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

Extensive experience with replantation and transplantation surgery has accrued since the development of microvascular surgery. However, circulation often fails to return to a tissue after a temporary period of vascular obstruction, even if the vascular anastomoses are perfect. This circulation failure is known as the "no-reflow phenomenon." The authors investigated the effectiveness of fluorocarbon (FC) in preventing this condition using the free epigastric flap of the rabbit. When the flaps were immersed in oxygenated FC during the ischemic period, the survival rate of the flap was 100% and 80% in 12 and 24 hours of ischemia, respectively. These survival rates were higher than those in control animals (20%). Although further studies are necessary for clinical application, it is suggested that the FC immersion technique has a definite potential for prevention of the no-reflow phenomenon in tissue transplantation and replantation surgery.
 ...
PMID:An experimental study on the effect of fluorocarbon on the preservation of free skin flaps in the rabbit. 683 99

Small intestinal mucosal lesions are reported in clinical shock and are commonly found in experimental shock. Experimental series in which shock is induced by regional intestinal ischemia or IV infusion of live Escherichia coli in cats or by graded intestinal vascular occlusion in rats are described. In all series mucosal damage was related to pronounced hypotension or mortality. In the cat models myocardial dysfunction was demonstrated in vivo by IV volume load and recording of changes in left ventricular filling pressure as related to cardiac performance. Following intestinal ischemia in cats and intestinal vascular obstruction in rats the intestinal venous plasma was found to contain cardiotoxic factors when tested in vitro. It is proposed that the development of small intestinal mucosa lesions in shock tends to further aggravate hypotension by causing intestinal release of cardioinhibitory material.
 ...
PMID:An evaluation of the functional implications of the intestinal mucosal lesions in shock. 713 50

The effect of thrombolytic therapy is well-documented in acute myocardial infarction. In acute cerebral infarction, thrombolytic therapy has been evaluated in small series of patients. The point of thrombolytic therapy is to avoid or reduce ischemic damage of neuronal tissue by rapid arterial recanalization. In thrombolytic therapy of cerebral vascular occlusion, the pathophysiology of reperfusion needs further investigation and documentation. This review describes studies of thrombolysis in embolic stroke using animals embolized by intracarotid injections of blood clots. Vascular occlusion was demonstrated by angiography and measurement of cerebral blood flow. Thrombolytic therapy with recombinant tissue-type plasminogen activator was initiated after varying periods of time. Reperfusion, cellular function, and brain damage were examined by angiography and by clinical and pathoanatomical examination. Based mainly on results from our own investigations, the following theses concerning ischemic stroke were made: (a) Cerebral infarction caused by arterial occlusion is due to delayed, incomplete, or no reperfusion. Spasms, or hemodynamic mechanisms, seem to be of only minor importance. (b) Early thrombolytic therapy in animal models increases the degree of reperfusion and reduces brain damage, clinical deficits, and mortality. (c) Early arterial reperfusion reduces cerebral infarction and related edema. With early reperfusion, the extent of brain damage correlates to the length of the delay from onset of ischemia. (d) Cerebral stunning is caused by arterial occlusion followed by very early spontaneous or induced reperfusion, as neurons temporarily lose their functional capabilities without dying. (e) Multiple embolic microclots in experimental stroke result in more brain damage than a single macroclot, and with clots the extent of brain damage is dependent on the structural composition and volume of emboli. (f) The ability to recanalization in experimental embolic stroke is related to the amount of red cells in the emboli and inversely related to the volume of emboli and to the fibrin content and density of the clots. (g) Infarct-limiting effects in experimental stroke can be obtained by ischemic neuroprotectants or by hypothermia, either alone or with thrombolytic therapy, which then reduces brain damage further.
 ...
PMID:Thrombolytic therapy in experimental embolic stroke. 781 66

Twenty-six hepatic resections were performed using vascular clamping lasting more than one hour. The average duration of continuous normothermic ischemia was 67.0 +/- 7.5 minutes (plus or minus standard error of the mean) (range of 60 to 85 minutes). Vascular occlusion consisted of simple portal triad clamping in 14 patients and of hepatic vascular exclusion in 12. Extensive hepatectomy was performed upon more than 80 percent of the patients. One postoperative death was recorded. Extensive complications occurred in eight patients, including one case of hepatic failure. Postoperative changes in hepatic function tests were mild and transient. The rate of postoperative complications was higher in the group of patients with chronic hepatic disease (77.8 versus 11.8 percent, p < 0.005). Prolonged hepatic ischemia should not be considered a risk factor in patients with normal livers, whereas morbidity and mortality rates are seriously affected by the presence of chronic hepatic disease.
 ...
PMID:Hepatic resection with ischemia of the liver exceeding one hour. 816 81

