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At least 19 recordsLinked to original sources

PubMed1985

A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.

We have previously described a subpopulation of patients with septic shock who had a reversible depression of radionuclide-determined left ventricular ejection fraction (EF). To investigate the mechanism of this myocardial depression, an in vitro model of mammalian myocardial cell performance was established employing primary spontaneously beating rat myocardial cells. The contraction of a single cardiac cell was quantitated by recording the changes in area occupied by the cell during contraction and relaxation. In 20 septic shock patients during the acute phase, the mean left ventricular EF was decreased (mean = 0.33, normal mean = 0.50), and serum obtained during this acute phase induced a mean (+/- standard error of the mean) 33 +/- 4% decrease in extent and 25 +/- 4% decrease in velocity of myocardial cell shortening during contraction (P less than 0.001). In contrast, serum obtained from 11 of these same patients before shock (n = 2) or after recovery (n = 9) of the left ventricular EF (mean = 0.50) showed a return toward normal in extent and velocity of shortening (P less than 0.001). Sera from 17 critically ill nonseptic patients, from 10 patients with structural heart disease as a cause for a depressed EF, and from 12 healthy laboratory personnel, induced no significant changes in in vitro myocardial cell performance. In 20 patients during the acute phase of septic shock, the decreased EF in vivo demonstrated a significant correlation (r = +0.52, P less than 0.01) with a decrease in the extent of myocardial cell shortening in vitro. The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substance in producing the reversible cardiomyopathy seen during septic shock in humans.

Adolescent↗

PubMed2003

Septic shock.

Septic shock remains an important cause of death and serious morbidity in medical, surgical and obstetric illness. Many patients with septic shock succumb despite aggressive therapy. Any microorganism can initiate septic shock; the pathophysiology of the disease is not clear; the clinical manifestation is not specific; and there is no reliable laboratory result to diagnose septic shock before it is late. Moreover, despite increasingly complex modes of mechanical ventilation, sophisticated respiratory and hemodynamic monitoring, and a continually expanding array of potent antibiotics, the overall mortality from septic shock remained constant. Better outcome is more likely when recognition is early and treatment is much more aggressive. Therefore, where there is suspicion of septic shock: commence fluid resuscitation, administer oxygen, take blood, urine, and other fluids for culture, commence intravenous broad-spectrum antibiotics, pass a urethral catheter, determine the cause of sepsis and remove if possible, consult for expert medical advice and possible patient transfer to intensive care units, and provide supportive care to involved organ systems.

Anti-Bacterial Agents↗

PubMed2001

Replacement therapy with hydrocortisone in catecholamine-dependent septic shock.

Septic shock is one of the leading causes of death in intensive care units world-wide. Scientists have made great improvements in understanding mechanisms of inflammation, and the sequence of activation of the various pro- and anti-inflammatory markers is now well known. In contrast, physicians have failed to improve survival from septic shock despite the development of specific targets at various points in the cytokine cascade considered to have a key role in host survival in sepsis. Corticosteroids were among the first anti-inflammatory drugs to be tested in large randomized controlled trials. These trials showed that patients with septic shock did not benefit from a short course of large doses of steroids. More recent findings highlighting the role of the integrity of the hypothalamic-pituitary-adrenal axis to respond appropriately to a septic insult, have led to a re-appraisal of the use of steroids in septic shock. Several randomized controlled trials have evaluated the efficacy of a replacement therapy with hydrocortisone in severe sepsis. These trials strongly suggest that this replacement therapy reduces the morbidity of septic shock and may favorably affect survival from septic shock.

Animals↗

PubMed2006

Effects of verapamil and nifedipine on different parameters in lipopolysaccharide-induced septic shock.

