 0.7 micrograms/ml; P less than 0.01) rats. Survival time (8.6 +/- 0.2 hours) was significantly enhanced by essential fatty acid-deficiency (10.2 +/- 0.4 hours; P less than 0.01) or indomethacin treatment (13.3 +/- 0.6 hours; P less than 0.01). These studies show that fecal peritonitis is associated with increased synthesis of thromboxane A2 and prostacyclin and suggest that these arachidonic acid metabolites may play a role in the pathophysiology of septic shock.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"133-45"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17806625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Thoracic duct lymph flow after pancreatitis: role in circulatory collapse. 胰腺炎后胸导管淋巴流动:在循环衰竭中的作用。
Advances in shock research Pub Date : 1982-01-01
A B Malik, R J Mullins, P S Barie, D R Bell, B C Lee
{"title":"Thoracic duct lymph flow after pancreatitis: role in circulatory collapse.","authors":"A B Malik,&nbsp;R J Mullins,&nbsp;P S Barie,&nbsp;D R Bell,&nbsp;B C Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We examined the effects of acute hemorrhagic pancreatitis on thoracic duct lymph flow and its protein concentration. Thoracic duct lymph flow increased and the protein concentration decreased. These changes in the lymph were associated with steady decreases in arterial pressure and cardiac output and increase in systemic vascular resistance. The results suggest that the increased lymph flow and decreased protein concentration were due to either an ultrafiltration causing a dilution of the lymph protein concentration or to the heterogeneous origin of thoracic duct lymph such that redistribution of blood flow to the essential beds (eg, kidneys) after arterial hypotension altered the lymph flow and its protein concentration. The increase in filtration and the absence of a compensatory \"autotransfusion\" during arterial hypotension may be a mechanism contributing to circulatory shock in acute pancreatitis.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"81-9"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
An evaluation of the functional implications of the intestinal mucosal lesions in shock. 休克后肠黏膜病变的功能意义评价。
Advances in shock research Pub Date : 1982-01-01
U Haglund, A Falk, E Haglind, H E Myrvold, O Lundgren
{"title":"An evaluation of the functional implications of the intestinal mucosal lesions in shock.","authors":"U Haglund,&nbsp;A Falk,&nbsp;E Haglind,&nbsp;H E Myrvold,&nbsp;O Lundgren","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Small intestinal mucosal lesions are reported in clinical shock and are commonly found in experimental shock. Experimental series in which shock is induced by regional intestinal ischemia or IV infusion of live Escherichia coli in cats or by graded intestinal vascular occlusion in rats are described. In all series mucosal damage was related to pronounced hypotension or mortality. In the cat models myocardial dysfunction was demonstrated in vivo by IV volume load and recording of changes in left ventricular filling pressure as related to cardiac performance. Following intestinal ischemia in cats and intestinal vascular obstruction in rats the intestinal venous plasma was found to contain cardiotoxic factors when tested in vitro. It is proposed that the development of small intestinal mucosa lesions in shock tends to further aggravate hypotension by causing intestinal release of cardioinhibitory material.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"91-7"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sequestration of fibronectin at the site of an injury. 纤维连接蛋白在损伤部位的隔离。
Advances in shock research Pub Date : 1982-01-01
A C Reese, J E Doran, B D Callaway, A R Mansberger
{"title":"Sequestration of fibronectin at the site of an injury.","authors":"A C Reese,&nbsp;J E Doran,&nbsp;B D Callaway,&nbsp;A R Mansberger","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Fibronectin (Fn), a normal serum protein which appears to have important roles in wound healing and in reticuloendothelial system function, is depressed by most types of trauma. Fn is released into the tissue at the site of an injury which suggests the depression is the result of Fn sequestration at the wound site. A competitive inhibition assay for Fn was used to measure the concentration of Fn in fluid draining the site of a radical mastectomy and the level in concurrently obtained plasma. Plasma levels of Fn were significantly depressed following surgery but were returning toward normal by 24 hours postsurgery. The concentration of Fn in drainage fluid collected two hours postop was slightly but significantly lower than the plasma collected simultaneously. By 8 hours after surgery, drainage fluid levels were significantly higher than that in concurrently obtained plasma, and the difference was even more pronounced at 24 hours postop. Fn in the drainage fluid retained opsonic activity but at a lower level than the opsonic activity in plasma. The higher concentration of Fn in drainage fluid than in plasma appears to be due to binding of the Fn to tissue debris in the exudate, which prevents the reentry of Fn into the vascular compartment.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"119-27"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Importance of hypoxic pulmonary vasoconstriction with atelectasis. 缺氧肺血管收缩伴肺不张的重要性。
Advances in shock research Pub Date : 1982-01-01
B E Marshall
{"title":"Importance of hypoxic pulmonary vasoconstriction with atelectasis.","authors":"B E Marshall","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This survey summarizes information on various factors that determine responses to hypoxic pulmonary vasoconstriction. The emphasis is on the clinical relevance of these responses for atelectasis. Flow diversion reduces the functional effect of lung collapse by redistributing the pulmonary blood flow so as to promote restoration of arterial oxygen tension. The factors shown to influence the outcome include size of the atelectactic segment, mixed venous oxygen tension, intrapleural and intraalveolar pressure (transpulmonary pressure), cardiac output, and pulmonary transmural vascular pressure.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Reduced ambient temperature blocks the ability of naloxone to prevent endotoxin-induced hypotension. 降低的环境温度阻断了纳洛酮预防内毒素诱导的低血压的能力。
