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

Twelve patients with isolated extremity injuries had 14 compartment syndromes of the feet. An interstitial pressure of more than 30 mm of mercury in either the central or interosseous compartment was considered pathologic and was treated by fasciotomy, performed dorsally in nine feet and medially in five. Open reduction of fractures amenable to internal fixation (eight tarsometatarsal, three calcaneus, and one metatarsal) was performed after completion of the fasciotomies. The fasciotomy wounds were covered by primary split-thickness skin excision (three), delayed split-thickness skin grafting (eight), and delayed primary wound closure (three). Patients were evaluated at a mean of 22 months (range, 17-36 months) after injury, and the examination was directed specifically toward symptoms and signs of myoneural ischemia. Absolute compartment pressure measurements are more accurate than clinical findings in the diagnosis of a compartment syndrome of the foot. Fasciotomy may be performed medially or dorsally, depending on the configuration of the pattern of fracture or dislocation. To ensure satisfactory results, all compartments should be decompressed, and the pressures remeasured after the completion of fasciotomy.
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PMID:Management of compartment syndromes of the foot. 168 May 91

Vascular mechanisms play an important but controversial role in the pathogenesis of acute pancreatitis. In experimental animals, injection of wax, powder, air, mercury, and microspheres into the pancreatic artery causes pancreatitis by end artery occlusion with resulting cellular infarction. Larger microspheres do not cause pancreatitis because collateral blood flow is preserved. Clinical evidence, such as microthrombi and atheromatous emboli in the pancreatic artery of patients with pancreatitis, supports pancreatic infarction as an etiologic agent. Experimental and clinical studies have suggested that pancreatic ischemia may also cause pancreatitis, but these studies have not been conclusive. We have compared five hours of total occlusion of the pancreaticoduodenal artery along with four hours of reperfusion to bile injection into the pancreatic duct as causes of pancreatitis. Bile injection caused a significant increase in serum amylase, activation of trypsin in pancreatic exudate, and histologic evidence of necrotizing pancreatitis. Pancreatic blood flow decreased as pancreatitis developed. Ischemia for five hours did not cause a significant increase in serum amylase or activation of trypsin in pancreatic exudate. Only edema was seen histologically, but there was no necrosis. Pancreatic blood flow increased with reperfusion. We believe ischemia aggravates, but does not initiate pancreatitis. Ischemia does not induce inflammation and necrosis in the pancreas, although infarction does.
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PMID:Mechanisms of acute pancreatitis. Vascular etiology. 174 44

Measurement of arterial flow is a very old practice, and intra-arterial recordings of pressure and flow have long served as a reference for experimental studies (fig. 1). The definition of a hemodynamic state is inconceivable unless these two parameters are associated. The electromagnetic method using an intra-arterial sensor measures pulsatile flow. Now, technological advances have led to the appearance of other methods providing measurement of mean (plethysmography) and nonpulsatile flow. As a result, there has been considerable confusion between mean arterial and pulsatile arterial flow (Fig. 2). Various studies have emphasized the physiological importance of pulsatile arterial flow and thus the interest in measuring it. The recording of mean flow has often proved disappointing because values are comparable in groups of normal subjects and those with arterial disease. Mean arterial flow can be measured by isotopic methods and plethysmography. Xenon-133 clearance is the isotopic method most often used. Since determination of microcirculatory flow at rest proved of no use, it was necessary to add a hyperemia test reactive to ischemia to differentiate patients with artery disease from normal subjects. Methods involving technetium and thallium have been little used since they require the presence of a nuclear medicine center and are not easily reproducible. There are numerous plethysmographic methods, but only those are studied here which allow measurement of arterial flow. Plethysmography by venous occlusion measures arterial flow by recording the increase in limb volume. The sensor is a mercury strain gauge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Measurement of arterial flow in the limbs: plethysmography, isotopes, electromagnetic methods]. 217 49

