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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemorrhagic shock causes a severe suppression of cellular immunity and an increased susceptibility to sepsis that may be due to increased release of prostaglandin E2 by macrophages. Since chloroquine inhibits the secretion of prostaglandin E2 by macrophages in vitro, the effects of chloroquine administration in vivo following hemorrhagic shock on macrophage prostaglandin E2 secretion and on depressed cellular immunity were examined. Inbred C3H/HeN male mice, aged 6 to 8 weeks, were bled to a mean blood pressure of 35 mm Hg, which was maintained for 60 minutes, and adequately, resuscitated. Mice then received intramuscular injections of either saline (vehicle) or chloroquine (10 mg/kg of body weight). Prostaglandin E2 in macrophage supernatants (radioimmunoassay) concanavalin A-dependent splenocyte proliferation, and interleukin 2 in splenocyte supernatants (CTLL 20 interleukin 2-dependent proliferation) were determined 2 or 24 hours later. Hemorrhage caused a significant decrease of splenocyte proliferation (47%) and interleukin 2 release (49%) at 24 hours, while prostaglandin E2 secretion from macrophages was elevated at 2 hours. Chloroquine treatment attenuated depression of splenocyte functions and reduced prostaglandin E2 release. Furthermore, chloroquine treatment decreased the mortality of septic mice after hemorrhage to levels comparable with those of sham-operated mice. Thus, chloroquine may be a useful adjunct in the clinical setting for the treatment of shock-induced immunodepression and increased susceptibility to sepsis following hemorrhage.
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PMID:Chloroquine attenuates hemorrhagic shock-induced immunosuppression and decreases susceptibility to sepsis. 173 52

Although it is known that interferon-gamma synthesis and macrophage functions are depressed after hemorrhage, it remains to be determined whether systemic administration of interferon-gamma has any effect on hemorrhage-induced depression of macrophage and splenocyte functions. To study this, C3H/HEN mice were bled to a mean blood pressure of 35 mm Hg, maintained for 60 minutes, and followed by adequate fluid resuscitation. The mice then received either 1000 units interferon-gamma or saline solution (vehicle). Peritoneal (pM phi) and splenic (sM phi) macrophages and splenocytes were isolated 24 hours later. PM phi antigen presentation was measured by coculturing pM phi with the D10.G4.1 cell clone. Major histocompatibility complex class II (Ia) antigen expression was determined by direct immunofluorescence. Cytokine release by pM phi, sM phi, and splenocytes was assessed with specific bioassays. For survival studies, mice were subjected to sepsis 3 days after hemorrhage. Treatment with interferon-gamma restored (p less than or equal to 0.05) hemorrhage-induced suppression of pM phi antigen presentation capacity and Ia antigen expression and increased (p less than or equal to 0.05) interleukin-1 and tumor necrosis factor release by pM phi and sM phi, as well as splenocyte proliferation (p less than or equal to 0.05). Interferon-gamma also decreased (p less than or equal to 0.007) the susceptibility to sepsis after hemorrhage. Thus interferon-gamma represents a potent agent for treating hemorrhagic shock-induced immunosuppression and for increasing the ability of the host defense system to combat bacterial infections after hemorrhage.
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PMID:Interferon-gamma attenuates hemorrhage-induced suppression of macrophage and splenocyte functions and decreases susceptibility to sepsis. 173 88

