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)

Cecal ligation and puncture (CLP) were performed in rats. After 4 hr (early sepsis) and 16 hr (late sepsis), platelet morphology and function were studied. At 16 hr, platelet counts for the CLP group were significantly lower than for the sham-operated control group. Low maximum aggregation rates (MAR) and decreased platelet counts were elicited in platelet-rich plasma with 4 M ADP and 2 micrograms/ml collagen. However, with platelet counts equalized, MAR for the CLP group increased significantly, especially after 16 hr. The platelet-large cell rate and platelet distribution width decreased temporarily at 4 hr, then rose significantly at 16 hr. No significant changes were observed in the mean platelet volume after 4 hr, but there were significant increases after 16 hr. Total adenine nucleotide (TAN) levels within the platelets rose significantly in the CLP group, suggesting the appearance during the late sepsis of large, heavy platelets or adenine nucleotide-rich platelets. The platelet adenylate pool was divided into granular and cytoplasmic fractions, respectively characterized by ADP and ATP increases. However, no septicemia-related differences were noted in the degree of binding between goat antirat fibrinogen and platelet surface glycoprotein IIb/IIIa complex. Internal environment changes in the platelets indicated that during septicemia hyperfunctional or hypersensitive platelets with a latent capacity for active aggregation and release appeared in the circulation. Hypercoagulability in septicemia involves activation of coagulation factors, stimulation of the coagulation cascade, volume changes accompanying increased platelet TAN content, and changes in AN distribution in the two pools. These findings significantly increase our understanding of the transition from the prethrombotic state to thrombosis in septicemia.
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PMID:Platelet size and function in septic rats: changes in the adenylate pool. 217 92

The percutaneous placement of intravascular devices creates a portal for microbial invasion that can result in local infections or septicemia. In nature, resistance to "exist site" infection in percutaneous organs, such as teeth, is prevented by a dense collagen/epithelial barrier. A new percutaneous access device has been developed that incorporates a porous polyurethane "button" at the subdermal level. This device promotes the development of a collagen/epithelial interface, thus inhibiting sinus formation. Twelve percutaneous access devices (PCADS) were implanted in calves; eight devices were utilized for venting of, and hard wire passage to, an implantable left ventricular assist device (LVAD) and served as controls. Four devices were utilized for long-term vascular access. The PCADS remained in situ for 2-127 days (mean 70). Excellent healing was apparent in all cases, and no exit site or catheter related infections occurred. Histologic examination demonstrated fibroblastic in-growth and collagen deposition within the porous polyurethane, which provides a barrier to epithelial migration and firmly anchors the device. These PCADS appear to reduce exit site infections and may improve upon currently available long-term vascular access catheters.
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PMID:Development of a polyurethane percutaneous access device for long-term vascular access. 225 96

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

The infection with Erysipelas rhusiopathiae demonstrates that it is possible to characterize the significance of predisposing factors. The virulence of the agent is most important among the exogenous factors; it determines decisively the course of the disease: 1. paracute course as septicemia; 2. chronic course as polyarthritis; 3. subclinical course nearly without any symptoms. The immune status and the genotype of the host are predominant out of endogenous factors. The importance of immunity is known since a long time. A series of field observations supported the potential genetical influence in the pig. Within the hereditability an association to the MHC (in special genetic lines of rats to the RT 1 system of the MHC) was most recently determined in inbred laboratory animals. Additionally several environmental conditions, which can be summarized as stress, and as endogenous factor the age of the animals are relevant for the pathogenesis of the erysipelas infection. A non variable but most important disposition for special tissues are the so-called "borderline tissues", where accumulation, sedimentation and persistence of bacterial antigens are wellknown as described earlier. This phenomenon is determined by hemodynamic manifestation and quantifiably regulated by cytokines especially interleukin (IL 1) as well as by the tumor necrosis factor (TNF alpha) and prostaglandin PgE2. Additionally the cross reactivity of antibodies of Erysipelas rhusiopathiae against most specific collagen of type II, IX and XI in the pig and in laboratory animals was elaborated. This autoimmune phenomenon called "immunologic mimicry" supports besides the special physiologic conditions as niche of defense a very successful evolutionary adaptation of the agent.
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PMID:[Erysipelas as a disease factor]. 268 51

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


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