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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute fatal pulmonary embolism is one cause of sudden death which should be guarded against. It is the most often missed diagnosis in sudden death cases within the hospital. Clinical pictures of 10 patients with acute fatal pulmonary embolism proved by autopsy were examined to elucidate the problems of diagnosis, and to look for an effective treatment, and a method of prevention. Common risk factors were old age and immobility due to stroke or postoperative state. Common past histories were hypertension, diabetes mellitus, obesity, atrial fibrillation and hyperlipidemia. Electrocardiogram and echocardiogram showed that in these patients there was definite evidence of acute right ventricular overload. High doses of intravenous urokinase should be given whenever acute cardiovascular collapse develops in such high risk patients. Emergent pulmonary angiogram and pulmonary embolectomy could be life-saving in patients with acute massive pulmonary embolism. Prevention is, however, the best treatment. In addition to anticoagulation medication, frequent change of body position and early mobilization are important precautions to prevent fatal pulmonary embolism developing in such patients.
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PMID:[Acute fatal pulmonary embolism: its prevention, diagnosis and treatment]. 236 72

Various interventions are available to assist in the management of patients with pulmonary embolism. Most are reserved for patients who either fail standard systemic anticoagulation therapy or are not candidates for anticoagulant therapy. The most common intervention is placement of a vena caval filter. Several different filter devices are available, most of which may be placed percutaneously. Pulmonary thrombolysis with urokinase or streptokinase may be appropriate in some patients with severe, symptomatic pulmonary embolism. Finally, pulmonary embolectomy by means of either a transvenous catheter or surgical technique may be necessary in cases of refractory cardiovascular collapse.
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PMID:Interventions in pulmonary embolism. 269 5

The history and physical examination were assessed in 215 patients with acute pulmonary embolism uncomplicated by preexisting cardiac or pulmonary disease. The patients had been included in the Urokinase Pulmonary Embolism Trial or the Urokinase-Streptokinase Embolism Trial. Presenting syndromes were (1) circulatory collapse with shock (10 percent) or syncope (9 percent); (2) pulmonary infarction with hemoptysis (25 percent) or pleuritic pain and no hemoptysis (41 percent); (3) uncomplicated embolism characterized by dyspnea (12 percent) or nonpleuritic pain usually with tachypnea (3 percent) or deep venous thrombosis with tachypnea (0.5 percent). The most frequent symptoms were dyspnea (84 percent), pleuritic pain (74 percent), apprehension (63 percent) and cough (50 percent). Hemoptysis occurred in only 28 percent. Dyspnea, hemoptysis or pleuritic pain occurred separately or in combination in 94 percent. All three occurred in only 22 percent. The most frequent signs were tachypnea (respiration ate 20/min or more) (85 percent), tachycardia (heart rate 100 beats/min or more) (58 percent), accentuated pulmonary component of the second heart sound (57 percent) and rales (56 percent). Signs of deep venous thrombosis were present in only 41 percent and a pleural friction rub was present in only 18 percent. Either dyspnea or tachypnea occurred in 96 percent. Dyspnea, tachypnea or deep venous thrombosis occurred in 99 percent. As a group, the identified clinical manifestations, although nonspecific, are strongly suggestive of acute pulmonary embolism. Conversely, acute pulmonary embolism was rarely identified in the absence of dyspnea, tachypnea or deep venous thrombosis.
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PMID:History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. 746 69