We compared the early and late pulmonary effects of human recombinant tumor necrosis factor (TNF) and interleukin 1 (IL-1) challenges in awake dogs with chronic tracheostomies. Serial blood gas analysis, bronchoalveolar lavage (BAL) with cell and protein analysis, intravascular catheter hemodynamics, and radionuclide left ventricular ejection fractions (LVEF) were determined before and after infusion of TNF (60 micrograms/kg body wt, n = 8), IL-1 (1,000 micrograms/kg body wt, n = 6), or heat-inactivated IL-1 (n = 6, controls). Controls given heat-inactivated IL-1 had no changes (P = NS) in any pulmonary parameter throughout the study. Animals given IL-1 had a transient increase (P less than 0.05) in BAL neutrophil concentration 1 day after infusion but no other changes (P = NS) in pulmonary function throughout the study. Animals given TNF had early (0-4 h) decreases (P less than 0.05) in arterial PO2, increases (P less than 0.05) in physiological shunt fraction and alveolar-to-arterial PO2 gradient, and a high mortality rate (50%). In TNF animals, volume challenges at 4 h were associated (P less than 0.05) with death and noncardiogenic pulmonary edema. In TNF survivors, hypoxemia persisted for 2-3 days and was associated with increases (P less than 0.05) in alveolar protein and neutrophil concentration on days 1 and 3, respectively, which in survivors returned to near normal over 6-21 days. Animals challenged with TNF and not IL-1 had reversible depression of LVEF similar in time course to abnormalities in arterial PO2. In this study, TNF (but not IL-1) challenges were lethal and produced acute pulmonary dysfunction sustained over days (reversible in survivors) that was similar to that seen in human septic shock. The ability of TNF to induce pulmonary injury similar to bacterial shock suggests that TNF is a key mediator of sepsis-induced lung injury. Furthermore, because TNF challenge induced both sustained pulmonary and cardiac injury, TNF may be a common pathway for the multiple organ dysfunction that occurs during septic shock.
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PMID:TNF but not IL-1 in dogs causes lethal lung injury and multiple organ dysfunction similar to human sepsis. 176

We analyzed 8 cases of meningococcal septic shock diagnosed in a three year period. The age varied from 20 months to 10 years (mean: 4.8 years). Two patients died. Every child was monitored with a Swan-Ganz catheter 5 F or 7F, placed on by puncture of internal jugular or subclavicular veins. Of this hemodynamic study, we can conclude that in septic shock, there is a myocardial depression, that persist for several days, and improves with dopamine and dobutamine. In addition to this, in sepsis exists a pulmonary hypertension that makes worse the prognosis.
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PMID:[Hemodynamic study in meningococcal septic shock]. 177 67

The aim of the present study was to determine whether hearts that demonstrate depressed myocardial reserves as a result of sustained hypermetabolic sepsis would show a potentiation of the dysfunction after an infusion of high doses of alcohol. We have previously shown that myocardial depression is present in hearts removed from hypermetabolic septic rats. Acute alcohol administration has also been shown to have a negative inotropic effect on the heart. In this study, myocardial function was assessed under in vitro conditions in which preload could be varied and aortic outflow resistance controlled and thus heart function could be determined under both low and high workloads. The alcohol-infused group increased cardiac performance as a function of increasing preload similarly to the controls. Heart rate, however, was significantly elevated compared with control. Isolated hearts from septic, saline-infused animals showed depressed cardiac performance both in terms of stroke volume and myocardial work over a range of preloads. The septic, alcohol-infused animals did not show this depression. Thus, a loss of myocardial reserve was demonstrable in hearts isolated from septic, saline-infused rats but not in septic, alcohol-infused rats. Alcohol, at least acutely, seemed to reverse or ameliorate the loss of myocardial reserve induced by sepsis possibly by increasing the ability of the heart to fill during diastole and thus perform volume work.
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PMID:Function of isolated hearts from septic, saline-infused, and septic, alcohol-infused rats. 178 83

The primary function of the cardio-respiratory system is to meet the oxygen demands of the various organs and tissues and to remove metabolic wastes. The cellular O2 supply in the critically ill patient afflicted with severe infection, sepsis or ARDS is impaired not only by reduced O2 transport to the tissue due to myocardial depression caused by inadequate preloading and depressed contractility, but also by inadequate blood flow at the regional and microcirculatory levels. To obtain adequate tissue oxygenation despite derangements of the microcirculation, it is useful to aim for a hyperdynamic circulatory state that provides a supramaximal O2 transport. The best way to achieve this goal is first to optimize cardiac filling pressures, i.e. to the upper range of normal, and then to improve cardiac output using inotropic support. Only when the arterial pressure remains too low despite these measures is the use of vasopressors indicated.
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PMID:[Oxygen transport and tissue oxygenation in critically ill patients--value of volumes and vasoactive substances]. 181 5