The relationship between blood flow and metabolism was studied in halothane-anaesthetized, normothermic rats submitted to 30 min global ischemia by four-vessel occlusion. Phosphocreatine (PCr), ATP, intracellular pH and intracellular magnesium (pMg) were measured by 31P NMR spectroscopy, and blood flow by laser Doppler flowmetry. Prior to ischemia the PCr/ATP ratio of fully relaxed spectra was 2.4 +/- 0.3, intracellular pH was 7.26 +/- 0.15 and pMg was 3.26 +/- 0.13. Vascular occlusion led to complete cessation of blood flow in four out of eight rats, and to incomplete ischaemia (< 10% of control) in the other four animals. During vascular occlusion EEG flattened and energy metabolism broke down in all but one animal with a residual blood flow of 8% of control. pH declined to 6.70 +/- 0.08. The speed of electrophysiological and metabolic recovery after 30 min ischemia varied considerably from animal to animal. Variability depended mainly on the recirculation delay (i.e., the interval from vascular release to normalization of blood flow) but was independent of residual blood flow during ischemia, pre-ischemic glucose, ischemic or post-ischemic acidosis, or the degree of post-ischemic hypoperfusion. After 3 h recirculation PCr and intracellular pH returned to normal but pMg was slightly increased, and ATP was reduced by up to 50% in all animals except the rat with incomplete breakdown of energy metabolism during ischemia. The dissociation between PCr and ATP is attributed to a loss of total adenylate, the severity of which depends on the quality of post-ischemic recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Simultaneous 31P NMR spectroscopy and laser Doppler flowmetry of rat brain during global ischemia and reperfusion. 849 45

This study investigated the vascular effect of ferromagnetic obstruction of cochlear blood vessels in the guinea pig using dual-channel laser Doppler flowmetry. To improve this technique, we tested new types of magnets and iron spheres. In so doing, the cochlear temperature was lowered selectively and general hypothermia was avoided. The success of vascular impairment in the inner ear was found to depend on the experimental conditions used. Given normothermic conditions (38 degrees C body temperature), a clear reduction in cochlear blood flow (CBF) was found in only about 30% of the animals tested when an aluminium-nickel-cobalt alloy magnet and carbonyl iron spheres were used, while this ratio increased to about 80% under general hypothermia (33 degrees C). Using a stronger neodymium-iron-boron magnet and smaller-sized iron spheres, we found the success of vascular obstruction to be approximately 70% under normothermia and 100% with local hypothermia (to 33 degrees C) of the cochlea. Although the extent of vascular impairment revealed a considerable interindividual variation, the present findings demonstrate that ferromagnetic intervention in CBF with dual-channel laser Doppler flowmetry can be used to investigate the effect of quantified cochlear ischemia on inner ear physiology in the guinea pig model and test various therapeutic strategies.
 ...
PMID:Laser Doppler measurements of inner ear blood flow during experimental thrombosis of cochlear blood vessels in the guinea pig. 906 62

Ischemia is known to be a cause of hepatocellular apoptosis and atrophy in experimental animals, but the effect of vascular obstruction on such lesions in the normal or cirrhotic human liver has not been studied. The purpose of this study was to investigate the role of ischemia in the development of apoptosis, atrophy, and nodular hyperplasia in cirrhotic and noncirrhotic human livers. Apoptosis, focal atrophy, and nodular hyperplasia were semiquantitated in 203 liver specimens obtained at transplantation, segmental resection, or autopsy. These parameters were correlated with etiology, stage, activity, and acute and healed portal vein thrombosis (PVT). Large numbers of apoptotic cells were found in livers with acute PVT (17.2/medium-power field [MPF]) and in infarcts of Zahn caused by obstruction of portal veins (PVs) by tumor (16.4/MPF). Smaller numbers of apoptotic cells were found in cirrhosis of various etiologies (3.8-10.0/MPF) and rarely in normal livers (0.16/MPF). Evidence of healed PVT was found in 47% of cirrhotic livers and was associated with nodular hyperplasia (58% vs. 32%, P < .01) and focal atrophy (79% vs. 49%, P < .002). Apoptotic cells were found equally in those with and without healed PVT (40% vs. 38%, not significant). These observations suggest that apoptosis is a transient response to acute ischemia and that atrophy and nodular hyperplasia are chronic responses to ischemia. Vascular obstruction may be an important cause of the apoptosis and atrophy, which are found in nodular regenerative hyperplasia (NRH), infarct of Zahn, chronic hepatitis, and cirrhosis.
 ...
PMID:Role of ischemia in causing apoptosis, atrophy, and nodular hyperplasia in human liver. 925 44

