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)

Between 1983 and 1986, 23 athletes were evaluated for arm and hand complaints. Eleven players had symptoms of thoracic outlet compression. Severe arm fatigue (eight patients) and finger ischemia (three patients) were the presenting symptoms. In the remaining 12 athletes, symptoms of hand ischemia were predominant. Noninvasive testing with Doppler ultrasonography and duplex scanning (positional testing and finger systolic pressure recording) and cold immersion were used to aid in diagnosis. In the 11 athletes with thoracic outlet compression, arteriography confirmed the finding with compression of the subclavian artery in five, the axillary artery in one, both subclavian and axillary arteries in two, posterior humeral circumflex artery in one, and subclavian aneurysm in two. Compression of the suprascapular artery was identified in four, the subscapular artery in two, and the posterior humeral circumflex artery in one. Thrombosis of a first baseman's ulnar artery and occlusion of the palmar arch in a frisbee player were documented by arteriography. Decompression of the thoracic outlet consisted of anterior scalenectomy in five, pectoralis minor muscle division in one, and resection of both muscles in two. Removal of cervical rib with interposed vein graft was performed in the two players with arterial aneurysm. Hand ischemia in the remaining athletes was treated conservatively with Dextran-heparin infusion for acute ischemia. Repeat noninvasive study of all players demonstrated absence of compression in their playing position, and all have resumed their playing careers. Hand ischemia in athletes can be evaluated noninvasively and treated conservatively. Resection of hypertrophied muscles to decompress the thoracic outlet together with release of branch artery compression in selected athletes promotes perfusion to arm and shoulder muscles and helps to avoid the catastrophic complication of repetitive trauma leading to sudden arterial thrombosis.
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PMID:Upper extremity arterial injury in athletes. 291 27

Reperfusion injury following prolonged ischemia is thought to be caused primarily by microvascular failure. The aim of the present study was to investigate whether prophylactic isovolemic hemodilution with Dextran 60 (hct 30%) could improve microvascular perfusion after 4 h of pressure-induced ischemia in skeletal muscle. In 28 Syrian golden hamsters (6-8 weeks/60-80 g b. wt.) a dorsal skinfold chamber and permanent arterial and venous catheters were implanted under Nembutal anesthesia (50 mg/kg b. wt.). Following a recovery period of 48 h pressure-induced ischemia was applied to the skeletal muscle within the skinfold chamber by means of a transparent stamp. Quantitative analyses of microhemodynamics were performed in the awake animal prior to and 15 min, 1, 2, 4 and 24 h after ischemia using vital fluorescence microscopy. In non-treated animals, functional capillary density decreased after 4 h of ischemia to 30% of the initial values (P less than 0.001); after 24-h reperfusion only 50% of the initially perfused capillaries were reperfused (P less than 0.001). The heterogeneity of functional capillary density increased after ischemia to a maximum of 2.19 +/- 0.94 as compared to 0.48 +/- 0.11 prior to ischemia. Capillary RBC-velocity suffered a marked reduction in the early reperfusion phase and did not recover up to the 24-h observation time. In contrast, prophylactic isovolemic hemodilution was associated with only a small and reversible reduction of functional capillary density after 4-h ischemia. At 24-h reperfusion 90% of the initially perfused capillaries were reperfused. Capillary RBC-velocity was reduced in the early reperfusion phase, but returned to normal values within 24 h. Thus, prophylactic isovolemic hemodilution resulted in a marked reduction of microvascular reperfusion failure in skeletal muscle. A hematocrit lower than normal prior to ischemia provides better conditions for capillary reperfusion after prolonged ischemia.
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PMID:Quantitative analysis of microcirculatory disorders after prolonged ischemia in skeletal muscle. Therapeutic effects of prophylactic isovolemic hemodilution. 342 Feb 98

A technique for producing a reliable, clinically applicable, and highly reproducible canine model of nonocclusive mesenteric ischemia was developed. Following left thoracotomy in 10 dogs, a 1 mm diameter soft polyethylene tube was inserted into the pericardial space via a small puncture site. This tube was sealed in place with cyanoacrylate tissue adhesive. A solution of 10% Dextran 40 in saline was infused into the pericardial space until a 50% reduction (as monitored by electromagnetic flowmeter) in superior mesenteric artery flow (SMAQ) was obtained. Without additional intrapericardial infusion of the Dextran solution, SMAQ was reduced 51 +/- 4% to 54 +/- 3% of control values during a 60 minute post-tamponade observation period. During the same time. Cardiac output was depressed between 40 +/- 8% and 54 +/- 3%, and right atrial pressure remained elevated between 164 +/- 15% and 171 +/- 15%. Systemic arterial pressure initially dropped 28 +/- 5% but compensated to within 11 +/- 5% of pre-tamponade level at 60 minutes. The stability of this model is well suited for evaluating new experimental diagnostic and therapeutic procedures.
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PMID:A reproducible canine model of nonocclusive mesenteric ischemia. 617 68

