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

To overcome the hemorrhagic complications that may occur during extracorporeal circulatory support for post cardiotomy shock patients, a heparinized circuit was introduced into the percutaneous cardiopulmonary support system and decreased systemically administered heparin during bypass. Heparin coated percutaneous cardiopulmonary support with low dose systemic heparinization was instituted in 13 patients (6 men and 7 women, mean age 62.2 +/- 8.5 years) who experienced circulatory collapse after cardiac surgery. Of the 13 patients, 9 could not be weaned from cardiopulmonary bypass and 4 had circulatory collapse in the operating room or in the intensive care unit. The duration of support ranged from 1 to 66 hr (mean 27.4 +/- 26.7), and the flow rate ranged from 1 to 3 L/min (2.2 +/- 0.5). An activated coagulation time of about 150 sec was maintained with or without minimal systematically administered heparin. Of the patients cannulated, 77% (10 of 13) were successfully weaned from percutaneous cardiopulmonary support and 39% (5 to 13) were long-term survivors. The causes of death were sepsis in three, progressive heart failure in three, lower leg ischemia in one, and vital infection in one. From the results of clinical or post mortem examinations, there was no massive bleeding or evidence of thromboembolism in the major organs. From observations made within 12 hr of initiation of percutaneous cardiopulmonary support, there was no significant decrease in the number of platelets, but platelet count had significantly decreased 24 hr after initiation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin coated percutaneous cardiopulmonary support for the treatment of circulatory collapse after cardiac surgery. 785 34

Ischemia/reperfusion mechanisms contribute to lung injury after transplantation, pulmonary embolism, and resolution of atelectasis. Alveolar tissue becomes hypoxic and deprived of substrate only when both ventilation and perfusion are interrupted, a situation modeled in vivo by complete, unilateral lung collapse. Because previously hypoxic mitochondria may be an important intracellular source of superoxide and hydrogen peroxide (H2O2) during reperfusion and re-oxygenation, the authors, in this study, investigated whether mitochondrial H2O2 release changed as a result of lung hypoxia/hypoperfusion resulting from collapse. Mitochondria were isolated from hypoxic (previously collapsed) right or contralateral left rabbits' lungs and from control rabbits' lungs. Mitochondrial H2O2 release, a marker of superoxide production, was measured fluorometrically after incubation with or without 1 mmol/L cyanide and 0.1 mmol/L nicotinamide adenine dinucleotide. Mitochondrial recovery was determined by assaying succinate dehydrogenase activity in mitochondrial preparations and lung homogenates. Lung succinate dehydrogenase activity and mitochondrial recovery were comparable among groups. Calculated lung mitochondrial content did not change (control subjects: left 7.9 +/- 0.5, right 13.8 +/- 1.7; hypoxic: left 10.3 +/- 1.3, right 10.5 +/- 2.4, all mg mitochondrial protein/lung). Mitochondria released hydrogen peroxide at approximately 5.6 nmol/h/mg pro in buffer alone and 14.8 nmol/h/mg pro in buffer with cyanide and nicotinamide adenine dinucleotide. However, lung collapse and resulting hypoxia caused no change in mitochondrial number or capacity to release H2O2 in vitro. Based on these findings, it is suggested that other sources of reactive oxygen metabolites, including xanthine oxidase and activated neutrophils, contribute to the oxidant injury observed in this model.
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PMID:Hydrogen peroxide release by mitochondria from normal and hypoxic lungs. 794 83

We used an intact in vivo canine model of pulmonary ischemia-reperfusion injury to evaluate whether the bronchial circulation or reverse pulmonary venous blood flow would protect the lung from injury during 2 h of unilateral pulmonary arterial (PA) occlusion and lung deflation. Serial measurements of regional extravascular density and transcapillary protein flux were made after reperfusion by using the quantitative imaging technique of positron emission tomography. Twenty-one animals were divided into four experimental groups. In all experimental groups, the left PA was clamped and the left lung was allowed to collapse and remain unventilated for a period of 2 h. In addition, in group I (n = 5) the left bronchial circulation was disrupted and the left pulmonary veins were clamped, in group II (n = 5) the bronchial circulation and the pulmonary veins were left intact, in group III (n = 6) the bronchial circulation was left intact but the pulmonary veins were clamped, and in group IV (n = 5) the bronchial circulation was disrupted but the pulmonary veins remained patent. The rate of protein flux in the left lung was increased only in group I (complete ischemia with lung deflation) [mean 195 x 10(-4) min-1 (range 85-453 x 10(-4) min-1) at 0.25 h and 114 x 10(-4) min-1 (range 22-200 x 10(-4) min-1) at 3 h] after reventilation and PA reperfusion (normal = 49 +/- 31 x 10(-4) min-1). Extravascular density increased significantly from 0.25 to 3 h only in group I.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bronchial and reverse pulmonary venous blood flow protect the lung from ischemia-reperfusion injury. 800 21

