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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When keratome-sliced pig epidermis was floated on Hank's balanced salt solution, we observed a rapid decrease in the intracellular level of cyclic GMP. A portion of the lost cyclic GMP was detected in the incubation medium. When the epidermis was kept in air at room temperature, the cyclic GMP level also decreased rapidly but to a lesser degree. Incubating the epidermal slice at 37 degrees C in Hank's balanced salt solution with the addition of 3-isobutyl-1-methyl xanthine (IBMX) prevented the decrease. Also, after the cyclic GMP level had fallen, it could be raised to be the in vitro level by the addition of IBMX. Increased amounts of cyclic GMP were detectable in the medium in this case. These data indicate that the decrease in cyclic GMP in ischemic epidermis is due to sudden activation of epidermal cyclic GMP-phosphodiesterase and also in part due to leakage of cyclic GMP extracellularly. In contrast to the rapid decline in the cyclic GMP level, ischemia caused a rapid and transient increase in epidermal cyclic AMP. This confirms previous data by ourselves and by others (Br J Dermatol 92: 249-254, 1975; J Invest Dermatol 68:125-127, 1977). These "ischemic effects" must be avoided in order to measure the "in vivo level" of cyclic nucleotides in epidermis.
J Invest Dermatol 1979 Sep
PMID:Cyclic GMP System in epidermis: I. Effect of ischemia. 8 73

Reactive hyperemia following ischemia in cutaneous tissue of human fingers was studied in 6 normal persons and 9 patients suffering from generalized scleroderma. Ischemia lasting 6 or 12 min was induced by inflating a cuff placed around the proximal phalanx to 300 mm Hg. Blood flow was measured by the local atraumatic 133Xenon wash-out technique. The following parameters were calculated: (1) Maximum blood flow was calculated from the steepest part of the wash-out curve following release of the cuff. (2) Excess cumulative blood flow, i.e., the integrated blood flow from release of cuff until preischemic blood flow values were obtained, minus preischemic blood flow times duration of ischemia. (3) Repayment, i.e., excess cumulative blood flow in percent of preischemic blood flow times duration of ischemia. Maximum blood flow, excess cumulative blood flow and repayment was decreased in the patients compared to normals. This might be due to structural changes of the blood vessel walls and/or functional changes of the vascular smooth muscle cells in scleroderma.
J Invest Dermatol 1978 Oct
PMID:Reactive hyperemia in cutaneous tissue in generalized scleroderma. 35 21

In this paper the authors try to specify the leg ulcers physiopathology. They have first studied the vascular deficits, and they are able to conclude that this deficit is not the only factor responsible for the thrombosis. They try to rediscover the factors which could lead to the thrombosis, on the created local conditions (circulatory slackening, cooling, ischemia), by using clinical and biological "check-ups" as well as an exploration of the clotting. In many patients we find an anomaly such as: clotting "check-ups" disturbance, thrombocyte hyperaggregability, fibrinolysis deficit, antithrombin III deficit, cryoprecipitate, circulating immune complexes, hepatic "check-up" alteration. It is difficult to establish an accurate relation between these anomalies and a thrombosis but the frequent existence of such anomalies makes us think that they play a part in the ulcerations coming-up.
Ann Dermatol Venereol
PMID:[Leg ulcer. Vascular and thrombosis factors. Each responsibility of those factors? (author's transl)]. 50 59

On electron microscopy of the endothelial cells of a patient with cutaneous and CNS symptoms of malignant atrophic papulosis, paramyxovirus-like particles could be seen in the cytoplasm. These particles were interpreted as degenerative changes that were due to ischemia. Coagulation studies showed increased thrombocyte aggregation, and treatment with the platelet-suppressive drugs, aspirin and dipyridamole, was instituted. This treatment resulted in a normal thrombocyte aggregation after eight months and complete clinical remission, which still persisted four months after cessation of therapy.
Arch Dermatol 1978 Nov
PMID:Malignant atrophic papulosis: treatment with aspirin and dipyridamole. 71 20

The endogenous level of epidermal cyclic AMP does not remain constant but increases rapidly and transiently after removal of the tissue; this is known as the "ischemia" effect. UVB-irradiated epidermis which shows increased beta-adrenergic response revealed an increased ischemia effect, while psoriatic involved epidermis which shows decreased beta-adrenergic response revealed a decreased ischemia effect. Because of the similar rise-and-fall pattern between the ischemia effect and the beta-adrenergic response, the mechanism of the ischemia effect was investigated, especially in terms of the beta-adrenergic relationship. The ischemic rise of epidermal cyclic AMP was well preserved after 6 h pretreatment at 4 degrees C, and, following the pretreatment, the skin markedly increased its cyclic AMP level by the 37 degrees C treatment with 1 mM isobutylmethyl xanthine. The addition of propranolol or cimetidine at the time of 37 degrees C treatment (following the 4 degrees C pretreatment) had no effect on the ischemia effect; both skin groups markedly increased their cyclic AMP levels to an extent similar to that of the control skin. However, the addition of propranolol at the time of both preincubation (at 4 degrees C) and incubation (at 37 degrees C) markedly decreased the ischemic rise of cyclic AMP. Similar treatment by cimetidine had no effect on the ischemia effect. There was no significant difference in cyclic AMP phosphodiesterase activities among skin groups by propranolol or cimetidine pretreatment. These results indicate that the so-called ischemic rise of epidermal cyclic AMP is actually the beta-adrenergic adenylate cyclase-dependent process. Our results also indicate that the magnitude of the "ischemic" rise of cyclic AMP is generally parallel to the beta-adrenergic responsiveness of epidermis.
J Invest Dermatol 1986 Mar
PMID:"Ischemic" rise of epidermal cyclic AMP is a beta-adrenergic adenylate cyclase-dependent process. 242 5