Postoperative abdominal adhesion formation can undo the reconstructive work of the infertility surgeon. Adhesions can form in as little as three hours after surgery. Most adhesions are transient and lyse spontaneously within 72 hours of surgery. Such factors as tissue trauma, anoxia and ischemia cause a reduction in plasminogen activator activity that is strongly correlated with the persistence and progression of postoperative adhesions. Adhesions can be prevented by a proper and meticulous surgical technique emphasizing preservation of tissue without abrasion, anoxia or ischemia. Dextran, antiprostaglandins, antibiotics, steroids, antihistamines, anticoagulants and enzymes have various roles. Our current regimen involves Hyskon, Motrin and deoxycycline.
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PMID:Formation and prevention of postoperative abdominal adhesions. 672 92

Acute hemorrhage in premature infants occurs as the result of obstetrical complications, birth trauma, or operative procedures. This study evaluates the response of the preterm piglet to acute hemorrhage and resuscitation. Piglets delivered by Caesarean section 7-14 days preterm underwent acute arterial/venous hemorrhage (20 cc/kg). At 0, 15, and 60 min after hemorrhage, hemodynamic parameters and regional blood flows (reference organ technique) were measured. Animals were then resuscitated with shed blood (20 cc/kg), crystalloid (60 cc/kg), or colloid (dextran 40, 20 cc/kg) with study parameters obtained 30 min later (statistical analysis by ANOVA). Significant decreases in blood pressure (BP) and cardiac output (CO) occurred after hemorrhage. BP and CO were reestablished to near control levels following resuscitation with blood and crystalloid. Dextran failed to return BP to baseline; however, it resulted in CO 1.7 x control. Heart and CNS blood flow were not significantly influenced by hemorrhage; however, dextran increased flows to these organs significantly above control levels. In the kidney and small bowel, flows decreased significantly following hemorrhage; blood and crystalloid restored flows to near baseline, while dextran resulted in flows significantly greater. In summary, the preterm piglet responds to hemorrhage with maintenance of blood flow to the heart and brain and significantly decreased flows to the kidney and small intestine. Flows following resuscitation with blood and crystalloid are comparable to those in control. Dextran resuscitation resulted in flows significantly greater than baseline; this response might be detrimental with ongoing hemorrhage and/or prolonged ischemia.
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PMID:Regional blood flow redistribution in preterm piglets with hemorrhage and resuscitation. 763 Jan 33

Optimal techniques of heart-lung preservation are yet to be defined. The aim of this study was to develop, in a canine model, a method of heart-lung preservation which would permit distant procurement of the organs. The animals were divided into 2 groups. In the experimental group (N = 6) the method of preservation consisted of cold cardioplegic arrest of the heart with St. Thomas' Hospital solution containing superoxide dismutase, catalase and deferoxamine, followed by cold pulmonary artery flush with modified Euro-Collins solution to which prostaglandin E1, superoxide dismutase, catalase, deferoxamine and Dextran 40 were added. Following harvesting, the heart-lung block was stored for 8 hours in cold (4 degrees C) Euro-Collins solution containing superoxide dismutase, catalase, deferoxamine, lactobionic acid, raffinose, mannitol, Dextran 40, magnesium sulfate, insulin and penicillin. In the control group (n = 6), the heart-lung block underwent the same treatment as the experimental group except that lactobionic acid, raffinose and insulin were omitted from the storage solution, and that oxygen radical scavengers were excluded from the cardioplegic, pneumoplegic and storage solutions. Histologic and electron microscopic examinations of heart-lung specimens taken before and after 8 hours cold storage of the organs suggested that our preservation technique may be effective in preventing ischemia-induced injury.
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PMID:Heart-lung protection from ischemic injury during 8 hour hypothermic preservation. 771 31