Postlactational involution of the mammary gland is characterized by two distinct physiological events: apoptosis of the secretory, epithelial cells undergoing programmed cell death, and proteolytic degradation of the mammary gland basement membrane. We examined the spatial and temporal patterns of apoptotic cells in relation to those of proteinases during involution of the BALB/c mouse mammary gland. Apoptosis was almost absent during lactation but became evident at day 2 of involution, when beta-casein gene expression was still high. Apoptotic cells were then seen at least up to day 8 of involution, when beta-casein gene expression was being extinguished. Expression of sulfated glycoprotein-2 (SGP-2), interleukin-1 beta converting enzyme (ICE) and tissue inhibitor of metalloproteinases-1 was upregulated at day 2, when apoptotic cells were seen initially. Expression of the matrix metalloproteinases gelatinase A and stromelysin-1 and the serine proteinase urokinase-type plasminogen activator, which was low during lactation, was strongly upregulated in parallel starting at day 4 after weaning, coinciding with start of the collapse of the lobulo-alveolar structures and the intensive tissue remodeling in involution. The major sites of mRNA synthesis for these proteinases were fibroblast-like cells in the periductal stroma and stromal cells surrounding the collapsed alveoli, suggesting that the degradative phase of involution is due to a specialized mesenchymal-epithelial interaction. To elucidate the functional role of these proteinases during involution, at the onset of weaning we treated mice systemically with the glucocorticoid hydrocortisone, which is known to inhibit mammary gland involution. Although the initial wave of apoptotic cells appeared in the lumina of the gland, the dramatic regression and tissue remodeling usually evident by day 5 was substantially inhibited by systemic treatment with hydrocortisone. mRNA and protein for gelatinase A, stromelysin-1 and uPA were weakly induced, if at all, in hydrocortisone-treated mice. Furthermore, mRNA for membrane-type matrix metalloproteinase decreased after hydrocortisone treatment and paralleled the almost complete inhibition of activation of latent gelatinase A. Concomitantly, the gland filled with an overabundance of milk. Our data support the hypothesis that there are at least two distinct phases of involution: an initial phase, characterized by induction of the apoptosis-associated genes SGP-2 and ICE and apoptosis of fully differentiated mammary epithelial cells without visible degradation of the extracellular matrix, and a second phase, characterized by extracellular matrix remodeling and altered mesenchymal-epithelial interactions, followed by apoptosis of cells that are losing differentiated functions.
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PMID:Two distinct phases of apoptosis in mammary gland involution: proteinase-independent and -dependent pathways. 856 29

An otherwise healthy 36-year-old housewife was diagnosed with advanced cancer of the stomach 5 months after her third parturition. Surgery was performed with the patient under total intravenous anesthesia combined with continuous epidural anesthesia. The course of anesthesia and the operative course were uneventful until the abdominal skin was sutured, when unexplained severe circulatory collapse developed. A widely dissociated PETCO2- PaCO2 suggested pulmonary embolism, and the findings of transesophageal echocardiography corroborated the diagnosis. Infusion of 480,000 units of urokinase in 30 minutes was immediately started via a Swan-Ganz catheter, and intravenous heparin 10,000 units in 24 hours, was administrated continuously. The pulmonary circulation was restored 30 minutes after the start of therapy, resulting in rapid recovery of the patient's systemic circulatory and acid-base status. The patient was safely extubated 19 hours postoperatively.
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PMID:[A survival case of intraoperative pulmonary embolism diagnosed early by transesophageal echocardiography]. 925 14

A prior study has reported that a rapid recanalization therapy of cerebral embolism, using liquid jet impacts generated by the interaction of gas bubbles with shock waves, can potentially penetrate through thrombi in as little as a few microseconds with very efficient ablation (Kodama et al. 1997). The present study was undertaken to examine the liquid jet impact effect on fibrinolysis in a tube model of an internal carotid artery. First, the conditions for generating the maximum penetration depth of liquid jets in the tube were investigated. Gelatin was used to mimic thrombi. The shock wave was generated by detonating a silver azide pellet weighing about a few micrograms located in a balloon catheter. The collapse of the inserted gas bubbles and the subsequent liquid jet formation were recorded with high-speed photography. Second, thrombi were formed using fresh human blood from healthy volunteers. The fibrinolysis induced by the liquid jet impact with urokinase was explored. This was conducted under selected conditions based on the experiment using the gelatin. Fibrinolysis was calculated as the percentage of the weight loss of the thrombus. Fibrinolysis with urokinase alone and with a single liquid jet impact with urokinase was 1.9 +/- 3.7% (n = 16) and 20.0 +/- 9.0% (n = 35), respectively, for an incubation time of 60 min. Statistical differences were obtained between all groups (ANOVA). These results suggest that liquid jet impact thrombolysis has the potential to be a rapid and effective therapeutic modality in recanalization therapy for patients with cerebral embolism and other clinical conditions of intra-arterial thrombosis.
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PMID:Liquid jets, accelerated thrombolysis: a study for revascularization of cerebral embolism. 1046 27