Little is known of the endorphins' role in sepsis-induced respiratory distress and naloxone's effect as a treatment of it. Thirteen piglets were infused with live Escherichia coli at a rate of 2 to 10 x 10(8) colony-forming units per hour for six hours or until death and were divided into two groups: the septic control group (n = 8), and the naloxone-treated group (n = 5), which received 8 mg/kg/h of naloxone by continuous infusion. The results showed a significant reduction of QS/QT, VD/VT, and arterial carbon dioxide pressure at one hour and a significant increase of arterial carbon dioxide pressure and minute ventilation at 1, 3, and 4 hours in the naloxone-treated group, compared with the untreated septic group. None of the piglets in the naloxone-treated group developed ventilatory depression, while 75% of those in the untreated septic group did. Among the latter ficial effects of naloxone are likely related to its action on the central and peripheral respiratory regulatory mechanisms. A transient protection of the cardiac output and relatively decreased extravascular lung water with naloxone treatment may also, in part, improve the ventilation-perfusion maldistribution and secondarily reduce QS/QT and VD/VT.
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PMID:[Prevention of septic ventilatory depression with naloxone]. 181 74

So-called "Postoperative Erythroderma" was experienced in a 68 year-old man who received CABG for unstable angina. After a seemingly uneventful recovery, he revealed high grade fever on 13th post operative day (POD), rashes over the whole body on 15th POD and pancytopenia on 20th POD. He died of sepsis, multiple organ failure and DIC on 21st POD. Blood transfusion (concentrated red cell: 3 units) was done on operation. In this case, the rate of premature and atypical lymphocytes increased, and the ratio of OKT4 (helper)/OKT8 (suppressor) decreased. These findings of the examination suggested that there was a possibility of cell-mediated immunological depression. We considered this to be acute GVHD after blood transfusion.
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PMID:[A case of "postoperative erythroderma" following coronary artery bypass grafting operation]. 183 33

The quality of analgesia and incidence of side effects when using a continuous subarachnoid infusion of diamorphine were assessed in 28 postoperative patients who had undergone major abdominal or lower limb surgery. Excellent pain relief was obtained without depression of the respiratory rate. Four patients complained of headache, and 50% of those patients not already catheterized preoperatively subsequently required it for urinary retention. There was no evidence of sepsis related to the indwelling subarachnoid catheter.
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PMID:Initial experience of continuous subarachnoid diamorphine infusion for postoperative pain relief. 195

Since the sepsis syndrome is associated with depressed vascular reactivity, it may be incorrect to assume that pharmacologically mediated changes in cardiac output will be proportionately distributed at the regional level of the circulation. We examined the effect of hyperdynamic sepsis and the concurrent administration of the vasodilatory prostaglandin (PGE1) on the regional distribution of blood flows (Q) in unanesthetized sheep rendered septic by cecal ligation and perforation. Systemic Q progressively increased throughout a 48-h study period after cecal ligation and perforation. Simultaneously, organ Q, measured by the radioactive microsphere technique, was depressed to the pancreas, but increased to the heart, gallbladder, brain, and colon; the increased Q to both heart and gallbladder was greater than the simultaneous increase in systemic Q in this septic study. With the infusion of PGE1 (1 microgram/kg/min), mean arterial perfusing pressures fell, while the cardiac index increased further over that recorded during the 48-h septic study. Despite this depression in arterial pressures, the only significant effect of PGE1 on the interorgan distribution of Q was in the renal circulation, where it was demonstrated that kidney Q fell. We conclude that (1) hyperdynamic and normotensive sepsis exerted nonhomogeneous effects on the distribution of organ Q, and (2) an increased systemic Q during PGE1 infusion was proportionately distributed to all organs, except the kidneys, where Q paradoxically fell. The latter finding suggests that the regulation of kidney Q may be depressed across the normal range of arterial perfusing pressures in the sepsis syndrome. Further investigation is essential to understand the effect of clinical interventions on the control of tissue O2 flux at both the regional and microregional levels of the circulation.
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PMID:Effect of PGE1 on altered distribution of regional blood flows in hyperdynamic sepsis. 195 17


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