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

The present study has defined conditions whereby a reversible form of ischemia-induced ARF can be produced in the dog. Unlike previous studies [9-11] which examined the acute phase of NE-induced ARF, this study demonstrates the feasibility of using the model for the longitudinal study of ARF. Such a model may be useful in studying the pathologic and physiologic changes which occur during different phases of ARF. Perhaps most important, this model should also provide a setting in which treatment measures, either prophylactic or therapeutic for ARF, can be examined.
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PMID:Norepinephrine-induced acute renal failure: a reversible ischemic model of acute renal failure. 69 76

Calcium-channel blockers (CCBs) have been shown to afford protection against acute (ARF) and chronic renal failure (CRF). The effects of CCBs against acute renal injury occur at both the vascular and tubular epithelial level. At the vascular level, experimental ARF-associated loss of renal autoregulation and hypersensitivity to renal nerve stimulation has been shown to be reversed by CCBs. These beneficial vascular effects of CCBs occur on the background of the finding that renal ischemic injury is associated with an increase in cellular Ca2+ concentration. A rise in tubular epithelial Ca2+ concentration also occurs very early after a renal ischemic insult. This effect of ischemia is associated with evidence of membrane depolarization, opening of slow calcium channels, increased cellular Ca2+ uptake, and reversal by CCBs. There is evidence that the increased cellular Ca2+ uptake activates phospholipases, which prolong and increase membrane damage. Experimental CRF is also associated with increased renal cellular Ca2+ concentration, an effect that can be attenuated by CCBs. The CCBs probably slow progression of CRF by both cytoprotective and antihypertensive effects. These findings of vascular and tubular effects of CCBs in experimental ARF and CRF have led to their clinical use to prevent initial dysfunction of cadaveric kidney transplants, cyclosporine nephrotoxicity, radiocontrast-induced ARF, and progression of CRF. Randomized clinical studies are necessary to further examine the efficacy of CCBs in ARF and CRF.
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PMID:Role of calcium-channel blockers in preventing acute and chronic renal injury. 172 16

The course of the early postoperative period has been analysed in 325 patients with acute thrombosis and embolism; the results of 104 autopsies have been reviewed and macro- and microscopic lung studies have been performed using light microscopy. It has been established that broncho-pulmonary complications are most frequently encountered in the early postoperative period. Morphological changes in the lungs are proportional to the duration and severity of acute ischemia. In durable and severe ischemia the changes are progressing and are characterized by the elements of the "shock" lung. The morphological changes observed specify mechanisms of the onset of acute respiratory failure and broncho-pulmonary complications. They must be taken into consideration during intensive therapy.
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PMID:[Pathology of the lungs in patients with acute arterial obstruction in the lower extremities]. 183 Jul 29

Patients who acquire sepsis, ARDS, ARF, or MSOF subsequent to multiple trauma have a high mortality rate. The pathophysiology of these complications is complex and is thought to involve ischemia, the generation of mediators, alterations in regional perfusion, and cellular oxygen use. Because of the critical nature of the patient with these complications, nursing care requires indepth knowledge as well as competent nursing management, necessitating use of both the art and science of nursing.
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PMID:Complications of multiple trauma. 267 90

Fifty-three section examinations of peritonitis with a history of 1 to 30 days were performed to microscopically study viscera and their microcirculatory bed. They revealed microcirculatory disturbances and their consequences that were characteristic of shock. They were most of all pronounced in the kidneys and lungs. The kidneys showed blood dumping with cortical ischemia, which was accompanied with dystrophic changes in the proximal nephroepithelium or focal acute renal failure (ARF) in half the cases. Seven cases displayed advanced ARF of over 8-10-day history with regeneration in the damaged tubules. There were pulmonary microcirculatory disturbances in 27 cases, 10 of them having clinical signs of the "shock" lung, i.e. dys- and atelectases, alveolar bleedings, hyalin membranes, which might be a cause of acute respiratory failure.
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PMID:[Significance of bacterial shock to thanatogenesis in peritonitis]. 277 91

Bilateral blindness resulting from optic atrophy is an unusual complication following shock and cardio-respiratory arrest. This report describes a patient with acute respiratory failure due to pneumococcal pneumonia being treated with very high levels of positive end expiratory pressure who developed bilateral blindness following cardiac arrest. This unfortunate complication most likely resulted from increased intraocular pressure and low systemic perfusion pressure synergistically causing ischemia of the optic nerves.
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PMID:Bilateral optic atrophy after cardiac arrest in a patient with acute respiratory failure on positive pressure ventilation. 283 2

Infusion of prostacyclin (PGI2) reportedly attenuates renal ischemic injury in the dog and the rat. In the dog, PGI2 is a potent renal vasodilator; in the rat a direct action on the renal vasculature is not always apparent. To determine whether or not the protective effect of PGI2 on postischemic ARF was hemodynamically mediated, studies were performed in uninephrectomized Sprague-Dawley rats before and after a 40 minute period of complete renal artery occlusion. In response to the preischemic infusion of PGI2 for 30 minutes at 160 ng/kg body wt/min i.v. (N = 7), MAP and RBF fell to 86 +/- 7% (P less than 0.0001) and 84 +/- 9% (P less than 0.05) of baseline values, respectively. RVR initially declined to 81 +/- 9% of baseline values (P less than 0.025) but returned to 102 +/- 13% of baseline values prior to the period of ischemia. Following the period of ischemia, reflow of blood in the rats receiving PGI2 was delayed when compared to rats not receiving PGI2 (N = 7). RBF returned to only 76 +/- 19% of the initial values in PGI2-treated rats (P less than 0.01) but to 90 +/- 12% of the initial values in rats receiving buffer alone (NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of prostacyclin on postischemic acute renal failure in the rat. 332 94

