Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recurrences of CNS infarction often lead to progressive neurologic disability in sickle cell anemia. To prevent such reccurrence, a periodic blood transfusion program was begun in 1969. Currently, 27 patients are on this regimen. Before inclusion in the program, 12 patients had had one to nine CNS recurrences each. Since the program was started, two patients have had transient CNS ischemia. There were no other recurrences and none of the patients have shown progression of neurologic abnormalities. In addition, there was a striking decrease in bacterial infection and pain. We conclude that periodic transfusions are effective in preventing recurrent CNS infarction in sickle cell anemia. The benefits must be weighed against the potentially serious problem of iron overload, as evidenced by moderately elevated serum ferritin values.
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PMID:Periodic transfusions for sickle cell anemia and CNS infarction. 51 76

A 33-year-old male patient with hepatitis B surface antigen positive cirrhosis, received 2 courses of endoscopic injection sclerotherapy for bleeding esophageal varices. A Streptococcus viridans brain abscess developed 2 weeks after the first sclerotherapy (or 1 week after the second sclerotherapy). In cirrhotic patients, an increase in pulmonary vasodilatation and pulmonary arteriovenous shunting has been well recognized. Sclerosant as well as bacteria may pass through a pulmonary arteriovenous shunt and reach the brain, directly after an infection of esophageal varices. Brain ischemia and a bacterial infection may occur at the same time, this can accelerate the development of a pyogenic brain abscess. Careful observation for the early detection and treatment of infection following endoscopic sclerotherapy is essential.
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PMID:Brain abscess following endoscopic injection sclerotherapy: report of a case. 168 87

Lyophilized type I collagen (L.C.) can stimulate wound healing by recruiting a number of different cell types (i.e. platelets and macrophages) and proteins (i.e. fibronectin). Platelets and macrophages produce locally-acting growth factors that in turn induce fibroblast and epidermal migration, angiogenesis and increase matrix synthesis. Chronic leg ulcers (C.L.U.) are the end result of microvascular failure owing to ischemia and stasis. When L.C. has been used in the treatment of C.L.U. we have observed that: a) it is significantly more effective in stimulating the healing of chronic venous ulcers when compared to hydrocolloids (p less than .05), the two products being applied upon half of the same ulcer; b) in the treatment of C.L.U. due to arterial obstruction L.C. is more effective than hydrocolloids without achieving statistical significance; c) it is very effective in the treatment of C.L.U. in thalassaemic patients; d) telethermographic studies have demonstrated an increase of blood perfusion and histological studies have shown the stimulation of angiogenesis, fibropoiesis and epidermal growth; e) the application of L.C. determines the maximum obtainable increase also under conditions of proven cicatrization difficulty; and f) enzymatic degradation of L.C. has not promoted any bacterial infection and no local or generalized sensibilization phenomena have been observed. We can conclude that L.C. is a pharmacological approach to wound healing, directly interfering with cellular and non-cellular components, and significantly improves the reparative process when delayed.
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PMID:Lyophilized type-I collagen and chronic leg ulcers. 172 86

Chronic pyelonephritis (c.p.) is by definition an infectious tubulo-interstitial nephritis. It has to be differentiated from other etiologic forms of tubulo-interstitial nephritis. Therefore strict morphological criteria are needed for diagnosis. The characteristic lesion is a large cortico-medullary scar overlying a dilated chronically inflammed calyx. The macroscopic aspect and the histologic survey picture are more important than histologic details. A diagnosis on renal biopsies is therefore not warranted. Vesico-renal reflux and papillary morphology play an important pathogenetic role. Beside the more common focal scar a diffuse form of scarring can be observed. A limited number of conditions only have to be considered in differential diagnosis. The Ask-Upmark kidney seems to be a special form of c.p. related to urinary tract infection and reflux in early infancy. Pelvi-calyceal lithiasis without superimposed infection causes a picture very similar to a pyelonephritic scar. A reliable differentiation between c.p. and analgesic nephropathy may cause problems in endstage kidneys with sloughed off papillae. Various mechanisms of renal damage such as bacterial infection, immunological mediated inflammation, leakage of urinary constituents into the interstitium especially Tamm-Horsfall-protein and ischemia have to be considered. Despite the frequency of urinary tract infections chronic progressive pyelonephritis is rare. Predisposing factors are needed for progression of the disease. These include congenital or acquired urinary tract obstruction, vesico-renal reflux and papillary damage with intrarenal obstruction to the urinary flow. Other important factors are focal and segmental glomerulosclerosis and hypertension.
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PMID:[Chronic pyelonephritis and its differential diagnosis. A disease changing with time]. 248 12

