Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compared prophylactic administration of either intragastric misoprostol (200 micrograms four times a day), a prostaglandin E1 analog, or bolus intravenous cimetidine (300 mg every 6 hours) in preventing stress lesions and stress bleeding in 127 adult postoperative patients who required mechanical ventilation and also had developed hypotension or sepsis. Both drug treatments were equally effective in preventing the development of diffuse gastritis (greater than 10 gastric hemorrhagic lesions) and in preventing upper gastrointestinal hemorrhage (UGIH). The combined data from both groups showed that for the 44 (35%) patients who died, death was significantly associated with the presence at study entry of renal failure (64% of 25 patients with renal failure died), hepatic failure (57% of 23 patients) or coagulopathy (62% of 29 patients) (p less than 0.02 for each), and with the number of organ system failures at study entry (48% of 69 patients with multiple organ system failures died, p less than 0.001). Death was also significantly associated with the presence of adult respiratory distress syndrome (ARDS) at study entry or the development of ARDS (63% of 24 patients with ARDS died, p less than 0.001), and the development of UGIH (5% of 93 patients with known bleeding outcome died, p less than 0.05). The number of stress lesions that developed was significantly associated with subsequent UGIH (p less than 0.001). Additional organ system failure developed during the study in 31% of the 127 patients, as did diffuse gastritis in 20% of 111 patients who had a follow-up endoscopy. These results demonstrate that postoperative patients who require mechanical ventilation and have hypotension or sepsis are at significant risk for the development of stress gastric lesions and multiple organ system failure even when prophylaxis for stress ulcers is provided. Furthermore, the presence of ARDS, renal failure, hepatic failure, coagulopathy, and UGIH are significantly associated with death.
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PMID:Stress ulcers and organ failure in intubated patients in surgical intensive care units. 155 13

The effects of the anticoagulants, heparin and low molecular weight heparin (LMWH), and the antiplatelet agents, prostaglandin E1 (PGE1) and aspirin, on endotoxin-induced renal insufficiency not induced by prerenal factors, were investigated using rabbits to evaluate the clinical usefulness of these drugs and their possible involvement in the activation of hemostasis in renal insufficiency. The intravenous administration of PEG1, at 0.4 microgram/kg/min, or aspirin, at 5 mg/kg, significantly restored all the parameters of renal function measured in the present study, namely, effective renal plasma flow, glomerular filtration rate and urine N-acetyl-beta-D-glucosaminidase, as well as histological renal ischemic changes. On the other hand, neither heparin nor LMWH, even at a high dose, improved any parameter. As the antiplatelet effect is the common property of PGE1 and aspirin, it is suggested that the activation of platelets may be prerequisite to the occurrence of renal insufficiency induced by endotoxin. The results of this study thus show that PGE1 or aspirin may be applied in clinical use for renal insufficiency complicated by sepsis or endotoxemia.
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PMID:The possible involvement of platelet activation in endotoxin-induced renal insufficiency in a rabbit model. 166 36

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

In this study we investigated the effects of right atrial infusion of PGE1 (RAIPGE1) in doses from 40 to 500 ng/kg/min on sepsis-induced pulmonary artery hypertension (SIPAH). Thirteen pigs were randomized into a time-course group (n = 6) and a PGE1-treated group (n = 7). Pulmonary hypertension (PAH) was induced with the infusion of Pseudomonas Aeruginosa (PsAr) at a concentration of 2 X 10(8) CFU/20 kg/min in both groups. The infusion of PsAr caused a significant and persistent rise in mean pulmonary artery pressure (MPA), pulmonary vascular resistance (PVRI), right ventricular compliance (RVC), RV dp/dt, and right ventricular stroke work index (RVSWI), 30 min after the onset of infusion (P less than 0.05 vs baseline). Systemic hemodynamics and gas exchange were not affected throughout the 3-hr period of infusion (P = NS); however, left ventricular compliance (LVC) was depressed at a MPA greater than 35 mm Hg. The RAIPGE1 following SIPAH caused a concentration-dependent reduction above 40 ng/kg/min of MPA, PVRI, RVSWI, and RV dp/dt (P less than 0.05, 120 and 500 ng/kg/min vs PAH). RVC returned to baseline values during the infusion of PGE1. Systemic hemodynamics, including oxygen delivery and extraction, were unaffected by the infusion of PGE1, but LVC was improved (P less than 0.05, PGE1 500 vs PAH). The infusion of PGE1 caused a concentration-dependent rise in shunt fraction (Qs/Qt) and alveolararterial oxygen gradients which reached statistical significance during the infusion of 500 ng/kg/min. Our data show that RAIPGE1 is effective in ameliorating RV and pulmonary hemodynamics, but at the largest dose it negatively affects gas exchange.
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PMID:Efficacy of right atrial infusion of PGE1 in sepsis-induced pulmonary hypertension. 212 41