Advances in shock research Pub Date : 1982-01-01
H F Janssen, J L Pugh, L O Lutherer
{"title":"Reduced ambient temperature blocks the ability of naloxone to prevent endotoxin-induced hypotension.","authors":"H F Janssen,&nbsp;J L Pugh,&nbsp;L O Lutherer","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"117-24"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17353371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Studies on the effects of vasodilating agents in addition to volume therapy in endotoxic shock. 血管舒张剂与容量治疗在内源性休克中的作用研究。
Advances in shock research Pub Date : 1982-01-01
F W Schmahl, B Urbaschek, G Richardt, K Knorpp, M Frank, K Drysch, H Heckers
{"title":"Studies on the effects of vasodilating agents in addition to volume therapy in endotoxic shock.","authors":"F W Schmahl,&nbsp;B Urbaschek,&nbsp;G Richardt,&nbsp;K Knorpp,&nbsp;M Frank,&nbsp;K Drysch,&nbsp;H Heckers","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"7 ","pages":"179-84"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17247846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Exogenous amino acids as fuel in shock. 外源性氨基酸作为休克的燃料。
Advances in shock research Pub Date : 1982-01-01
A M Daniel, B Kapadia, L D MacLean
{"title":"Exogenous amino acids as fuel in shock.","authors":"A M Daniel,&nbsp;B Kapadia,&nbsp;L D MacLean","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It has been suggested that in shock branched-chain amino acids are preferentially oxidized resulting in continued proteolysis and stimulated gluconeogenesis. To determine if exogenous amino acids could be used as fuel in shock, dogs rendered hypotensive by controlled cardiac tamponade and normotensive controls were infused with amino acid mixtures and individual amino acids. When Nephramine, a mixture rich in branched-chain amino acids, was infused, plasma alpha-amino nitrogen levels rose but urea output did not increase in either the control state or in shock, suggesting that these amino acids were not rapidly deaminated to serve as fuels. Travasol, which in addition contained large amounts of alanine and glycine, tripled urea output in the controls and doubled it in shock. The limit of urea production was reached in both groups at 35 mumoles urea/minute/kg. In the Travasol-infused animals plasma alpha-amino nitrogen levels were maintained in normotension but rose sharply in shock. When glycine alone was infused into five dogs in shock urea production rate was 30.6 + 2.1 mumoles/minute/kg; with alanine the same value was 22.5 + 2.2 mumoles/minute/kg. In both cases plasma alpha-amino nitrogen levels were high, suggesting that transport of these amino acids into the cell was slow in shock. In four dogs in shock glycine-14C was added to the glycine infusate as a tracer. At radioactive equilibrium 28% of the label infused appeared in CO2; another 22% appeared in glucose. It is concluded that of all the amino acids tested only glycine and alanine are deaminated rapidly enough to serve as exogenous fuels in shock.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"163-70"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17866234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Arteriolar to venular red cell and plasma dispersion in hemorrhage- and endotoxin-shocked cats. 出血和内毒素休克猫的动脉到静脉红细胞和血浆分散。
Advances in shock research Pub Date : 1982-01-01
C H Baker
{"title":"Arteriolar to venular red cell and plasma dispersion in hemorrhage- and endotoxin-shocked cats.","authors":"C H Baker","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The passage of red cells is more rapid than for plasma through the microcirculation of most tissues. The effects of hemorrhage (13 ml/kg) and endotoxin (3 mg/kg) on this phenomenon were studied in the exposed mesentery of cats anesthetized with Dial-urethane using epi-illumination fluorescence or transillumination television microscopy. Femoral artery pressure, arteriolar pressure, and arteriolar and venular diameters were measured. FITC-dextran, the plasma label, and DTAF-labeled red cells (DTAF-RBCs) or sulphemoglobin-labeled RBCs (SH-RBCs) were injected as a bolus (0.005 ml in 0.5 seconds) into a small branch of the mesenteric artery at control and after the experimental procedure. Animals were hemorrhaged from the left femoral artery (13 ml/kg) or injected IV with endotoxin. Time-concentration curves were recorded from video tape recordings of the passage of the indicator by videodensitometry for determination of the mean transit times (t). During hemorrhage and endotoxin the arterial pressure decreased significantly as did the arteriolar flow velocity. Following hemorrhage arteriolar and venular diameters and arteriolar pressures decreased significantly. Postendotoxin, arteriolar and venular diameters increased and arteriolar pressures did not decrease significantly. During control the t of labeled red cells was exceeded significantly by those of FITC-dextran in all microvascular segments. Following hemorrhage the t of the two indicators were increased significantly but were not significantly different in the arterioles. However, they were different in the venules. One hour after endotoxin t was significantly increased in all segments and further increased at three hours. However, the labeled red cell values were still exceeded by the FITC-dextran values at both times. It would appear that the differences in t would be abolished by vasoconstriction reducing axial streaming and plasma skimming whereas vasodilation does not change these phenomena.</p>","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"8 ","pages":"35-51"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18152648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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