Septic shock has a high mortality rate due to the hypotension and circulatory disorder that occurs during its pathogenesis. Recently, humoral factors such as cytokines and nitric oxide became important in the complex pathophysiology of septic shock because there is a close relationship between the determined levels of these humoral factors and the responses to the therapy and survival periods. Verapamil and nifedipine are calcium channel blockers commonly used in the pharmacotherapy of cardiovascular disorders. In the present study these drugs were investigated in the rat septic shock model. In vivo hemodynamic parameters were recorded using a data acquisition system in endotoxin-induced septic shock in rats. The animals were followed for 5 h and blood pressure, rectal temperature, and ECG were recorded. Blood samples were collected at 1 h and 5 h time points after the injection of endotoxin, and serological samples were stored at -25 degrees C. Subsequently, tumor necrosis factor-alpha, interleukin-10 (enzyme-linked immunosorbent assay), and nitrite (Griess reagent) were determined in these serological samples. Significant correlations were observed between these humoral factors and the disordered hemodynamic factors. A reversal of changes was observed in the levels of serum cytokines, nitrite levels, and hemodynamic parameters with verapamil and nifedipine preadministration (P<0.05). Additionally, superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) were determined in livers obtained from these animals at the end of the experiments, and these results were compared to hemodynamic parameters and cytokines. Nifedipine and verapamil increased the levels of MDA and SOD but did not change catalase activity.

Animals↗

PubMed2001

[Septic shock].

Septic shock is the most severe systemic inflammatory response to infection. Despite recent progress in prevention and critical care therapy, this syndrome is the most common cause of death in intensive care units. Major advances have been realized recently in the understanding of septic shock. Cellular receptors involved in bacterial recognition have been identified as Toll-like receptors. After bacterial challenge, these receptors become activated and initiate in septic shock patients a biphasic immunological response associated with coagulation disorders. Genetic variability among humans and their predisposition towards pathologic inflammatory responses have also been demonstrated. These current views on the pathophysiological aspects of septic shock open new therapeutic perspectives which should change the prognosis of this syndrome.

Bacterial Infections↗

PubMed1992

Systemic hemodynamic abnormalities and vasopressor therapy in sepsis and septic shock.

Septic shock, a distributive form of shock, is a common and lethal disease characterized by tachycardia, hypotension, normal or elevated cardiac index, and decreased systemic vascular resistance (SVR). For 2 to 4 days after onset of shock, the left ventricular ejection fraction (LVEF) is depressed; with adequate volume replacement, the left ventricle dilates and cardiac output (CO) is maintained or increased. In survivors, these abnormalities reverse to normal within 7 to 10 days. The myocardial depression found in patients with septic shock is not associated with global myocardial ischemia. In our animal model of sepsis, myocardial depression is not associated with impaired myocardial high-energy stores, or abnormal myocardial oxygen utilization. However, septic animals have histopathologic evidence of coronary nonocclusive microvascular damage and myocyte injury. The majority of human deaths caused by septic shock are related to the peripheral vascular dysfunction and multiorgan system failure that occurs over time. The pathophysiology of this disease is complex. Clinical and experimental evidence support the notion that myocardial depression, peripheral vascular abnormalities, and multiorgan dysfunction result from the combined effect of exogenous and endogenous mediators (eg, endotoxin, cytokines, and nitric oxide) released during septic shock. Although conventional therapy with fluids, vasopressors, and antibiotics is effective, the disease still has a high mortality rate. Studies investigating the effects of bacterial toxins and potentially harmful host mediators offer the greatest hope in finding new ways to eradicate this highly lethal disease.

Animals↗

PubMed1997

A comparison of the peritoneal cell population of pregnant rabbits after LPS or TNF-alpha induced septic shock.

Septic shock is a catastrophic consequence of invasive infection. Unfortunately, recent advances in surgical and medical sciences have not significantly reduced the overall mortality from septic shock. Bacterial antigens stimulate a cascade of cytokine release; each cytokine helps the host to overcome infection, but their excessive production causes them to trigger events that lead to septic syndrome and shock. Tumour necrosis factor (TNF-alpha) has a pivotal role in orchestrating the events leading to septic shock. Intraperitoneal administration of certain substances can increase the number and phagocytic activity of cells, which reach naturally the site of infection. Activation of the immunity cells in the peritoneal cavity and their immunocompetence are found to be responsible for the organism protection against abdominal cavity infections. Macrophages, lymphocytes and granulocytes of low activity in the non-stimulated peritoneal cavity become significant due to the influence of numerous biologically active substances. This study was designed to determine the peritoneal response to local administration of LPS or TNF-alpha in the course of experimental septic shock.