Posttraumatic acute cholecystitis is an often unrecognized and potentially fatal complication seen among patients hospitalized for trauma, and differs in etiology from cholecystitis which develops de novo. The cause, although not yet clearly defined, is believed to be related to bile stasis, ischemia, bacterial infection, sepsis, the activation of factor XII, and the Shwarzman reaction. A case is described in which a 53-year-old man with pelvic fractures developed acute acalculous cholecystitis and died of multiple organ failure 3 weeks following cholecystectomy. The histopathological findings are also reported; these are most likely attributed to the Shwarzman reaction or the activation of the factor XII pathways. There has been a tendency to regard posttraumatic acute acalculous cholecystitis as induced by trauma, and calculous as mere coincidence. We believe, however, that it is not calculous but histopathological findings that determine whether acute cholecystitis following trauma was more than coincidence or just mere coincidence. Although progress in clinical care has improved the chances of survival of severely traumatized patients, posttraumatic acute cholecystitis has been increasing in frequency. We cannot be careful enough in judging the relationship of this fatal complication to the initial trauma.
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PMID:Posttraumatic acute cholecystitis. Relationship to the initial trauma. 360 14

The normal bacterial flora of the skin represents an important host defense mechanism against invasion by potentially pathogenic organisms. This flora is primarily composed of aerobic diphtheroids (Corynebacterium species), anaerobic diphtheroids (Propriono-bacterium acnes), and coagulase-negative staphylococci. Gram-negative bacilli may be present in limited numbers in intertriginous areas. Localized cutaneous infections occur in ostensibly normal hosts, often after trivial trauma, examples being streptococcal or staphylococcal impetigo, staphylococcal furunculosis, or more unusual infections due to agents such as Mycobacterium marinum. When the skin is injured more extensively by trauma, burns, ischemia with ulceration, or iatrogenic manipulations, or when host immunologic defenses are suppressed, more severe infections are likely to supervene, and the threat of systemic dissemination of infecting microorganisms increases. Cutaneous infection in immunosuppressed hosts may involve the same pyogenic bacteria that affect normal subjects or it may involve a variety of opportunistic invaders, including herpes viruses, gram-negative bacilli, mycobacteria, and deep or superficial mycoses. The skin may also be affected by infections whose primary site lies elsewhere in the body. Cutaneous manifestations may be secondary to hematogenous seeding of the causative agent or to the effects of toxins or immune complexes. Certain microbial agents may initiate a wide variety of cutaneous lesions, depending on route of infection and the status of the host. Thus, cutaneous lesions attributable to Pseudomonas aeruginosa range from "green nail syndrome" and self-limited folliculitis to ecthyma gangrenosum. Similarly, group A streptococci may produce pyoderma, cellulitis, lymphangitis, erysipelas, or scarlet fever. We recently described a syndrome of recurrent cellulitis in the saphenous vein donor extremities of patients who have undergone coronary artery bypass grafts. Most patients have associated tinea pedis. The pathophysiologic aspects of this syndrome are probably multifactorial, involving compromise of lymphatic or venous drainage, bacterial infection, elaboration of bacterial toxins, and hypersensitivity to bacterial or fungal products, or both. Coagulase-negative staphylococci are exhibiting a more prominent pathogenic potential than heretofore. When they infect immunosuppressed hosts or patients with indwelling intravascular catheters or cardiac prostheses, coagulase-negative staphylococci may cause life-threatening disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cutaneous infections: microbiologic and epidemiologic considerations. 637 67

A major determinant of survival in patients with advanced viral or bacterial infection, or following severe trauma or burns complicated by multiple organ failure, is the combination of clinical signs termed the systemic inflammatory response syndrome (SIRS). SIRS is characterized by hypotension, tachypnea, hypo- or hyperthermia and leukocytosis as well as other clinical signs and symptoms, including a depression in myocardial contractile function. Heart failure complicating systemic sepsis or other causes of SIRS is usually not accompanied by coronary artery ischemia due to hypotension, myocardial necrosis, or marked cardiac interstitial inflammatory infiltrates, and thus the cause of cardiac contractile dysfunction in this syndrome has remained unclear. However, recent evidence has implicated an endogenous nitric oxide (NO) signalling pathway within cardiac myocytes and other cellular constituents of cardiac muscle, including the microvascular endothelium, as a possible contributor to the pathogenesis of heart failure in this syndrome. Cardiac myocytes are now known to express both constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities. Activation of cNOS appears to modulate cardiac myocyte responsiveness to muscarinic cholinergic and beta-adrenergic receptor stimulation. Induction of iNOS by soluble inflammatory mediators, including cytokines, causes a marked depression in myocyte contractile responsiveness to beta-adrenergic agonists. Thus, inappropriate activation of cNOS or excessive or prolonged induction of iNOS in the myocardium may contribute to cardiac dysfunction complicating SIRS.
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PMID:Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. 753 82