Since decubitus, one of the common lesions, is not yet fully under medical control, it still offers serious problems. The incidence of this lesion once comprised about 12% of the patients hospitalized in a geriatric institution, and was responsible for the development of sepsis in about 20% of those cases. Although the incidence of this lesion has been declining, it still debilitates many geriatric patients, especially with neurological or malignant diseases. Care being necessary to disperse the pressure on the skin adjacent to the bone, many devices have been invented. The air-fluidized bed is especially effective in preventing and alleviating decubitus. However, a simple device utilizing polyvinyl sponge plates is worthy to try from the standpoint of cost-performance. Several surgical reparative manoeuvres as well as newly developed medicines, such as prostaglandin E1, etc. now promote favourable outcomes. However, the importance of basic preventive care, such as postural change with massage, local hygiene, nutrition, etc. cannot be ignored.
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PMID:[Decubitus]. 220 Sep 9

Adult respiratory distress syndrome is an inflammatory disorder of the lung parenchyma that results in severe respiratory failure. It is associated with sepsis syndrome and multiple organ failure and may be mediated by a variety of substances, several of which have been discussed in this article. Because sepsis syndrome, ARDS, and multiple organ failure are associated with a high mortality rate that has not been reduced significantly by supportive treatment, a rationale exists for therapeutic intervention with agents that affect the inflammatory cascade. Several of these agents, notably corticosteroids and prostaglandin E1, have been shown to be of no benefit in humans despite laboratory and animal studies suggesting their utility. Other agents, including surfactant, antiendotoxin antibodies, and NSAIDs, are undergoing clinical trials and may prove to be effective. A third group, including anti-TNF antibodies and pentoxifylline, are of theoretical benefit but await clinical trials.
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PMID:Pharmacologic treatment of the adult respiratory distress syndrome. 226 1

ARDS is a complication of septic and traumatic shock. It ranges from slight pulmonary dysfunction to forms so severe as to be incompatible with life. There seem to be initial pathogenic differences between sepsis-induced and trauma-induced ARDS, in that activation of granulocytes is primarily involved in the former and activation of the clotting system during a fibrinolysis-inhibition phase in the latter. In the later course the granulocyte-mediated and the coagulation-mediated injury can potentially amplify each other's effects in several positive feedback systems. In the end stage the two forms involve similar pathogenic mechanisms which may include production of oxygen radicals. Therapy aims primarily to eradicate the initiating event. Firm data support shock treatment with dextran-70 and early or prophylactic ventilator treatment using positive end-expiratory pressure. Despite lack of conclusive evidence, high-dose corticosteroids in one or two doses should be given very early, at least in sepsis-induced ARDS. Other agents which may be tried early in the course of ARDS include prostaglandin E1, cyclooxygenase inhibitors and oxygen radical scavengers.
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PMID:Adult respiratory distress syndrome. Pathogenesis and treatment. 242 88

There is considerable evidence from animal and human studies of sepsis and acute lung injury that prostacyclin and PGE1 may have a beneficial effect on tissue perfusion with a reduction in the severity of tissue damage associated with these disorders. As yet, there are no good data from controlled clinical trials that these agents improve survival and it is not clear whether in the future such data will be forthcoming. Nevertheless, using various physiological end-points, both prostaglandins seem to be beneficial in sepsis and when used in combination with the whole process of Intensive Therapy, may contribute to the survival of some cases. Although the assessment of combinations of agents designed to inhibit mediator release might be more useful, it remains to be seen whether the relatively insensitive controlled clinical trial, with survival as its endpoint, is the appropriate tool for assessing efficacy in the ITU. Perhaps, the 'consensus' approach has something to offer in this situation!
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PMID:The therapeutic value of vasodilator prostaglandins in multiple organ failure associated with sepsis. 306 68