Animals↗

PubMed1989

The pharmacotherapy of septic shock.

Septic shock is a common clinical problem in the intensive care setting. The high mortality rate associated with septic shock, regardless of age, reflects the inadequacy of available therapeutic approaches. The purpose of this article is to review the current pharmacologic approaches to the treatment of septic shock with an emphasis on the pathophysiologic correlations of these treatments.

Adrenergic Agonists↗

PubMed1990

Antibiotic therapy in septic shock.

Septic shock is a life-threatening illness characterized by hypotension, impaired organ function and/or failure, and metabolic abnormalities. Septic shock can develop in patients infected with a variety of gram-positive and gram-negative bacteria, viruses, fungi, rickettsiae, spirochetes, protozoa, and parasites. Immediate recognition, diagnosis, and treatment are key elements in reducing the morbidity and mortality associated with this condition. Rapid administration of appropriate antibiotics in correct doses plays a major role in patient survival. Infections with gram-negative bacteria appear to be associated with septic shock more than any other etiologic agent; therefore, antibiotic selection must include those drugs with superior gram-negative coverage. The selection of appropriate antibiotics should be based on sound clinical judgement plus knowledge of the antimicrobials used. The principles of rational therapy include the following: (1) know the type of microorganisms or suspected organism being treated; (2) be familiar with resistant organisms in both the community as well as the hospital; and (3) initiate combination therapy with a beta-lactam antibiotic plus an aminoglycoside or use monotherapy with either a carbapenem or selected third generation cephalosporin. After culture results are known, the antibiotic regimen should be narrowed to cover the specific infecting microorganism using the least expensive, least toxic antibiotic available. The beta-lactam antibiotics include all penicillins, cephalosporins, carbapenems, and monobactams. Penicillins with extensive gram-negative coverage include all the carboxy (carbenicillin, ticarcillin, and ticarcillin plus clavulanic acid) and ureido (piperacillin, mezlocillin, azlocillin) penicillins. The third generation cephalosporins (cefoperazone, cefotaxime, ceftazidime, ceftizoxime, ceftriaxone, and moxalactam) have the broadest gram-negative coverage within the cephalosporin family.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗

PubMed1993

Platelet-activating factor in septic shock.

Septic shock induced by endotoxins of Gram-negative bacteria, or toxins of Gram-positive bacteria and fungi, deserves particular interest because of its high mortality rate. In experimental animals, treatment with bacterial lipopolysaccharide (endotoxin of Gram-negative bacteria) mimics the symptoms of septic shock. Thus, this treatment has become an important method in animal models of septic shock. Endotoxin induces release of platelet-activating factor and cytokines, such as tumor necrosis factor and interleukins. Platelet-activating factor derived from macrophages, polymorphonuclear leukocytes, and platelets is a potent phospholipid inflammatory mediator that increases cell adhesion and activates endothelial cells by direct effect or through formation of toxic oxygen species and arachidonic acid metabolites, such as thromboxane A2 and leukotriene B4. Platelet-activating factor interacts with cytokines, and this interaction leads to an autocatalytic amplification of inflammatory mediator release. The release of inflammatory mediators by interaction of platelet-activating factor with cytokines is characterized by bell-shaped concentration-effect curves. For example, in a certain concentration range, platelet-activating factor or cytokines induce a mediator release that is proportional to the stimulation. However, over-stimulation may lead to a decrease of mediator release or a prevalence of the release of a single mediator. Down-regulatory processes may be brought about by platelet-activating factor-induced prostacyclin or adenosine release that activates adenylate cyclase and increases intracellular cyclic adenosine 3'5'-monophosphate concentrations. Down-regulation may protect inflammatory and endothelial cells from overstimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Implication of Toll-like receptor and tumor necrosis factor alpha signaling in septic shock.