A new cause of chronic interstitial fibrosis of the kidney, recently identified in Belgium, was found to be related to a slimming regimen that included Chinese herbs. Thirty-three biopsy-proven cases of this nephropathy are discussed, with special reference to the pathologic aspects. Extensive interstitial fibrosis with atrophy and loss of the tubules was the major lesion; it was predominantly located in the superficial cortex. The glomeruli were relatively spared. They nevertheless showed a mild collapse of the capillaries and wrinkling of the basement membrane. Thickening of Bowman's capsule was the rule. Interlobular and afferent arterioles showed thickening of their walls due to swelling of the endothelial cells. These aspects suggest that the primary lesions could be located in the vessel walls, leading to ischemia and interstitial fibrosis. On the other hand, they are characteristic enough to allow the pathologist to suspect the diagnosis even in the absence of an anamnesis of ingestion of Chinese herbs.
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PMID:Pathologic aspects of a newly described nephropathy related to the prolonged use of Chinese herbs. 804 21

Mechanical support for acute regional ischemia without hemodynamic collapse may be achieved percutaneously with an intraaortic balloon pump (IABP) or with transseptal left ventricular assist (TLVA) while awaiting revascularization. The relative benefits of these two percutaneous transfemoral techniques for the treatment of ischemia were compared in a representative animal model. During 90 minutes of regional coronary occlusion, four groups of 8 pigs were treated with either no support (control), IABP, TLVA, or both IABP and TLVA. Cardioplegic arrest for 30 minutes to simulate coronary grafting was followed by 180 minutes of global reperfusion on bypass. In all groups regional wall motion and interstitial pH in the area at risk were significantly depressed with ischemia, but wall motion fully recovered after reperfusion. However, histochemical staining of the area of necrosis/area at risk was significantly reduced with IABP versus control (20.2% versus 34.1%; p < 0.05) and further significantly reduced with TLVA and IABP + TLVA (10.7% and 6.7% versus IABP alone; p < 0.05). We conclude that in supporting even a modest-sized myocardial region at risk (12% of the left ventricle) the area that went on to infarction was significantly reduced with the use of TLVA over IABP. Regional wall motion and myocardial pH measurements did not reflect this difference in the early reperfusion period. The benefit of TLVA over IABP during more extensive or prolonged ischemia may have real clinical significance.
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PMID:Enhanced preservation of acutely ischemic myocardium with transseptal left ventricular assist. 814 23

Cocaine is one of the illicit hallucinogenic drugs which can be conveniently taken without resorting to parenteral administration. Almost all organs systems in the body are affected by its abuse. Complications involving the nervous, cardiovascular and reproduction systems have recently been published. In this report, complications relating to gastrointestinal system are reviewed. Acute ischemic syndromes are the most prominent gastrointestinal complication of cocaine use. Severe ischemia results from intense activation of alpha-adrenergic receptors in the mesentery. This ischemia results in gastropyloric ulcerations, gangrene and perforation of small as well as large intestine and colitis. Sudden collapse and deaths have been reported in "body packers" who swallow cocaine filled condoms in an effort to smuggle the drug through the customs. Several cases of acute hepatotoxicity and hepatocellular necrosis from cocaine use have also been reported.
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PMID:Gastrointestinal manifestations of cocaine addiction. 820 75

