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

A common although infrequently recognized complication associated with the use of a pneumatic tourniquet is profuse bleeding from the wound after deflation of the tourniquet. The purpose of this study was to determine whether intravascular coagulation and fibrinolysis could be induced in subhuman primates by tourniquet ischemia, and whether this phenomenon could be altered by pretreatment of the animal with heparin. It was shown that, after 2(1/2) hours of tourniquet ischemia, (400 mmHg) to one lower limb, fibrinogen levels were significantly lower (p < .005), antithrombin III levels were significantly lower (p < .05), plasminogen levels were significantly lower (p < .05), fibrin split products significantly higher (p < .025) and fibrinopeptide A levels were significantly higher (p < .02) than values measured simultaneously in the control limbs. After pre-treatment with sodium heparin, 30 units/kg, there was no change in antithrombin III levels or fibrinogen levels, but fibrin split products in the experimental limbs were significantly elevated (p < .05) when compared to control limbs. In both groups the abnormal levels returned to control levels 5-30 minutes after tourniquet deflation. We conclude that intravascular coagulation and fibrinolysis develop within ischemic subhuman primate limbs during tourniquet ischemia. Pretreatment with heparin prevents the consumption of fibrinogen and antithrombin III but does not prevent the increase in fibrin split products which was observed. It is possible that intravascular coagulation and fibrinolysis contribute to post tourniquet bleeding.
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PMID:Intravascular coagulation and fibrinolysis within primate extremities during tourniquet ischemia. 11 39

A postischemic edema in hind limbs of dogs occurred after a 5 hours tourniquet ischemia. The protein distribution of edematous liquid, serum and lymph has been investigated by immunoelectrophoretic analysis. Using different identification reactions it could be demonstrated, that edematous liquid only differs from serum because of additional appearance of fibrinogen, so corresponding qualitatively and in so far estimated quantitatively to serum plasma. In connection with the osmotic pressure factors and postischemic hyperemia, as they have been demonstrated up to now, the severe changes of permeability seem to be a main factor in pathogenesis of postischemic edemas.
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PMID:[The protein distribution in the postischemic edema of dogs in reference to pathogenesis (author's transl)]. 24 Feb 20

Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.
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PMID:Cerebral and retinal vascular complications of inflammatory bowel disease. 44 68

To evaluate the biological tolerance of the human liver to prolonged warm ischemia, two groups of extensive hepatic resection for tumor were compared. Group 1 (11 patients) performed with short hepatic inflow occlusion (7 [mean] +/- 2 [SEM] minutes), and group 2 (nine patients) operated with use of complete hepatic vascular exclusion and prolonged warm liver ischemia (38 [mean] +/- 5 [SEM] minutes). Comparison of biological values, such as transaminase, bilirubin, total protein, albumin, and fibrinogen levels, the platelet count, prothrombin complex, and proaccelerin level, did not show statistically significant differences between the two groups. Therefore, the hepatic warm ischemia period may be, if needed, safely extended beyond the classical 15 minutes. It lasted 65 minutes in one case without adverse effect. These clinical observations parallel recent experimental work and should destroy the myth of the high sensitivity of the liver to warm ischemia.
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PMID:Tolerance of the human liver to prolonged normothermic ischemia. A biological study of 20 patients submitted to extensive hepatectomy. 73 77

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Coagulation mechanisms were examined in the dog after a 70 per cent hepatectomy and the additional effect of varying periods of ischemia on the liver remnant. Dogs were submitted to a 70 per cent partial hepatectomy, and the liver remnant was rendered ischemic by occluding the vascular inflow. Portal decompression during ischemia was accomplished by allowing portal venous flow through the lobes subsequently resected. Dogs in the control group, those undergoing hepatectomy alone and those undergoing hepatectomy together with 60 minutes of ischemia time exhibited a fall in hemoglobin and hematocrit values, a transient leukocytosis, a small increase in kaolincephalin clotting time and a decline in platelet count but no significant thrombocytopenia. Prothrombin time was changed in dogs undergoing hepatectomy, but this was not affected by ischemia. The characteristic rise in plasma fibrinogen postoperatively was abolished, and fibrinogen levels were lower in dogs undergoing hepatectomy alone and fell significantly in dogs subjected to 30 to 60 minutes of ischemia of the liver remnant. Factors V and VII were decreased after hepatectomy, and Factor V was more severely reduced after 30 to 60 minutes of ischemia. There was no overt bleeding tendency. In ten dogs, the liver remnant was subjected to ischemia for 75 minutes. Four of these died within three days of operation, two with severe hypoglycemia and two with postoperative bleeding. All six surviving dogs exhibited gross coagulation defects. Prothrombin time rose, kaolin-cephalin clotting time increased and platelets fell to a greater degree than in any of the other dogs. Plasma fibrinogen level showed a profound fall, as did Factor V, the magnitude of these changes being greater than after a shorter period of ischemia. Factor VII was also decreased, but this did not appear to be related to the ischemic interval. In the clinical situation in which intrinsic coagulation mechanisms are shown to be impaired, treatment with Factor V and VII concentrates may be the best way of correcting the coagulation defect.
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PMID:The mechanism of impaired coagulation after partial hepatectomy in the dog. 93 55