Clinical cardiopulmonary transplantation is currently limited by the availability of suitable heart-lung donors. Distant graft procurement, with pretreatment, of the donor by intravenous prostaglandin E1 and cooling of the graft with pulmonary artery perfusion, is now clinically established and should increase the number of available donors. Between March 1981 and September 1986, 40 heart-lung transplantations were performed. The characteristics of the donor pool were analyzed. Gram stain of the donor tracheal aspirate revealed gram-positive bacteria in 80% and gram-negative organisms in 35%. Yeast was present on stain in 25% of the patients. Donor arterial oxygen tension was less than 100 torr inspired oxygen concentration 40%) repeatedly in one patient; this recipient died of lung failure at operation. Severe deterioration of allograft lung function was seen in 11 (27.5%) recipients. The causes of deterioration were substantial postoperative bleeding in six patients, sepsis in two, and acute rejection, poor lung function, and allograft heart failure in one patient each. HLA-A locus mismatch, poor donor alveolar-capillary gas exchange, tracheal colonization with heavy polymorphonuclear cells, and heavy bacteria and fungus resulted in increased operative mortality. Donor pretreatment with prostaglandin E1 was associated with improved survival. Recipient selection, emphasizing adequate liver function and absence of previous thoracic operation, careful surgical technique with minimal bleeding, and brief perfusion time were factors associated with improved survival. Early morbidity and mortality were principally related to recipient risk factors, and the strict criteria observed for selection of heart-lung donors were valid. The importance of appropriate recipient selection is underscored.
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PMID:Proper donor selection for heart-lung transplantation. The Stanford experience. 311 47

In 16 anesthetized pigs the cardiovascular effects of prostaglandin E1 and methylprednisolone (MPS) during E. coli sepsis were studied. Gated blood pool scans and hemodynamic studies were simultaneously performed. A control group, group I (n = 4), received volume loading alone; groups II, III, and IV received (each n = 4) volume loading after intravenous administration of MPS, prostaglandin E1, and both MPS and prostaglandin E1, respectively. Groups were formed by randomization, such that the effects of prostaglandin E1 (0.1 microgram/kg/min) and MPS (30 mg/kg) could be analyzed separately and in combination. Eight animals treated with prostaglandin E1 were compared with eight animals not receiving prostaglandin E1. The same method was applied to the MPS group. E. coli infusion resulted in an abrupt increase in pulmonary arterial pressure while systemic blood pressure gradually fell. Cardiac output decreased. Gated blood pool studies showed an increase in right ventricular end-diastolic volume and a decrease in right ventricular ejection fraction. Consequently, right-to-left ventricular end-diastolic volume ratio increased. Pulmonary arterial pressure was lowered in the treatment groups compared to control group. During volume loading right ventricular ejection fraction improved in the prostaglandin E1 group but remained low in the MPS group. Compared to control group, cardiac output did not change and mean systemic arterial pressure significantly decreased in the prostaglandin E1 group. Treatment with prostaglandin E1, MPS, or both drugs and volume loading did not reveal any difference between the four groups with respect to cardiac output, right and left ventricular volumes, and left ventricular ejection fraction. The present study indicates that in a porcine model of E. coli septic shock with acute pulmonary hypertension, prostaglandin E1 and MPS treatment decrease pulmonary vascular resistance but also systemic vascular resistance. Prior to and during volume loading right ventricular ejection fraction increased in the prostaglandin E1 group. However, neither prostaglandin E1 nor MPS improved right ventricular performance and forward flow during volume loading.
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PMID:Effects of vasodilators prostaglandin E1 and methylprednisolone on pulmonary hypertension and right ventricular performance during volume loading in porcine septic shock: a combined invasive and radionuclide study. 329 78


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