The case of a woman with systemic lupus erythematosus with unusual clinical, cutaneous and biologic features and lupus anticoagulant is presented. According to the literature this association is not fortuitous: a new syndrome characterized by the presence of a subgroup of antiphospholipid antibodies has been recognized. The cutaneous symptoms of this syndrome include: leg ulcers, livedo reticularis, widespread cutaneous necrosis and distal cutaneous ischemia. In our patient a nearly complete picture of the clinical and biologic features of this syndrome, including a characteristic retinal vein thrombosis is present.
G Ital Dermatol Venereol 1989 Mar
PMID:[Clinical manifestations associated with the presence of lupus anticoagulant]. 250 30

Intermittent digital ischemia is frequently resistant to therapy despite various treatment modalities. Recent studies have reported the successful treatment of intermittent digital ischemia with prostaglandin infusion therapy. We present a severe case of intermittent digital ischemia associated with mixed connective tissue disease, responsive to prostaglandin E1 infusion therapy.
J Am Acad Dermatol 1989 May
PMID:Prostaglandin infusion therapy for intermittent digital ischemia in a patient with mixed connective tissue disease. Case report and review of the literature. 265 23

The first application of human in vivo phosphorus (31P) magnetic resonance spectroscopy to analysis of skin metabolism is presented. Our results confirm that phosphocreatine is a major energy phosphometabolite in human skin. Human in vivo 31P spectroscopy utilizing a skin coil designed in our laboratory can have clinical applications in cutaneous surgery and clinical dermatology, and will facilitate understanding of the pathophysiology of skin disease. In vitro experiments with fresh human skin indicate that complete utilization of phosphocreatine is followed by utilization of adenosine triphosphate (ATP) molecules during ischemia. These experiments also suggest that the majority of phosphocreatine in human skin is localized in epidermal and papillary dermis.
J Dermatol Surg Oncol 1989 Nov
PMID:Human in vivo 31P spectroscopy of skin: potentially a powerful tool for noninvasive study of metabolism in a cutaneous tissue. 280 89

The clinical and histopathologic findings in 13 patients with lipomembranous changes in the subcutaneous adipose tissue as part of the inflammatory reaction are presented. Nine patients had clinical evidence of vascular disease and four had clinical evidence of connective tissue disease. Histopathologic evidence of endarteritis obliterans, venous stasis, and hemorrhage was present in more than half the patients, and the clinical lesion of liposclerosis was frequently present. These findings suggest that the histologic changes of lipomembranous panniculitis may be the result of an inflammatory reaction in patients who have the liposclerosis of venous insufficiency with connective tissue disease or previous leg ischemia or both.
J Am Acad Dermatol 1988 Jul
PMID:Lipomembranous changes in chronic panniculitis. 304 17

Two patients with the lupus anticoagulant exhibited unusual cutaneous manifestations. They both fulfilled four criteria for systemic lupus erythematosus and had experienced deep venous thrombosis. The first patient suffered from a leg ulcer that resembled a pyoderma gangrenosum. The second patient presented erythematous and purplish macules on the fingertips. The histologic studies showed only microthrombosis in the dermal vessels without vasculitis, although such lesions in systemic lupus erythematosus are usually attributed to vasculitis. The association of these cutaneous lesions with lupus anticoagulant has never been reported. It is likely that this association is not fortuitous. After a review of the literature, it seems possible to individualize a new syndrome characterized by the presence of a subgroup of antiphospholipid antibodies. Thrombosis, spontaneous abortions, neurologic manifestations, pulmonary hypertension, positive results of a Coombs' test, and thrombocytopenia can be included in this syndrome, which overlaps with systemic lupus erythematosus. Certain cutaneous symptoms are associated with the presence of lupus anticoagulant or other antiphospholipid antibodies: leg ulcers, distal cutaneous ischemia, widespread cutaneous necrosis, and livedo. They can be considered as the dermatologic manifestations of this syndrome.
J Am Acad Dermatol 1986 Aug
PMID:Cutaneous manifestations associated with the presence of the lupus anticoagulant. A report of two cases and a review of the literature. 309 56


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