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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of urinary trypsin inhibitor (UTI) on the number, morphology and function of platelets under septic state were studied in rat models of cecal ligation and puncture (CLP). At formation of CLP, 5,000 U/kg/h of UTI was serially administered intraperitoneally and blood was sampled after 16 hours. Comparative study among sham-operation group, CLP group, and CLP + UTI group revealed: 1) inhibition of the platelets of platelet counts and appearance of large-sized, active platelets by UTI in the CLP + UTI group, 2) increase of platelet maximum aggregation rate (MAR) by ADP and increase of collagen in the CLP group, while inhibition in the CLP + UTI group and 3) by HPLC evaluation of adenine nucleotide in the platelet, increased levels of total ATP and ADP in the CLP group, particularly, increases of ATP in the metabolic pool and ADP in the granular pool. CLP + UTI group did not show these changes in the adenylate pool. UTI was thus considered to stabilize the platelet cycle in sepsis. Platelets under septic state might be hyperactive, and thrombosis is easy to occur. UTI administration might work for maintaining constancy of the platelet internal environment and improve septic state because adenine nucleotide level in the platelet did not change in the CLP + UTI group through changed in the CLP group.
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PMID:[Effects of the administration of urinary trypsin inhibitor on the morphology and function of platelets in the rat septic models]. 232 1

The diagnosis of essential thrombocythemia in a cat was made by fulfilling the five applicable criteria set forth by the Polycythemia Vera Study Group for use in humans. The criteria were 1) a platelet count persistently above 600,000/microL, 2) a normal initial hematocrit that did not rise in response to iron therapy, 3) normal serum iron concentration, 4) absence of collagen fibrosis of the bone marrow, and 5) no cause for reactive thrombocytosis. In addition, normal thrombopoietin concentrations and splenic hypofunction were demonstrated. Melphalan was not effective in decreasing the platelet count and the cat died of sepsis.
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PMID:Essential thrombocythemia in a cat. 234 25

We have discussed the relationship between systemic illness, infection, and lung disease. As we have seen, patients with a wide variety of disease states, including advanced age, diabetes mellitus, alcoholism, collagen vascular disease, cancer, heart failure, and organ transplantation are potentially at increased risk for pneumonia because of disease-related impairments in host defenses. In addition, two virtually ubiquitous conditions in hospitalized patients, malnutrition and therapeutic interventions (especially with common medications), frequently add to the risk of airway invasion by bacterial pathogens. Systemic illness not only makes lung infection more common, but may adversely affect outcome and resolution, as well as determine the clinical presentation of pneumonia. In one particular population, the intubated and mechanically ventilated patient, the risk of infection is particularly high, and nosocomial pneumonia is a major cause of mortality. To the extent that the host response itself leads to the symptoms and signs of infection, systemically ill individuals may have subtle clinical features when serious bacterial invasion is present. Many components of the host defense system can become abnormal with serious illness, but a common mechanism that ties many systemic diseases to pneumonia is an alteration in airway epithelial cell receptivity for bacteria, namely, bacterial adherence, a process that mediates airway colonization, the first pathogenetic step on the road to pneumonia. The impetus for understanding how serious illness promotes lung infection is that once these mechanisms are identified, potential preventative strategies to minimize infection risk in the individual with systemic disease may be developed. The relationship among systemic illness, the lung, and infection also exists in a different direction: infection of a systemic nature (the septic syndrome) can lead to disease in the lung (ARDS). We have described the features of the septic syndrome and identified how it may lead to lung injury, usually by indirect means, through activation of inflammatory mediators that are carried to the lung via the vasculature. Although it is frequently impossible to predict which specific patient with systemic sepsis will develop acute lung injury, the current state of knowledge does permit us to identify high-risk individuals. Surprisingly, clinical assessment rather than biochemical testing is the best predictor of the development of acute lung injury. Patients with severe injury, profound shock and multiple systemic insults are most prone to acute lung injury in the presence of systemic sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Respiratory infections and acute lung injury in systemic illness. 268 63

Using an enzyme-linked immunosorbent assay, we measured the concentration of fibronectin containing an extra type III domain (ED1) in the circulation of humans. Plasma levels of ED1 + fibronectin averaged 2.8 +/- 1.0 micrograms/ml in healthy individuals and did not differ substantially according to age or sex. In comparison with those from normal subjects, plasma samples obtained from patients with collagen vascular disorders contained increased average levels of ED1 + fibronectin. Among this group, levels of ED1 + fibronectin were significantly greater in samples taken from individuals with clinical evidence of vasculitis. Although levels of total (ED1 + plus ED1 -) fibronectin were also elevated in plasma samples from patients with vasculitis, only the concentration of the ED1 + variant correlated with severity of disease in two patients examined serially. Elevations in plasma content of ED1 + fibronectin, but not total fibronectin, were also noted in patients with acute vascular tissue injury associated with major trauma or sepsis syndrome. Western blot examination revealed the presence of intact dimeric ED1 + fibronectin in the circulation of all patients studied, although fragments bearing the ED1 were also detected. Human plasma normally contains small quantities of soluble ED1 + ("cellular") fibronectin, and these levels are increased in disorders involving vascular injury.
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PMID:Elevated plasma levels of ED1+ ("cellular") fibronectin in patients with vascular injury. 271 81