The aim of this study was to determine whether the formation of edema that occurs secondary to the neutrophil-dependent increase in microvascular permeability contributes to the genesis of no-reflow in postischemic skeletal muscle. To address this issue, four experimental approaches were used. In the first group, capillary perfusion was assessed in nonischemic canine gracilis muscles in which interstitial fluid volume was increased to a level similar to that in postischemic muscle. In the second and third groups, edema formation was prevented in postischemic skeletal muscles by administration of phalloidin or a hypertonic hyperosmotic saline-dextran solution (HSD; 7.5% saline-6% Dextran 70), and the extent of capillary no-reflow was assessed. In the final group of experiments, a monoclonal antibody (MAb) that binds to the common beta-subunit of the leukocyte integrin CD11/CD18 (MAb IB4) was administered after the development of postischemic edema, and capillary perfusion was determined. Formation of edema in nonischemic preparations and ischemia-reperfusion (I-R) were associated with marked reduction in the number of patent capillaries per fiber (1.2 +/- 0.1 and 0.4 +/- 0.1, respectively) compared with nonedematous nonischemic controls (2.5 +/- 0.3). Treatment with phalloidin or HSD prevented edema formation and attenuated the reduction in the number of patent capillaries per fiber (1.62 +/- 0.2 and 1.71 +/- 0.2, respectively) induced by I-R, whereas administration of MAb IB4 after the formation of edema in reperfused muscles failed to limit capillary no-reflow (0.5 +/- 0.1 patent capillaries/fiber).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Leukocyte adhesion, edema, and development of postischemic capillary no-reflow. 794 78

Mucosal injury caused by ischemia and reperfusion has been well documented with the small intestine, but little is known about the colon. In the present study, the effect of warm and cold ischemia on the canine colon was studied and compared to that on the small intestine. After in situ flushing, the small intestine and the colon from six beagle dogs were removed and stored for 0.5, 1.5, and 3 hr at 37 degrees C (warm ischemia) or for 1, 6, 12, 24, 36, and 48 hr at 4 degrees C (cold ischemia). Electrophysiology, permeability, biochemistry, and histopathology of the specimens at each ischemic period and after reperfusion in the Ussing chamber were determined. Warm and cold ischemia induced duration-dependent suppression of electrophysiology in both organs, but the colonic mucosa retained higher activity of absorptive enterocytes and cryptic cells than the small intestine. Only the colon showed increased permeability of FITC-conjugated Dextran from the mucosal surface to the submucosal layer after prolonged ischemia. Changes in adenine nucleotides and purine catabolites were not markedly different between the organs. Histopathologic abnormalities during ischemia and after reperfusion were more serious with the small intestine than with the colon. Compared to warm ischemia, hypothermia lessened or delayed these morphofunctional derangements in both organs, which became universally worsened after reperfusion. Colonic mucosa receives morphofunctional derangements from ischemia and reperfusion, but the severity of the damage was much less severe in the colon than in the small intestine.
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PMID:Effect of ischemia on the canine large bowel: a comparison with the small intestine. 860 7

We report a case of the heparin-induced thrombocytopenia and thrombosis syndrome presenting with acute ischemia of a lower limb. The patient was successfully treated by withdrawal of heparin products, intraarterial urokinase, and platelet anti-aggregation therapy consisting of Dextran and aspirin.
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PMID:The heparin-induced thrombocytopenia and thrombosis syndrome: treatment with intraarterial urokinase and systemic platelet aggregation inhibitors. 866 73

Pulmonary endothelial cells are known to be fundamental for lung preservation and one of the most serious limiting factors observed during transplantation is the stress to which these cells are subjected. On this premise, strenuous efforts should be made to select and employ the preservation solution best able to prolong ischemia time and thus prevent cytotoxic effects. The aim of this study was to identify the solution with minimum toxicity on endothelial cells. For this purpose, we analysed the noxious effect of solutions such as Euro Collins (ECS), Belzer (UWS) and Low-potassium Dextran (LPD) on endothelial cells after 12 hours of incubation at 10 degrees C. For each solution, we examined the modifications produced on the nuclei, mitochondria and cellular wall of human pulmonary-artery endothelial cells by transmission electron microscopy and recorded the results on an ultrastructural grading scale. As regards morphological alterations incompatible with cell life, the most cytotoxic solution proved to be ECS. UWS and LPD, on the contrary, appeared to preserve cells relatively well, and no perceptible difference was observed between the two solutions. In conclusion, it is interesting to note that although ECS is widely used for lung preservation, the results of our study indicate that a 12 hours at 10 degrees C in this solution may exert adverse effect on pulmonary endothelial cells.
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PMID:Morphological changes of human pulmonary-artery endothelial cells after 12-hours hypothermic storage in organ-preservation solutions. 888 90


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