We tested the hypothesis that endothelial nitric oxide synthase (eNOS) modulates angiogenesis in two animal models in which therapeutic angiogenesis has been characterized as a compensatory response to tissue ischemia. We first administered L-arginine, previously shown to augment endogenous production of NO, to normal rabbits with operatively induced hindlimb ischemia. Angiogenesis in the ischemic hindlimb was significantly improved by dietary supplementation with L-arginine, compared to placebo-treated controls; angiographically evident vascularity in the ischemic limb, hemodynamic indices of limb perfusion, capillary density, and vasomotor reactivity in the collateral vessel-dependent ischemic limb were all improved by oral L-arginine supplementation. A murine model of operatively induced hindlimb ischemia was used to investigate the impact of targeted disruption of the gene encoding for ENOS on angiogenesis. Angiogenesis in the ischemic hindlimb was significantly impaired in eNOS-/- mice versus wild-type controls evaluated by either laser Doppler flow analysis or capillary density measurement. Impaired angiogenesis in eNOS-/- mice was not improved by administration of vascular endothelial growth factor (VEGF), suggesting that eNOS acts downstream from VEGF. Thus, (a) eNOS is a downstream mediator for in vivo angiogenesis, and (b) promoting eNOS activity by L-arginine supplementation accelerates in vivo angiogenesis. These findings suggest that defective endothelial NO synthesis may limit angiogenesis in patients with endothelial dysfunction related to atherosclerosis, and that oral L-arginine supplementation constitutes a potential therapeutic strategy for accelerating angiogenesis in patients with advanced vascular obstruction.
 ...
PMID:Nitric oxide synthase modulates angiogenesis in response to tissue ischemia. 961 28

Acute renal failure (ARF) is characterized by an acute decrease in glomerular filtration rate (GFR). ARF complicates 4% to 23% of intensive care unit admissions, and is associated with a mortality of approximately 50% among critically ill patients. In the intensive care setting the term ARF is usually applied to acute tubular necrosis (ATN), a form of intrinsic ARF caused by ischemia or nephrotoxins. Pathophysiological mechanisms involved in the decline in GFR include tubular obstruction caused by detachment of tubular epithelial cells from the basement membrane and back-leak of glomerular filtrate as a consequence of disruption of the epithelial cell layer. Vascular mechanisms involved in the pathophysiology of ATN are vasoconstriction due to an imbalance between vasoconstrictive and vasodilatory mediators and vascular obstruction caused by cell aggregation. Currently, there is no real time method to monitor renal function comparable to the real time monitoring of blood pressure or arterial oxygen saturation. Urinary output does not reflect glomerular filtration which may be critically reduced despite normal urine volumes and creatinine clearance still provides the clinically most applicable estimate of GFR. Tubular function can be assessed using the fractional excretion of sodium or the ratio of urinary and serum osmolality; both parameters can be obtained from spot samples of urine and serum and no urinary sampling period is necessary. However, both parameters are strongly affected by the administration of loop diuretics and high fluid and sodium inputs which are common in the intensive care unit. We determined the day to day variability of creatinine clearance, fractional excretion of sodium and the urinary to serum osmolality ratio in critically ill patients without renal dysfunction (i.e. creatinine clearance in the normal range) and found differences of 16% for creatinine clearance, 79% for fractional excretion of sodium and 22% for urinary to serum osmolality ratio. Treatment of ARF is mainly supportive and there is no clinically accepted therapy that attenuates the course of ATN. Treatment of the underlying disease and renal replacement therapy are the main options for the treatment of patients with ARF. In critically ill patients continuous venovenous hemo(dia)filtration is the first choice because it provides more hemodynamic and metabolic stability than intermittent therapy. Acute life-threatening hyperkalemia is an indication for intermittent hemodialysis because of the higher efficacy of dialysis in the clearance of low molecular weight substances.
 ...
PMID:[Acute kidney failure. Physiopathology--clinical diagnosis--therapy]. 1084 May 48

The clinical presentation of mesenteric ischemia depends on the site, grade, and cause of vascular obstruction; the degree of collateralization; and the stage of disease. Patients in the early stages of ischemia typically have abdominal pain out of context with an unimpressive abdominal examination. It is during this stage that medical and endovascular techniques can be most effective. After signs of peritonitis are present (signaling bowel infarction), surgical exploration and bowel resection are necessary. Chronic mesenteric ischemia induced by stenotic arteriosclerosis should be treated with percutaneous transluminal angioplasty and stenting (PTAS). Chronic mesenteric arterial occlusions are better handled with bypass surgery. Acute embolic or thrombotic ischemia is surgically treated after medical resuscitation. Endovascular techniques may be applicable in selected patients (usually in those with subacute symptoms), but thrombolytic therapy should be avoided if intestinal infarction is suspected. Non-occlusive mesenteric ischemia requires a rapid correction of the predisposing hypotension or sepsis followed by papaverine infusion into the superior mesenteric artery. Celiac artery compression syndrome requiring treatment is best treated with surgical release of the median arcuate ligament; PTAS should not be performed. Mesenteric venous occlusion should be treated with anticoagulation. Surgical exploration and bowel resection is necessary in patients presenting with acute signs and symptoms, reserving thrombolytic therapy for early, mildly symptomatic, thromboses in whom there is no contraindication to thrombolysis.
 ...
PMID:Mesenteric Vascular Disease. 1134 65


<< Previous 1 2 3 4 5 Next >>