Advances in shock research最新文献

Pharmacologic support in cardiogenic shock. 心源性休克的药物支持。

Advances in shock research Pub Date : 1983-01-01

R E Rude

{"title":"Pharmacologic support in cardiogenic shock.","authors":"R E Rude","doi":"","DOIUrl":"","url":null,"abstract":"Cardiogenic shock is a relatively specific clinical syndrome characterized by decreased cardiac output, elevated left ventricular filling pressure, and arterial hypotension with vital organ hypoperfusion. It most commonly occurs as the consequence of extensive left ventricular damage due to myocardial infarction. The prognosis of patients with cardiogenic shock is very poor, because by definition there are no readily correctable metabolic, hemodynamic, humoral, or infectious problems whose treatment may lead to improved circulatory function. Pharmacologic support of the patient with cardiogenic shock plays a major role in clinical management. Diuretics, inotropic agents, and vasodilator drugs all have a place in the management of selected patients with low output states and cardiogenic shock following myocardial infarction. Diuretics such as furosemide may be used to relieve symptoms of pulmonary congestion, but are not effective in reversing hypotension or vital organ hypoperfusion; in advanced shock states with acute renal failure, they may be totally ineffective. The most commonly employed and effective inotropic agents are the sympathomimetic amines dopamine and dobutamine, which have complex effects on important variables in cardiogenic shock, including the heart's inotropic and chronotropic states, myocardial oxygen requirements, left ventricular filling pressure, and peripheral vascular tone. All inotropic agents have the capacity to intensify myocardial ischemia because they may increase myocardial oxygen requirements in the face of limited arterial blood flow; isoproterenol, epinephrine, and norepinephrine appear to be particularly troublesome in this regard. Vasodilator agents (phentolamine, nitroprusside, and nitroglycerin) have also been used to alter left ventricular loading conditions in patients otherwise supported by inotropic drugs, and may be particularly useful in the management of \"mechanical\" complications of infarction such as mitral regurgitation and interventricular septal rupture. The use of these drugs, just as that of inotropic agents, must be tailored to specific hemodynamic abnormalities documented in individual patients.","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"35-49"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410041","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

Calcium entry blockers: potential applications in shock. 钙进入阻滞剂:在休克中的潜在应用。

Advances in shock research Pub Date : 1983-01-01

M L Hess, L J Greenfield

{"title":"Calcium entry blockers: potential applications in shock.","authors":"M L Hess, L J Greenfield","doi":"","DOIUrl":"","url":null,"abstract":"Failure of the myocardium and vascular smooth muscle to maintain intracellular calcium homeostasis results in intracellular calcium overload leading in turn to cell death and tissue necrosis. This phenomenon can occur in myocardium in response to such diverse etiologies as catecholamine-induced necrosis, prolonged periods of hypoxia, low-flow states, and reperfusion of a previously ischemic vascular bed. Such conditions exist in the shock syndrome with its various etiologies. Cardiogenic shock is associated with primary myocardial failure and a low-flow state. The later stages of septic and endotoxin shock are associated with increasing peripheral vascular resistance and decreasing cardiac output. Experimental and clinical hemorrhagic shock are both associated with prolonged periods of low flow, and then with subsequent transfusion, reperfusion of previously ischemic vascular beds occurs. Therefore, in the shock syndrome, at least the potential for intracellular calcium overload exists. It is the purpose of this communication to discuss the pathophysiologic sequence of the shock syndrome, to illustrate the potential role of intracellular calcium overload in the progression of shock, to present a data base of the use of slow calcium channel blockers in the study of shock, and to suggest a future study of calcium entry blockers as potential therapeutic agents in the shock syndrome.","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"15-25"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410179","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

Proceedings of the Fifth Annual Conference on Shock. Smugglers' Notch, Vermont, June, 1982. Part 2. 第五届休克年会论文集。走私者槽口，佛蒙特州，1982年6月第2部分。

Advances in shock research Pub Date : 1983-01-01

引用次数: 0

The role of endogenous opiates in shock: introductory comments. 内源性阿片类药物在休克中的作用:导论。

Advances in shock research Pub Date : 1983-01-01

J W Holaday, D G Reynolds

引用次数: 0

Role of toxic oxygen products from phagocytic cells in tissue injury. 吞噬细胞有毒氧产物在组织损伤中的作用。

Advances in shock research Pub Date : 1983-01-01

P A Ward

{"title":"Role of toxic oxygen products from phagocytic cells in tissue injury.","authors":"P A Ward","doi":"","DOIUrl":"","url":null,"abstract":"The generation of toxic oxygen products from activated phagocytic cells represents an important pathogenic mechanism in tissue damage associated with inflammatory reactions that are characterized by the involvement of neutrophils or other phagocytic cells. The production of these toxic products from activated phagocytic cells is related to receptor activation on the surface of the cells. Most emphasis has been placed on studies in the lung where the production of these toxic metabolites by phagocytic cells, either in the vasculature or in the airway compartment of the lungs, has been demonstrated to result in endothelial cell injury or damage and destruction of alveolar lining cells. In some cases these reactions are progressive, resulting in parenchymal collapse and fibrosis. Naturally occurring protective factors have been demonstrated both within cells and in the plasma and interstitial fluid compartments. Although there is increasing evidence that in the shock syndrome complement activation products and toxic oxygen metabolites from activated leukocytes play important roles, the most direct evidence for related mechanisms comes in detailed studies of immune complex induced injury where a role for both O-2 and H2O2 has been clearly demonstrated. These facts indicate that toxic oxygen metabolites from activated phagocytic cells play important roles in a variety of pathological situations, and have provided new insights into intervention therapy.","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"10 ","pages":"27-34"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17370339","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