The division of the venous circulation in to two sectors, one constituted by the superficial and deep venous trunks (macrocirculation) and the other by the capillaries and precapillary venules (microcirculation), is surely schematical but aids the comprehension of many hemodynamic effects connected to hampered venous return and to the incompetence of the valvular devices. In fact many of the effects of stasis and venous hypertension (oedema, red cell diapedesis, skin dystrophies) cannot be explained merely by hydraulic mechanisms but require a primary alteration of the microvascular wall associated with structural changes of the perivascular connective tissue. The alterations that occur in microcirculation are of the utmost importance in the formation of the venules ulcerations. The passage of fibrinogen through large pores in the venules of the patients affected by venous hypertension derived from venous insufficiency creates a pericapillary fibrin deposition that cannot be removed because of inadequate blood and tissue fibrinolysis. This accumulation acts as a barrier to the diffusion of oxygen and other nutrients, determining a stasis dermatitis that may lead to tissue necrosis and ulceration. The more precise knowledge of the phenomena connected with the venous stasis at the level of microcirculation (pericapillary fibrin deposition, endothelial ischemia, blocked lymphatic drainage) will not only allow a deeper comprehension of the clinical signs but hopefully will lead to a more effective treatment of the postphlebitic syndrome.
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PMID:[Physiopathology of venous stasis at the microcirculation level]. 129 20

Following liver transplantation, the decision to retransplant in cases in which graft function is marginal must be taken early. Plasma coagulation factor monitoring was evaluated as an early predictor of graft failure requiring retransplantation in the first posttransplant week. Plasma levels of fibrinogen, factors V, VII, VIII, IX, antithrombin III, protein C, and plasminogen were measured in all patients at 0, 12, 24, 48, 72, 96, and 120 hours posttransplant in 46 patients who received 56 grafts and results were compared between livers that failed early (group 1) and those that functioned adequately (group 2). Six grafts were included in group 1: one patient died before retransplantation, four were retransplanted once, and one patient was retransplanted twice. Three grafts had primary nonfunction (PNF), 2 had obstructed portal veins, and 1 had a long period of warm ischemia during the initial transplant. In group 1, plasma levels of factor V were significantly lower than in group 2 at 24, 48, and 72 hours posttransplant (21.2% +/- 14.2%, 12.4% +/- 4.5%, and 13.0% +/- 5.0% v 39.1% +/- 23.9%, 48.8% +/- 31.9%, and 60.9% +/- 25.9%; P less than .05, P less than .01, and P less than .005, respectively). Similarly, plasma levels of factor VII were significantly lower in group 1 over the same period of time (7.3% +/- 2.7%, 4.2% +/- 1.8%, and 4.7% +/- 2.5% v 27.4% +/- 17.1%, 34.1% +/- 21.6%, and 34.8% +/- 18.6%, respectively; P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coagulation plasma factor levels are early indicators of graft nonfunction following liver transplantation in children. 150 Oct 1

Some mechanisms of clinical improvement of peripheral atherosclerosis were studied on the basis of changes occurred in hemorheological parameters and lipid spectrum in 107 patients with atherosclerosis obliterans of the lower extremity vessels who had undergone 166 courses (468 sessions) of therapeutical plasmapheresis. In addition to improved lower extremity blood flow in 94.8% of patients with Stage II ischemia and 78.2% with Stage III, clinically improved cerebral circulation was seen in 87.6% and clinically better coronary circulation in 85.2%. This suggests definite unique hemodynamic effects of plasmapheresis. The paper also indicates that there are at least three mechanisms providing a positive clinical effect of plasmapheresis in peripheral atherosclerosis: (1) peripheral macro- and microhemodynamic improvement due to decreased levels of plasma and perimembrane fibrinogen and increased erythrocyte deformability; (2) a decrease in thrombus risk due to lower fibrinogen levels and fibrinolytic activation; (3) monitoring risk factors of atherosclerosis due to lower levels of atherogenic lipoproteins, triglycerides, and cholesterol.
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PMID:[Mechanisms of the positive clinical effect of plasmapheresis for arteriosclerosis obliterans in the lower extremities]. 152 41

This study compared the function of reduced grafts prepared in situ or ex vivo and transplanted immediately or after 4 hr of cold storage. Measurements of acid/base balance, plasma electrolytes, albumin, and urea showed no differences between groups. There was no difference between the increase and decline of plasma AST in recipients of grafts transplanted immediately after either ex vivo or in situ reduction; the increase in plasma AST of recipients of stored grafts was up to 10-fold and persisted until the end of the study at 7 days, with some decline. Plasma fibrinogen decreased intraoperatively but levels were restored within 24 hr in all groups; plasma prothrombin and partial thromboplastin times were not significantly disturbed. The patterns of decline and return of tissue adenine nucleotides were similar in all groups. While the regenerative response measured by tissue thymidine kinase and mitotic figures was not different between the groups, comparison with results from a group of partially hepatectomized animals showed a 3-4-fold depression in response in reduced liver grafts. The contributions of the effects of ischemia, flushing, and preservation to the depressed regenerative response of reduced liver grafts need to be determined. The present studies suggest however, that with regard to functional assessment, results are not affected either by ex vivo or in situ reduction of the graft, or by cold storage for 4 hr.
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PMID:Ex vivo versus in situ resection of segmental liver grafts in pigs--a comparison in immediate and four-hour-stored grafts. 158 63


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