Septic shock is initiated by a systemic inflammatory response to microbial infection that frequently leads to impaired perfusion and multiple organ failure. Because of its high risk of death, septic shock is a major problem particularly for patients in the intensive care unit. In general, bacterial lipopolysaccharide (LPS) is a strong activator of various immune responses and stimulates monocytes/macrophages to release a variety of inflammatory cytokines. However, overproduction of inflammatory factors in response to bacterial infections is known to cause septic shock, similar to that induced by LPS. Studies of LPS-signaling pathways and downstream inflammatory cytokines may have critical implications in the treatment of sepsis. In recent years, there has been significant progress in understanding the signaling pathways activated by LPS and its receptor Toll-like receptor 4 (TLR4), as well as by tumor necrosis factor alpha (TNFalpha), a potent inflammatory cytokine induced by LPS stimulation. This review briefly summarizes our current knowledge of these signaling pathways and critical signal transducers. Characterization of key signal transducers may allow us to identify tractable, novel targets for the therapeutic interventions of sepsis.

Adaptor Proteins, Signal Transducing↗

PubMed1980

[Hemodynamics during septic shock].

Septic shock usually induces a hyperdynamic state characterized by normal or high cardiac output, associated with a fall in peripheral resistances which is responsible for arterial hypotension; when the evolution is prolonged it usually leads to a low output syndrome with elevated peripheral resistances, suggesting the hemodynamic pattern of hypovolemic shock. All intermediate situations can be observed within these extremes. The hyperdynamic state corresponds to a decrease in aortic impedance, which is indirectly related to the effects of endotoxin on vascular bed. The low output syndrome is more usual at the advanced stage and corresponds to the intervention of associated factors such as progressive hypovolemia and/or myocardial dysfunction. In certain cases--e.g. peritonitis--septic shock is immediately associated with hypovolemia. Many hypotheses have been advanced to explain the circulatory, cardiac and metabolic effects of septic shock. The effect of kinines on the circulation appears to predominate but there are still many unanswered questions concerning the real sequence of events. Hemodynamic monitoring is of great advantage in identifying the type of circulatory distortion, determining its severity, guiding therapy and evaluating its effects.

Adult↗

PubMed1978

A new model for the study of septic shock.

Septic shock was produced in 28 healthy mongrel dogs by injecting 10(8) Escherichia coli organisms per kilogram into the gallbladder following division of the cystic artery and duct. Based upon the circulatory responses and the mortality, two distinct groups emerged. In one, the cardiac index decreased significantly, and the total peripheral resistance was elevated. In the other, the cardiac index increased significantly, and the total peripheral resistance was significantly lower. The average survival time in the former group was three days and, in the latter, five days. The physiopathology of this model is remarkably similar to that of human septic shock. Studies are planned to further describe this model to increase its utility in the study of septic shock.

Animals↗

PubMed2004

The role of vasopressin in vasodilatory septic shock.

Septic shock that requires therapy with adrenergic agents is associated with high rates of mortality. Inappropriately normal or low serum concentrations of vasopressin contribute to the development of hypotension during sepsis. We critically evaluated the role of administering exogenous vasopressin to patients with septic shock. A computerized search of MEDLINE from January 1966--December 2003 and a manual search of relevant journals for abstracts were conducted. Eleven retrospective, six prospective cohort, and four prospective randomized studies were identified. Most studies evaluated short-term infusions of vasopressin at 0.08 U/minute or less as add-on therapy in patients requiring adrenergic agents. The results show that starting vasopressin in patients with septic shock increases systemic vascular resistance and arterial blood pressure, thus reducing the dosage requirements of adrenergic agents. These effects are rapid and sustained. Substantial enhancement of urine production, likely due to increased glomerular filtration rate, was shown in several studies. A few studies demonstrated clinically significant reduced cardiac output or cardiac index after vasopressin was begun, necessitating cautious use in patients with cardiac dysfunction. Vasopressin was associated with ischemia of the mesenteric mucosa, skin, and myocardium; elevated hepatic transaminase and bilirubin concentrations; hyponatremia; and thrombocytopenia. Limiting the dosage to 0.03 U/minut or less may minimize the development of these adverse effects. Vasopressin 0.03 U/minute or less should be considered if response to one or two adrenergic agents is inadequate or as a method to reduce the dosage of adrenergic agents. At present, vasopressin therapy should not be started as first-line therapy. Additional studies are needed to determine the optimum dosage, duration, and place in therapy of vasopressin relative to adrenergic agents. A multicenter, comparative study of vasopressin 0.03 U/minute as add-on therapy is under way and should provide mortality data.