Adhesion molecules are responsible for PMN-endothelial cell interactions involved in both PMN-mediated endothelial injury (e.g., after ischemia-reperfusion injury) and PMN-mediated host defense against bacterial infection. Inhibition of PMN-endothelial adherence with CD18 and P-selectin mAb has been shown to ameliorate the tissue injury resulting from ischemia and reperfusion under a variety of experimental conditions. However, interference with PMN function may result in an increased risk of bacterial infection. Previous investigations suggest that CD18 blockade can lead to increased infectious risk. Little is known of the infectious risks associated with selectin blockade. We report the effects of P-selectin blockade (using mAb PB1.3) on bacteria-induced PMN emigration into the peritoneum and subcutaneous (s.c.) tissue in rabbits. Leukocyte and PMN emigration into the peritoneum 4 h after inoculation with 10 ml of 10(9) CFU/ml Escherichia coli was significant in saline-treated animals, and not different in animals pretreated with mAb PB1.3. Similarly, the incidence and severity of abscess formation 7 days after s.c. inoculation with Staphylococcus aureus (10(7), 10(8), or 10(9) CFU) was not increased in rabbits pretreated with mAb PB1.3 compared to saline. PMN emigration to the s.c. S. aureus was also similar in both saline and mAb PB1.3-treated animals, as determined by light microscopy. We conclude that P-selectin blockade with mAb PB1.3: 1) does not interfere with acute, E. coli-induced PMN emigration into the peritoneum, 2) does not increase the incidence or severity of S. aureus abscess formation in s.c. tissue, and 3) interferes less with PMN antibacterial host defense mechanisms than inhibition of CD18-mediated PMN adherence.
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PMID:P-selectin blockade does not impair leukocyte host defense against bacterial peritonitis and soft tissue infection in rabbits. 769 61

Recent studies indicate that the mucosa of the urinary bladder may play a major role in the maintenance of normal bladder function. The mucosal surface of the urinary bladder serves as a protective layer against the irritative solutes found in the urine. The integrity of this barrier can be broken by overdistension, anoxia, detergents, alcohols, bacterial infection and by contact with agents to which the mucosa has been sensitized. In view that both anoxia and ischemia can mediate a breakdown in the role of the mucosal layer as a permeability barrier, it is reasonable to assume that this function is dependent on cellular metabolism. As an initial investigation we have compared a variety of biochemical and metabolic parameters between the mucosal layer (consisting of the lamina propria, urothelium, and any connective tissue and vascular tissue within this layer); and the muscularis layer. The results of these studies demonstrated that the rate of glucose metabolism to lactic acid (LA) of the mucosa was more than three-fold greater than that of the smooth muscle. The rate of CO2 production of the mucosa was 60% greater than that of the unstimulated smooth muscle. The maximal activity of the mitochondrial enzyme citrate synthase was significantly greater in the mucosa than in the smooth muscle, however, the activity of malate dehydrogenase was similar for both tissues. The maximal activity of the cytosolic enzyme creatine kinase was more than two-fold greater in the bladder smooth muscle than in the mucosa; although the affinities of the creatine kinase isoforms of the mucosa were significantly greater than those of the muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic studies on rabbit bladder smooth muscle and mucosa. 826 70

Effect of hepatic ischemia and reperfusion on hepatic regeneration after 70% partial hepatectomy was evaluated in rats. Total hepatic ischemia by portal triad cross clamping (15 minutes) and reperfusion (15 minutes) was repeated two times during partial hepatectomy in the PS, non-PS, and G groups. In the C group, partial hepatectomy was made as a control without ischemia and reperfusion. In order to evaluate the effect of portal pooling, portal systemic shunt (PS shunt) was made by splenic transposition to subcutaneous space in the PS group, and compared with the non-PS group. Gadolinium chloride (GdCl3), the selective blocker of Kupffer (K) cell, was intravenously administered to the rat in the G group. Hepatic regeneration rates, labelling index of liver cells, rates of bacterial infection of mesenteric lymph nodes (MLN), blood levels of endotoxin (Ex) and tumor necrosis factor-alpha (TNF) were compared. Hepatic regeneration at 28 days was suppressed by total hepatic ischemia in the non-PS group. Increased positive rates of MLN culture and blood levels of Ex showed bacterial translocation induced by the portal pooling during portal triad clamping. PS shunt reduced both bacterial translocation and the suppression of hepatic regeneration occurred in the PS group. Hepatic regeneration was not suppressed and blood TNF level did not increased in the G group by the inhibition of K cell function. In conclusion, repeated total hepatic ischemia and reperfusion induced portal pooling, bacterial translocation, and activated K cell, then inhibited hepatic regeneration after partial hepatectomy.
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PMID:[Inhibitory effect of portal pooling, bacterial translocation, and Kupffer cell activation on hepatic regeneration after partial hepatectomy by repeated portal triad cross clamping in rats]. 828 11


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