Platelet activation releases thromboxane A2 and serotonin, which acts on blood vessels through a specific, 5-hydroxytryptamine (5-HT2) receptor. The development of ketanserin, the selective 5HT2 receptor blocker, has made it possible to explore the role of serotonin in patients with advanced atherosclerotic disease. Ketanserin in low doses (3 to 30 micrograms/kg) was administered intra-arterially to 23 patients with symptomatic peripheral occlusive vascular disease during peripheral angiography: an additional seven patients received a placebo. The angiographic response was evaluated by coded reading and by computer-assisted measurement of arterial segments in four anatomical regions (pelvis, thigh, knee, and lower leg). Hemodynamic changes were assessed by mercury strain gauge plethysmography and Doppler pressure measurement. Unequivocal vasodilatation was observed in zero of seven placebo-treated patients and in 13 of 23 (57%) treated patients primarily at the level of collateral vessels. Dilation of the geniculate arteries, a major source of collaterals to the calf, was associated with a significant increase in the blood flow delivery to the calf. There was a moderate drop of systemic blood pressure in patients who failed to respond with peripheral vasodilatation. Ketanserin induces hemodynamically significant vasodilatation in some patients with peripheral vascular disease, suggesting that serotonin may contribute to ischemia in some patients with advanced atherosclerosis.
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PMID:Atherosclerosis, peripheral arterial disease and the vascular response to ketanserin. 234 79

A variety of drugs and toxins can produce severe abdominal pain and, in some cases, a surgical abdomen. Toxins can be classified according to mechanisms of injury: 1. Corrosives often produce severe gastroenteritis and may result in gastric or esophageal perforations. Examples of corrosive substances include aspirin, iron, mercury, acids and alkali. 2. Drugs may cause intestinal ileus or obstruction by pharmacologic actions (i.e., anticholinergic drugs and narcotics) or by mechanical obstruction (charcoal and drug bezoars). 3. Abdominal pain simulating an acute abdomen may result from systemic effects of black widow spider envenomation or intoxication with heavy metals such as lead and arsenic. 4. Ischemic bowel disease may occur from use of vasoconstrictor drugs, such as ergotamines, amphetamines and cocaine, or may follow treatment with catecholamines or digitalis in critically ill patients. Small bowel ischemia is life-threatening and may require bowel resection. 5. Many drugs cause abdominal pain by directly injuring abdominal organs, such as the liver and pancreas. Antibiotic-associated colitis may present with abdominal pain and inflammatory diarrhea. Consideration of drugs and toxins plays an important role in the differential diagnosis of the acute abdomen.
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PMID:Toxicologic causes of acute abdominal disorders. 266 62

In previous work, we described a group of patients with angina-like chest pain and normal coronary arteries. These patients had impaired coronary vasodilator responses to the stress of rapid atrial pacing and to the administration of dipyridamole, a potent vasodilator of coronary arterioles. This abnormality appears to be localized to the prearteriolar microvascular bed. To determine whether these patients have a more generalized abnormality of vasodilator reserve, we used mercury-in-Silastic strain-gauge plethysmography to compare their hyperemic responses to forearm ischemia with those of normal controls. After 10 minutes of ischemia, peak forearm flow was 39.9 +/- 5.0 ml per minute per deciliter in the controls [corrected] and 31.7 +/- 10.5 in the patients [corrected] (21 percent reduction; 95 percent confidence interval, 4 percent to 37 percent). Flow responses were also significantly reduced after three and five minutes of ischemia. Correspondingly, the vascular resistance after ischemia was also consistently higher in the patients with microvascular angina. The degree of vasodilator impairment in the peripheral circulation correlated well with the degree of vasodilator impairment in the coronary circulation (r = 0.74; P less than 0.004). Thus, patients with microvascular angina appear to have an impairment of vasodilator reserve that affects not only their coronary circulation but also their peripheral arterial bed.
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PMID:Impaired forearm vasodilator reserve in patients with microvascular angina. Evidence of a generalized disorder of vascular function? 368 70

