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)

The caudal cruciate ligament assists the medial femorotibial ligament in supporting the medial aspect of the femorotibial joint. It also limits the outward rotation of the tibia during weight bearing. In two lame horses tearing of the caudal portion of the femoral attachment of the caudal cruciate ligament was recorded together with cracking and tearing of the medial meniscus. In one case, synovitis and restrictive fibrous periarthritis were the sequelae of secondary stifle sepsis.
Vet Rec 1987 Oct 03
PMID:Caudal cruciate ligament function and injury in the horse. 342 84

The incidence of lameness in herds visited by veterinary practitioners in winter (0.87 cases per 100 cows per month) was greater than in summer (0.71 cases per 100 cows per month). The relative proportions of leg lesions and underrun heel were higher, and those of foul-in-the-foot, interdigital hyperplasia and foreign body in the sole were lower in winter than in summer. In winter, leg lesions and aseptic laminitis were most common in cows housed in cowsheds, white line abscess in cows in strawyards and sole ulcer in cows in either cowsheds or cubicles with concrete yards. The overall incidence of lesions was lower in strawyard accommodation (0.71 cases per 100 cows per month) than in cubicles with yards (0.93 cases per 100 cows per month). Veterinary practitioners saw proportionally fewer cases of foul-in-the-foot but proportionally more cases of sole ulcer in larger than in smaller herds. The animal incidence of lameness ranged from 1.7 to 11.4 per cent among practices; in 20 practices which recorded a total of at least 100 lesions in both summer and winter there was a large variation in the proportions observed of each lesion. A principal component analysis contrasted those practices which tended to see mainly cases of white line abscess, white line separation, foul-in-the-foot and leg lesions with those which saw mainly cases of underrun heel, interdigital hyperplasia, punctured sole with pus and sole ulcer. Twenty-nine per cent of cases of underrun heel and 22 per cent of cases of both deep sepsis and interdigital hyperplasia occurred in conjunction with another lesion.
Vet Rec 1983 Nov 05
PMID:Effects of season, herd size, management system and veterinary practice on the lameness incidence in dairy cattle. 664 78

C1-Inhibitor (Berinert, C1 INH), a 104 kDa protein, inhibits complement components (C1 esterase) as well as enzymes of the contact phase of coagulation (Factor XII, Factor XI) and kallikrein, thus regulating kinin generation. C1 INH is used for the treatment of the hereditary angioneurotic edema. This paper will give a survey about the evidence in recent literature concerning the potential efficacy of the compound on other diseases associated with shock, capillary leakage and inflammation as well. In our own experiments we evaluated whether the compound could influence acute inflammatory reactions or the severe systemic inflammatory response syndrome (SIRS) as a consequence of an experimental septic shock. To prevent the sepsis-induced DIC we co-infused the thrombin inhibitors AT III or rec. hirudin in combination with C1 INH. Coinfusion of C1-inhibitor (50-200 U/kg x h) with either rec. hirudin or AT III significantly improved survival rate compared to thrombin inhibitor alone.
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PMID:Influence of C1-inhibitor on inflammation, edema and shock. 817 80

Chronic septic tenosynovitis with concurrent, associated focal osteomyelitis of the lateral proximal sesamoid bone was diagnosed in a seven-year-old thoroughbred gelding. Surgical management of this case consisted of open annular ligament desmotomy and curettage of the affected sesamoid. Following lavage of the digital sheath the incisional wound was closed but a 2 cm gap was left distally to allow for postoperative open drainage. The distal limb was bandaged and the horse treated with antibiotics and non-steroidal anti-inflammatories. Sepsis resolved and the horse made a gradual return to full work.
Vet Rec 1997 Aug 09
PMID:Septic tenosynovitis and focal osteomyelitis of the lateral proximal sesamoid bone in a thoroughbred gelding. 928 43

A four-year-old gelding was lame owing to a chronic septic common digital extensor tendon and sheath. The horse had been treated by open surgical lavage but the sepsis had recurred after three months. Physical, ultrasonographic, cytological and histological examinations confirmed chronic septic tenosynovitis and tendonitis. The entire intrathecal component of the common digital extensor tendon was resected under general anaesthesia and the synovial lining of the sheath was ablated. Postoperatively the horse regained good limb function and became sound.
Vet Rec 2000 Mar 25
PMID:Resection of the common digital extensor tendon in a gelding. 1080 83

Eight horses with synovial sepsis induced by trauma were treated by arthroscopic/tenoscopic debridement and lavage followed by the implantation of a gentamicin-impregnated collagen sponge. Seven of them responded favourably and were sound six months after treatment. The other underwent a further surgical procedure and recovered. Gentamicin-impregnated collagen sponges appear to be a safe and useful adjunct in the treatment of septic joints and tendon sheaths, and have the advantage of being bioabsorbable.
Vet Rec 2000 Aug 12
PMID:Treatment of traumatically induced synovial sepsis in horses with gentamicin-impregnated collagen sponges. 1098 61