Consensus regarding the use of thrombolysis to treat acute pulmonary embolism has not yet been reached. There is good evidence that thrombolytic agents dissolve clot more rapidly than heparin. However, proving that this benefit reduces the death rate from pulmonary embolism has been difficult. Each of the 3 thrombolytic agents (tissue type-plasminogen activator, streptokinase and urokinase) is equally efficacious at dissolving clot, but all are associated with an increased risk of major hemorrhage when compared with heparin. One evolving position is that, in addition to patients presenting in circulatory collapse, for whom thrombolysis has been demonstrated to be life-saving, a subgroup of patients may be identified by echocardiography, through its ability to assess right ventricular dysfunction, who should also be considered for thrombolytic therapy. It remains to be seen whether this approach can reduce the death rate associated with pulmonary embolism.
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PMID:Thrombolytic therapy for pulmonary embolism. 1112 28

We tested the effect of ACE inhibition on the survival of bovine retinal (REC) and choroidal (CEC) endothelial cells (EC) in culture. The ACE inhibitor captopril delayed the apoptotic tube collapse of REC on Matrigel for >15 days. Captopril treatment of confluent monolayers (2-8 weeks) followed by slow starvation (2-4 weeks) increased EC viability by approximately 200%. Two-week captopril exposures were sufficient to confer maximal protection. Only vehicle-treated EC demonstrated apoptotic features such as membrane blebbing and DNA laddering. By RT-PCR, the starvation marker p202 was upregulated only in starved cells. In REC, captopril upregulated the pro-survival proteins mortalin-2, uPA, and uPAR while downregulating the anti-growth sprouty-4 and tPA. In CEC, captopril also upregulated tPA and its inhibitor PAI-1. Amiloride (uPA inhibitor) blocked the captopril-induced increase in EC survival, secondary sprouting, and invasion in Matrigel. The pro-survival effects of captopril involve the reprogramming of genes involved in cell survival and immortalization.
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PMID:ACE inhibition actively promotes cell survival by altering gene expression. 1455 46

We report a case of hip arthroplasty done under epidural and general anaesthesia. The patient had two episodes of acute massive pulmonary embolism perioperatively. He received cardiopulmonary resuscitation for the cardiovascular collapse that ensued and was administered a single dose of urokinase inspite of having relative (major) contraindications to the same.
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PMID:Successful post-cardiopulmonary resuscitation urokinase therapy for massive perioperative pulmonary embolism - a case report. 1785 Nov 63

To investigate the feasibility and efficacy of angioplasty and stenting for symptomatic occlusion of carotid artery. From December 2004 to June 2009, 17 patients with progressive or reoccurred ischemic stroke or repeated transient ischemic attack resulted from the total occluded carotid artery underwent angioplasty and stenting were reviewed. All patients with successful procedure were followed up. Clinic and angiography data were documented prospectively. The median time from symptoms onset to procedure was 23 days (range 3-94 days). Twelve of the 17 patients (70%) were obtained technique success. Eight patients were observed the collapse of internal carotid artery between occluded location to origin of ophthalmic artery after the occlusion was patent. Two patients had clots which were solved with urokinase. The collapsed internal carotid artery was improved markedly in the compute tomography angiograph 7 days after the procedure. No any complications related procedures occurred. One patient died from myocardial infarct and one suffered from ischemic minor stroke in brainstem for a median follow-up of 346.5 days. One of 9 patients (11.1%) was observed in-stent stenosis in the follow-up angiography. Angioplasty and stenting was a potential alternative therapy for symptomatic occlusion of carotid artery. Further study is required to determine the safety of this treatment.
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PMID:Angioplasty and stenting for the occluded internal carotid artery. 2039 Mar 21


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