Proceedings of the Fifth Annual Conference on Shock. Smugglers' Notch, Vermont, June, 1982. Part 1. 第五届休克年会论文集。走私者槽口，佛蒙特州，1982年6月第1部分。

Advances in shock research Pub Date : 1983-01-01

引用次数: 0

Peripheral vascular adrenergic depression during hypotension induced by E coli endotoxin. 大肠杆菌内毒素致低血压时外周血管肾上腺素能抑制。

Advances in shock research Pub Date : 1983-01-01

R F Bond

{"title":"Peripheral vascular adrenergic depression during hypotension induced by E coli endotoxin.","authors":"R F Bond","doi":"","DOIUrl":"","url":null,"abstract":"Previous studies support the concept that most vascular beds exhibit some degree of blood flow autoregulation (ie, vasodilation) in response to a fall in local perfusion pressure. However, when systemic pressure is reduced by acute hemorrhage, this vasodilation is converted to vasoconstriction. This response is due to extrinsic influences (ie, elevated adrenergic activity) which overwhelm the intrinsic autoregulatory response. The objective of the present investigation was to compare the regional vascular behavior in selected tissues (ie, skeletal muscle, skin, mesenteric and renal) during local hypotension and systemic hypotension induced by stepwise hemorrhage and endotoxin. Previously published data on local hypotension accomplished by gradual occlusion of the arterial inflow, and systemic hypotension induced by stepwise hemorrhage were compared to systemic hypotension induced by IV administration of 2 mg/kg E coli endotoxin. The pressure/vascular conductance data suggest the following: 1) Skeletal muscle, mesenteric, and renal vasculature respond to local hypotension by autoregulating while skin exhibits passive vasoconstriction; 2) all four vascular beds respond to hemorrhage by intense vasoconstriction; and 3) all four vascular beds respond to endotoxin by vasodilating. The data are compatible with the concept that endotoxin inhibits the extrinsic compensatory vasoconstrictor response to systemic hypotension in all of these vascular beds.","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"9 ","pages":"157-69"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17931683","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

Serum complement levels in canine endotoxin shock: relation to survival and to corticosteroid therapy. 犬内毒素休克的血清补体水平:与生存和皮质类固醇治疗的关系。

Advances in shock research Pub Date : 1983-01-01

C H Shatney, R C Lillehei

{"title":"Serum complement levels in canine endotoxin shock: relation to survival and to corticosteroid therapy.","authors":"C H Shatney, R C Lillehei","doi":"","DOIUrl":"","url":null,"abstract":"Recent studies suggest prominent roles of the complement system in endotoxin shock and steroid-complement interactions in its treatment. To assess further the potential importance of the complement system in this condition, we measured serum total complement levels in dogs after an IV bolus of 1.5 mg/kg DIFCO E coli endotoxin. Dogs were assigned to control (C), dextran40 (LMD), or LMD + steroid groups. Corticosteroids, given IV 15 min after endotoxin, were 1) methylprednisolone sodium succinate (MPSS), 30 mg/kg; 2) dexamethasone sodium phosphate (DSP), 6 mg/kg; 3) hydrocortisone sodium succinate (HSS), 150 mg/kg; or 4) hydrocortisone sodium phosphate (HSP), 150 mg/kg. LMD was infused to maintain BP greater than 60% of preshock levels during the 4 h of monitoring. Survival rates at 48 h were C--7/24 (29%); LMD--3/12 (25%), MPSS--11/19 (59%) (P less than 0.1); DSP--9/14 (64%) (P less than 0.05); HSS--3/10 (30%) HSP--5/10 (50%). Within 15 min of endotoxin administration, serum complement titers fell at least 48% in all groups. Complement levels returned to the preshock range in only the LMD group. Mean complement levels of all survivors and nonsurvivors were nearly identical throughout the acute experiment. The results indicate that survival in canine endotoxin shock, with or without corticosteroid therapy, is not related to normalization of serum total complement titers during the first few hours after endotoxin injection.","PeriodicalId":75453,"journal":{"name":"Advances in shock research","volume":"9 ","pages":"265-74"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17256651","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

Prostaglandin synthetase inhibitors in endotoxin or septic shock--a review. 前列腺素合成酶抑制剂在内毒素或感染性休克中的应用综述。

Advances in shock research Pub Date : 1983-01-01

J R Fletcher

引用次数: 0

Renal hemodynamic alterations following administration of thiopental, diazepam, or ketamine to conscious hypovolemic dogs. 给有意识低血容量的狗服用硫喷妥钠、地西泮或氯胺酮后肾脏血流动力学的改变。

Advances in shock research Pub Date : 1983-01-01

L L Priano

引用次数: 0