Gentamicin-impregnated polymethylmethacrylate beads were used to treat infective arthritis in the small tarsal joints of 11 severely lame horses. Under general anaesthesia, between five and 10 beads were placed into a 7 to 8 mm tract drilled across the affected joint and, in all except one horse, they were left in place for 14 days. Two of the horses were euthanased for reasons other than persistent tarsal joint sepsis, but the other nine survived and seven of them returned to their previous level of athletic performance.
Vet Rec 2001 Mar 24
PMID:Treatment of sepsis in the small tarsal joints of 11 horses with gentamicin-impregnated polymethylmethacrylate beads. 1132 53

Sepsis induces recruitment of neutrophils and monocytes/macrophages in the lung and enhances host susceptibility to a secondary bacterial challenge. The phenotype and functions of recruited pulmonary intravascular monocytes/macrophages (PIMMs) in sepsis remain largely unknown. Therefore, we characterized PIMM recruitment and functions in a rat model of E. coli-induced sepsis. Male Sprague-Dawley rats were injected intraperitoneally with saline (n=10) and 48 hr after the saline treatment treated intravenously with either saline (n=5) or E. coli lipopolysachharide (LPS; 1.5 microg/kg body weight; n=5). A second group of 10 rats was infected intraperitoneally with E. coli (2x10(7) CFU/100 g) followed by intravenous injection of either saline (n=5) or LPS (n=5) 48 hr after the first treatment. Rats were euthanized at 6 hr after LPS treatment. Immunocytochemistry showed more PIMMs stained with ED-1 antibody, which specifically reacts with rat monocytes/macrophages, in rats infected with E. coli compared with the controls (P<0.05). LPS treatment of E. coli-infected rats increased the numbers of PIMMs (P<0.05) and induced more inflammation compared to other groups. Immuno-electron microscopy localized TNF-alpha, IL-10, and TGF-beta2 in recruited PIMMs in rats challenged with both E. coli and LPS. ELISA on lung homogenates showed higher concentrations of TNF-alpha, IL-10, and TGF-beta2 in rats treated with both E. coli and LPS compared with those treated with only LPS or E. coli (P<0.05). We conclude that ED-1-positive PIMMs are recruited in this model of sepsis and contain TNF-alpha, IL-10, and TGF-beta2.
Anat Rec A Discov Mol Cell Evol Biol 2006 Dec
PMID:Pulmonary intravascular monocytes/macrophages in a rat model of sepsis. 1707 48

Portal hypertension (PHT) is associated with a hyperdynamic state characterized by a high cardiac output, increased total blood volume, and a decreased splanchnic vascular resistance. This splanchnic vasodilation is a result of an important increase in local and systemic vasodilators (nitric oxide, carbon monoxide, prostacyclin, endocannabinoids, and so on), the presence of a splanchnic vascular hyporesponsiveness toward vasoconstrictors, and the development of mesenteric angiogenesis. All these mechanisms will be discussed in this review. To decompress the portal circulation in PHT, portosystemic collaterals will develop. The presence of these portosystemic shunts are responsible for major complications of PHT, namely bleeding from gastrointestinal varices, encephalopathy, and sepsis. Until recently, it was accepted that the formation of collaterals was due to opening of preexisting vascular channels, however, recent data suggest also the role of vascular remodeling and angiogenesis. These points are also discussed in detail.
Anat Rec (Hoboken) 2008 Jun
PMID:Hemodynamic changes in splanchnic blood vessels in portal hypertension. 1848 17

Sepsis causes significant alterations in the hepatic macro- and microcirculation. Diverging views exist on global hepatic blood flow during experimental sepsis because of the large variety in animal and sepsis models. Fluid-resuscitated clinical sepsis is characterized by ongoing liver ischemia due to a defective oxygen extraction despite enhanced perfusion. The effects of vasoactive agents on the hepatosplanchnic circulation are variable, mostly anecdotal, and depend on baseline perfusion, time of drug administration, and use of concomitant medication. Microvascular blood flow disturbances are thought to play a pivotal role in the development of sepsis-induced multiorgan failure. Redistribution of intrahepatic blood flow in concert with a complex interplay between sinusoidal endothelial cells, liver macrophages, and passing leukocytes lead to a decreased perfusion and blood flow velocity in the liver sinusoids. Activation and dysfunction of the endothelial cell barrier with subsequent invasion of neutrophils and formation of microthrombi further enhance liver tissue ischemia and damage. Substances that regulate (micro)vascular tone, such as nitric oxide, endothelin-1, and carbon monoxide, are highly active during sepsis. Possible interactions between these mediators are not well understood, and their therapeutic manipulation produces equivocal or disappointing results. Whether and how standard resuscitation therapy influences the hepatic microvascular response to sepsis is unknown. Indirect evidence supports the concept that improving the microcirculation may prevent or ameliorate sepsis-induced organ failure.
Anat Rec (Hoboken) 2008 Jun
PMID:Liver perfusion in sepsis, septic shock, and multiorgan failure. 1848 18


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