Approximately 20% of preterm rabbit pups develop spontaneous germinal matrix hemorrhages (GMH). To understand better the pathogenesis of GMH we studied the ultrastructure of germinal matrix (GM) blood vessels in rabbits delivered at gestational day 28. Regardless of luminal size, the walls of most GM vessels had the structural characteristics associated with a blood-brain barrier (BBB) and consisted of endothelial cells and pericytes, surrounded by GM cell processes. Endothelial cells ranged from voluminous to attenuated, with some cells containing intracytoplasmic, membrane-bound vacuoles, and luminal as well as abluminal cytoplasmic projections. Some short interendothelial junctions had no puncta adherentia, whereas long ones often possessed intermittent pores. In two animals with GMH, intact endothelial cells were separated by narrow and wide gaps filled with luminal contents that occasionally extended beyond the interendothelial opening. The basal lamina (BL) was ill-defined, thin, often discontinuous and of low electron density. Smooth muscle cells and collagen were not present, which precluded any classification into arteries, capillaries and veins. Germinal matrix cell processes lacking both micro- and intermediate filaments were haphazardly disposed around the blood vessel walls in place of astrocytic endplates. Recent reports indicate that an astrocytic environment may be necessary for the development of the interendothelial tight junctions and BL. The presence of "glial foot" processes that lack ultrastructural characteristics of mature astrocytes suggests that interendothelial junctions and basal laminae in the vessels of the ganglionic eminence may not have the necessary structural and functional potential to withstand the transmural pressures or the pathophysiological influence of hypertension, hyperosmolarity, sepsis, and other factors known to open the BBB and to contribute to GMH.
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PMID:Ultrastructure of blood vessels in the ganglionic eminence of premature rabbits with spontaneous germinal matrix hemorrhages. 273 55

Thirty-nine hospital-based cases of ischemic colitis were reviewed. There were 18 males and 21 females. Average age was 68.7 years (range, 18 to 92 years). Associated diseases among 13 patients younger than 65 included renal failure in seven patients and hematologic, vasculitic, or collagen vascular diseases in four. In 26 patients 65 or older, congestive heart failure was seen in 13, vascular disease in eight, and previous aortic surgery in four. Nineteen patients were treated nonsurgically and 8 died (42 percent mortality). Twenty patients (51 percent) underwent surgery: 18 had resection with colostomy or ileostomy and two had resection with reanastomosis; one patient underwent laparotomy followed by second-look exploration without resection. Thirteen of the 20 surgical patients died (65 percent mortality). Both patients who underwent reanastomosis died of sepsis. The data show a close association between ischemic colitis and a number of serious systemic diseases including renal failure, arteriosclerotic heart and vascular disease, and hematologic, vasculitic, and connective-tissue disease. A predilection for the right colon and sigmoid colon and splenic flexure was seen. A formidable mortality rate (53 percent) was found among patients treated both surgically and nonsurgically.
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PMID:Mortality from ischemic colitis. 279 81

The efficiency of a pure carbon prosthesis to reconstruct intra-articular ligamentous loss of substance was evaluated on 14 sheep with an 18-month follow-up study of recent and old ACL experimental injuries. Functional results showed a correlation between a tightened implant, the stability of the knee, and the absence of severe arthritis. The rupture strength of the newly formed ligament amounts to about 300 Newtons (N). That of the normal ACL amounts to 250-550 N. The structure gives a viscoelastic behavior to the prosthesis. This tissue was made of collagen fibers surrounding the carbon fibers and running generally in the direction of the ligament. In the osseous tunnels, the newly formed lamellar bone invaded and surrounded the implant. Carbon fiber fragmentation occurred, and fibers were found in the synovia and in the homolateral, inguinal, and paraaortic lymph nodes. No degeneration, necrosis of tissue, or cellular toxicity was found. On these bases, the carbon prosthesis was modified by adding a resorbable copolymer of polyglycollic (PGA) and polylactic acid (PLA) around the fibers and a resorbable sheath of the same polymer. This carbon-PGA/PLA prosthesis was used in 23 patients with a three- to 12-month follow-up period. Patients were evaluated by clinical tests and by functional control of the ligament. The indications for prosthetic replacement were: recent mop-end tears of the ACL, cruciate ligament reconstruction in chronic knee instability, and wide rotator cuff loss of substance. Five complications occurred because of hematomas and/or sepsis and prosthesis breakage. Eighteen of 23 patients had good clinical results with good function in five. The conclusions are that PGA/PLA produces a clean and flexible ligament, thus eliminating carbon fiber articular deposits and allowing a normal function. Inflammatory postoperative reactions seem to be more frequent than with other procedures and call for operative and clinical care in order to eliminate hematoma and sepsis. The efficiency of a rehabitable carbon-PGA/PLA prosthesis in intra-articular ligamentous defects in man will be confirmed only by controlled long-term clinical observations.
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PMID:Carbon-PGLA prostheses for ligament reconstruction. Experimental basis and short-term results in man. 298 86