Adult↗

PubMed1999

Nitric oxide in septic shock.

Septic shock is a major cause of death following trauma and is a persistent problem in surgical patients throughout the world. It is characterised by hypotension and vascular collapse, with a failure of the major organs within the body. The role of excessive nitric oxide (NO) production, following the cytokine-dependent induction of the inducible nitric oxide synthase (iNOS), in the development of septic shock is discussed. Emphasis is placed upon the signal-transduction process by which iNOS is induced and the role of NO in cellular energy dysfunction and the abnormal function of the cardiovascular system and liver during septic shock.

Animals↗

PubMed1979

Comparative haemodynamic effects of dopamine and dobutamine in septic shock.

Septic shock associated with depressed myocardial function generally requires the use of catecholamine. Currently dopamine is often selected. Dobutamine is a newly developed catecholamine which has been shown to be of value in severe cardiomyopathic disease. The aim of this work was to determine the most appropriate drug by comparing haemodynamic responses to dopamine and dobutamine in 19 studies carried out in 11 patients with septic shock and heart failure. Cardiac index increased siliarly with dopamine and dobutamine (33%), as did stroke volume (respectively 26.4 and 25%). Arterial pressure increased by 17% with dopamine whereas it did not significantly change with dobutamine due to reduction in vascular resistance of 19%. Dobutamine decreased filling pressure, either right (14%) of left (28%) whilst they slightly but unsignificantly increased with dopamine. Pulmonary shunting increased more with dopamine (47%) than with dobutamine (16%), but PaO2 remained constant with both. Since septic shock is characterized by lowered arterial pressure and vasodilatation it is concluded that effects of dopamine on capacitance and resistance vessels make this drug more suitable. In addition it selectively increases renal blood flow. Nevertheless dobutamine could be appropriate, in case of very high filling pressures, severe peripheral vasoconstriction, marked pulmonary shunting and in some cases where dopamine becomes ineffective.

Catecholamines↗

PubMed1989

Alterations in Gc levels and complexing in septic shock.

Septic shock involves increased generation of eicosanoids from arachidonic acid. Gc (vitamin D-binding protein) has been recently found to bind the parent molecule arachidonic acid but can also complex actin released as a result of tissue damage which causes displacement of bound arachidonic acid. Possible changes in serum levels of Gc and extent of complexing were therefore investigated in patients with gram-negative sepsis. As compared to healthy controls, serum levels of Gc were significantly decreased in patients with septic shock (P less than 0.01). Moreover, the percentages of Gc circulating in complexed form were significantly increased (P less than 0.01) and correlated strongly with disease severity, with levels often greater than 90% in patients who died (normal mean 8% +/- 3). These results suggest a hitherto unsuspected role for Gc in septic shock syndrome.

Actins↗

PubMed1963

SEPTIC SHOCK.

Septic shock may be defined as hypotension caused by bacteremia and accompanied by decreased peripheral blood flow, evidenced by oliguria. Clinically, a shaking chill is the warning signal. The immediate cause of hypotension is pooling of blood in the periphery, leading to decreased venous return: later, peripheral resistance falls and cardiac failure may occur. Irreversible shock is comparable to massive reactive hyperemia. Reticuloendothelial failure, histamine release, and toxic hypersensitivity may be factors in the pathogenesis of septic shock. Adrenal failure does not usually occur, but large doses of corticosteroid are employed therapeutically to counteract the effect of histamine release or hypersensitivity to endotoxin. The keys to successful therapy are time, antibiotics, vasopressors, cortisone and correction of acidosis.

Acidosis↗