Lower torso ischemia leads to acute respiratory failure, an event associated with the accumulation of inflammatory cells in the lungs. This study tests whether ischemia-induced eicosanoid synthesis leads to polymorphonuclear leukocyte (PMN) accumulation in the lungs. Anesthetized rats (N = 51) were randomized into five groups: nonischemic sham rats (N = 10); the remaining four groups were rats made ischemic for 4 hours with bilateral thigh tourniquets treated just before tourniquet release with saline vehicle (N = 17): the thromboxane (Tx) synthase inhibitor OKY-046 (Ono Pharmaceutica, Osaka, Japan) 2 mg/kg intravenously every 2 hours (N = 8); the lipoxygenase inhibitor diethylcarbamazine (DEC) (Sigma, St. Louis, MO) 0.2 mg/kg/min intravenously (N = 8); the platelet-activating factor receptor antagonist SRI (Sandoz Inc., East Hanover, NJ) 63-072 3 mg/kg intravenously every 30 minutes (N = 8). Four hours after ischemia, plasma TxB2 levels in the ischemic placebo-treated group was 3570 +/- 695 pg/mL, compared with 495 +/- 73 pg/mL in sham rats (p less than 0.001). Lung microscopy showed foci of proteinaceous exudate in alveoli and 121 +/- 10 PMN/20 high power fields (HPF) compared with 59 +/- 9 PMN/20 HPF in the sham group (p less than 0.001). One day after ischemia PMN accumulations remained elevated at 119 PMN/20 HPF. Pretreatment with OKY-046 led to reduced TxB2 levels of 149 +/- 17 pg/mL, normal lung histology, and 83 +/- 13 PMN/20 HPF, a value similar to that of the sham group and lower than that of the placebo-treated group (p less than 0.05). Treatment with DEC yielded TxB2 levels of 1419 +/- 492 pg/mL, which was lower than that of the placebo group (p less than 0.05) but higher than that of the sham group (p less than 0.05). Microscopy showed normal lungs with 79 +/- 7 PMN/20 HPF lower than the placebo group (p less than 0.05). SRI 63-072 did not inhibit Tx synthesis or leukosequestration in the lungs. Platelet counts decreased in all groups relative to sham animals (p less than 0.05). The results indicate that Tx synthesis induced by ischemia moderates PMN accumulations in the lungs. Inhibition of lipoxygenase is believed to prevent PMN accumulations both by limiting leukotriene-induced Tx synthesis as well as by limiting production of chemoattractants.
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PMID:Pulmonary leukosequestration induced by hind limb ischemia. 360 41

The pathophysiology and managements of right ventricular (RV) dysfunction in acute respiratory failure (ARF) is complicated. Results presented in this paper indicate that volume expansion may not be appropriate therapy to maintain or increase cardiac output (CO) when flow is reduced because of increased RV afterload. Volume will increase RV wall stress and O2 requirements so that despite increased preload, CO may fall. If RV afterload is significantly increased, such changes can occur despite a relatively normal RV end-diastolic pressure (RVEDP). Further, increased RV afterload and/or volume expansion can result in increased RV volumes and secondary alteration in left ventricular (LV) diastolic mechanics. Such changes, especially if wedge pressure increases, would tend to increase pulmonary edema. Also, because of potential changes in viscosity and pulmonary vascular resistance (PVR), packed red blood cells may not be indicated to increase CO, arterial O2 content and tissue O2 delivery in the setting of ARF. Therapy designed to reduce PVR may be appropriate to increase flow in the setting of increased RV afterload. However, such therapy may also reduce systemic vascular resistance, blood pressure (BP) and RV perfusion pressure. Such changes could lead to RV ischemia and reduced CO. Alternatively, agents which increased RV perfusion and/or contractility will increase CO by reducing RV end-diastolic and end-systolic volumes and may be the treatment of choice to increase flow when RV afterload is elevated.
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PMID:Treatment of right ventricular dysfunction in acute respiratory failure. 634 Sep 63

Acute respiratory failure, particularly if associated with sepsis, results in diffuse changes in pulmonary vascular geometry and the afterload characteristics against which the right ventricle must perform. Therapy in these patients frequently requires replacement of intravascular volume which, if pulmonary vascular resistance is abnormally elevated, may cause a substantial enlargement in right ventricular (RV) end-diastolic volume. The low compliance characteristics of the RV invalidate the use of filling pressure (CVP) as a guide to RV size. We have examined RV volume in critically ill patients by means of the gated 99TAc scan and noted a substantial increase in RV volume despite filling pressure in the upper normal range. This enlargement appears to encroach upon LV function because the ejection fraction of the LV remained high despite elevation of pulmonary capillary wedge pressure (PCWP). Older patients with "silent" right coronary artery disease may become hemodynamically limited during therapy for acute respiratory failure and sepsis due to RV enlargement, increased wall tension and RV ischemia, a condition not readily diagnosed at the bedside with the usual monitoring techniques.
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PMID:[Hemodynamic changes in acute respiratory insufficiency: the role of the right ventricle]. 731 51


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