Septic surgical patients often require fluid administration to maintain cardiovascular stability due, in part, to the sepsis-induced increase in vascular permeability and associated plasma volume depletion. Plasma fibronectin deficiency exists in such septic patients. We determined if maintenance of fibronectin levels by administration of fibronectin-rich human plasma cryoprecipitate would lower the resuscitative fluid volume needed for support of arterial pressure in septic postoperative sheep which were experimentally depleted of plasma fibronectin. Following a 2-hr postoperative baseline period, denatured collagen (gelatin, 8.7 mg/kg), which has a high affinity for fibronectin, was infused into both control and experimental sheep in order to acutely deplete plasma fibronectin. Sheep were then challenged both intraperitoneally and intravenously with live Pseudomonas (5 x 10(10) bacteria IP; 5 x 10(9) bacteria IV). Experimentals were given fresh plasma cryoprecipitate intravenously at a dose of 4 units bolus, followed by 3 units/hr for 5 hr. Controls received plasma cryoprecipitate selectively depleted of fibronectin by affinity chromatography. Bacterial challenge rapidly resulted in severe systemic hypotension. Ringer's lactate was infused intravenously into both groups at a rate sufficient to maintain a systemic arterial pressure of approximately 50 mm Hg with a maximum pulmonary artery wedge pressure of 15-18 mm Hg. Its rate of infusion was periodically adjusted to maintain this hemodynamic status. Comparison was made of the volume of Ringer's lactate required to maintain an arterial pressure of 50 mm Hg in both groups. Net fluid requirement was significantly (p less than 0.05) less in postoperative septic sheep (47.4 +/- 6.2 mg/kg/hr) treated with fibronectin-rich cryoprecipitate compared to the fluid requirement (71.7 +/- 4.7 mg/kg/hr) for postoperative septic sheep receiving fibronectin-deficient cryoprecipitate. Thus elevation of plasma fibronectin concentration lowers the fluid requirements needed for hemodynamic support in postoperative Gram-negative sepsis.
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PMID:Effect of fibronectin-rich human cryoprecipitate on fluid volume requirements in sheep during postoperative sepsis. 313 Apr 90

Immunoreactive plasma fibronectin depletion has been associated with the presence of collagen-fibronectin complexes in patients after trauma and in animal models of traumatic and burn injuries. However, the role of plasma fibronectin in the development of sepsis after traumatic and burn injuries in patients is unknown. Treatment of patients and animals with purified human plasma fibronectin ameliorates some of the clinical and metabolic effects of systemic endotoxemia. We report that the induction of immunoreactive plasma fibronectin deficiency by gelatin infusion is associated with enhanced effects of intraperitoneal Escherichia coli endotoxin injection. We have observed a significant increase in the concentrations of ammonia in plasma of treated rats compared with those in control rats administered the same dose of endotoxin.
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PMID:Enhanced endotoxin effects in plasma fibronectin-deficient rats. 329 66

Clinical studies of ARDS have been successful in determining the most common predisposing clinical disorders and the natural history of this syndrome. Sepsis, gastric aspiration, and major trauma are the most frequently associated high-risk factors. Overall mortality is in the range of 60% to 70%, but is even higher if ARDS is associated with sepsis, severe acidemia, or decreased renal function. It is evident that multisystem failure is responsible for death in many patients, as well as secondary pulmonary and extrapulmonary infections. Pathologic studies have provided descriptive information regarding the acute, subacute, and chronic phases of the syndrome, but little insight into the precise pathogenesis of the initial lung injury or the progressive fibrosing alveolitis and lung destruction that develops in some patients. There has been considerable circumstantial evidence from clinical studies implicating the neutrophil as a potentially important mediator of the early changes in lung endothelial and epithelial permeability. However, not all investigators have found the same alterations in neutrophil function in the circulation or in the lavage from the lungs of patients with ARDS. Also, the heterogeneous etiologies of ARDS make it difficult to be sure that there is a final common pathway for acute lung injury in all ARDS patients. In addition, there are a host of mediators, including products of complement activation and arachidonic acid metabolism, that may be important in amplifying the inflammatory response. Also, abnormalities of surfactant production and collagen turnover, as well as impaired host defenses in the lung, may contribute to the progressive respiratory failure that occurs in some ARDS patients, even though the acute, exudative phase of lung injury has resolved. Future human studies may provide useful information about the mechanisms of the acute lung injury through studies of circulating plasma markers, blood elements, and lavage fluids from high-risk patients. On the other hand, samples of cells and mediators from the airspaces with lavage still may not reflect the critical interactions of mediators and cells with the lung endothelium that lead to the protein-rich pulmonary edema that characterizes the first phase of ARDS. Thus, experimental studies must continue to study the details of the early phases of acute lung injury (see article by Flick, page 455). Finally, it is clear that treatment designed to reduce the severity and the incidence of ARDS must be started early, since the syndrome develops so rapidly in high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathophysiology of the adult respiratory distress syndrome. What have we learned from human studies? 333 57


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