Prior acute renal failure (ARF) induced by either glycerol (G) or mercury provides protection against rechallenge with the same agent or the other. To ascertain whether the widely employed ischemic renal failure model also shares a similar pathogenesis, two protocols were designed. In the first protocol, unilaterally nephrectomized rats with or without a prior episode of G-induced ARF two weeks previously were subjected to an ischemic insult [60-min total left renal artery clamp (LRAC)]. At 24 or 48 h after LRAC there was no difference in renal function in the rats with or without prior ARF. In the second protocol the sequence of G and ischemia was reversed. In rats having undergone LRAC two weeks prior to G, glomerular filtration rate was virtually identical from the right (control) and left (prior ARF) kidney (right, 138 +/- 30; left, 101 +/- 22 microliter/min/100 g body weight), and not different from rats receiving G alone. We conclude that protection against ARF conferred by prior insult is not a feature of all models.
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PMID:Protection against acute renal failure by prior acute renal failure: differences between myohemoglobinuric and ischemic models. 368 91

In this study, the tolerance of skeletal muscle to tourniquet application (ischemia) and to acute compartment syndrome (ischemia and pressure) was compared. In five animals, the cuff of a pneumatic tourniquet was inflated to 350 millimeters of mercury at the level of the thigh for three hours. In five other animals, an acute experimental compartment syndrome was created in one anterolateral compartment by autologous plasma infusion. The compartment pressure (measured by wick catheter) was maintained at a level equal to the mean arterial pressure for three hours. At three hours, reperfusion was established in both groups, either by tourniquet release or by decompressive fasciotomy and epimysiotomy. During both the ischemic period and a two-hour recovery period immediately thereafter, the mean intracellular pH and high-energy phosphate profile (levels of adenosine triphosphate and phosphocreatine) of the muscles of the anterolateral compartment were monitored non-invasively by phosphorus nuclear magnetic-resonance spectroscopy. Muscle biopsies were done the following day to take specimens for electron microscopic analysis of ultrastructural cellular degeneration. During ischemia, the cellular levels of phosphocreatine decreased at an identical rate in both groups. In contrast, the levels of adenosine triphosphate diminished rapidly in the animals with the compartment syndrome, but remained unchanged in the tourniquet group. Ischemic muscle acidosis was more severe in dogs with the compartment syndrome. In the tourniquet group, the phosphocreatine, adenosine triphosphate, and pH were all normal within fifteen minutes after release of the tourniquet, but these values remained depressed even two hours after fasciotomy in the group with compartment syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparative study of the tolerance of skeletal muscle to ischemia. Tourniquet application compared with acute compartment syndrome. 373 72

To characterize any digitalis-induced differences in intestinal blood flow autoregulation, we studied the circulatory responses of the rat intestine in control (n = 7) and chronically digitalized (n = 7) animals. Data were generated from denervated isoperfused small intestinal preparations. Arterial pressure, venous pressure, and oxygen consumption were continuously monitored. Determinations of intestinal blood flow allowed calculation of mesenteric vascular resistance and oxygen consumption. Animals underwent stepwise reductions in arterial pressure and acute venous hypertension (10 to 15 mm Hg). There were no differences in baseline hemodynamic or metabolic parameters in control (C) or digitalized (D) animals. Blood flow and oxygen consumption were autoregulated in both C and D rats until perfusion pressure decreased below 50 mm Hg. The response to acute venous hypertension was different. In D rats, venous hypertension resulted in increased vascular resistance (millimeters of mercury per milliliter per minute per 100 gm) [0.89 +/- 0.05 to 0.97 +/- 0.07; p less than 0.05], whereas C rats demonstrated no change [0.92 +/- 0.08 to 0.95 +/- 0.09]. The decrease in oxygen consumption in D rats (-14%) was slightly but significantly greater than that observed in C rats (-9%). Digitalized rats demonstrated a heightened myogenic response to acute venous hypertension with deleterious effects on vascular resistance and oxygen consumption. This reaction was intrinsic to the mesenteric circulation and not mediated by sympathetic nerves or central reflexes. Nonocclusive mesenteric ischemia in digitalized patients may reflect a similar abnormal response to the acute increases in portal pressure accompanying cardiac failure.
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PMID:Chronic digitalis administration alters mesenteric vascular reactivity. 382 Apr 9

Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular end-diastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction.
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PMID:Experimental myocardial infarction. IV. Reduction of left ventricular compliance in the healing phase. 491 78


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