The dynamics of the transmyocardial coronary flow patterns during normal and ischemic conditions are complex and relatively inaccessible to measurements. Therefore, theoretical analyses are needed to help in understanding these phenomena. The proposed model employs compartmental division to three layers, each with four vessel-size compartments which are characterized by resistance and compliance. These compartments are subjected to the extravascular compressive pressure (ECP) generated by cardiac contraction, which by modifying the transmural pressure causes changes in cross-sectional area of the vessels in each compartment continuously determining the resistance and capacitance values. Autoregulation and collaterals are also included in order to simulate the flow patterns during regional ischemia. Using these features, the model predicts the typical out of phase arterial and venous flow patterns. Systolic collapse of the large intramyocardial veins during the normal cycle, as well as systolic arteriolar collapse during ischemia are predicted. The transmural flow during ischemia is characterized by alternating flows between the layers. The ECP is considered here is two ways: (a) as a function of left ventricle (LV) pressure, decreasing linearly from endocardium to epicardium and (b) as the interstitial fluid pressure, employing a multilayer muscle-collagen model of the LV. While both of these approaches can describe the dynamics of coronary flow under normal conditions, only the second approach predicts the large compressive effects due to high ECP obtained at very low cavity pressure, resulting from significant muscle shortening and radial collagen stretch. This approach, combining a detailed description of transmural coronary circulation interacting with the contracting myocardium agrees with many observations on the dynamics of coronary flow and suggests that the type of LV mechanical model is important for that interaction.
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PMID:Coronary flow patterns in normal and ischemic hearts: transmyocardial and artery to vein distribution. 821 27

We have measured, directly and simultaneously, changes in extracellular volume and intra- and extracellular pH during ischemia in the isolated rat heart using 31P NMR spectroscopy. Hearts were perfused with buffer containing 15 mM sodium phenylphosphonate at pH 7.4. Wash in and wash out experiments showed that phenylphosphonate entered only the extracellular (interstitial, vascular and chamber) space of the heart and had no adverse effects on myocardial energetics, contractile function or coronary flow rate. Hearts were subjected to 28 min of total, global ischemia, during which the phenylphosphonate resonance area in the 31P NMR spectra decreased by 83%, indicating that extracellular fluid had moved rapidly from the heart to the bath surrounding the heart, partly as a result of vascular collapse. A separate, morphological study confirmed that 95% of the vasculature had collapsed by 28 min ischemia. Intra- and extracellular pH were determined from the chemical shifts of the P(i) and the phenylphosphonate resonances, respectively. In the pre-ischemic rat heart, intracellular pH was 7.15 +/- 0.03 and extracellular pH was 7.39 +/- 0.03. By 4 min of ischemia, intra- and extracellular pH were the same and decreased concomitantly throughout the remainder of ischemia to final values of 6.09 +/- 0.19 and 6.16 +/- 0.23, respectively. On reperfusion, the extracellular volume and pH returned to pre-ischemic levels within 1 min, but restoration of intracellular pH took > 2.5 min. Thus, a large volume of extracellular fluid moves out of the rat heart to the surrounding bath and the intra- and extracellular pH become the same during total, global ischemia.
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PMID:Extracellular volume and transsarcolemmal proton movement during ischemia and reperfusion: a 31P NMR spectroscopic study of the isovolumic rat heart. 821 28

The aim of the present study was to elucidate the role of mitochondria in the development of heart failure following ischemia/reperfusion. Although mitochondria were increasingly assumed to be responsible for the establishment of an oxidative stress situation the lack of suitable methods to prove it required new concepts for an evaluation of the validity of this hypothesis. The principal idea was to expose isolated mitochondria to metabolic conditions which are developed during ischemia/reperfusion in the cell (anoxia, lactogenesis) and study how they respond. Heart mitochondria treated in that way responded with an incomplete collapse of the transmembraneous proton gradient, thereby impairing respiration-linked ATP generation. The membrane effect affected also the proper control of e- transfer through redox-cycling ubisemiquinone. Electrons were found to leak at this site from its normal pathway to O2 suggesting that ubisemiquinone becomes an active O2.- generator. It was concluded from these observations that mitochondria are likely to play a pathogenetic role in the reperfusion injury of the heart both, by an impairment of energy conservation and their transition to a potent O2.(-)-radical generator. Furthermore, there is considerable evidence that the exogenous NADH-dehydrogenase of heart mitochondria is mainly responsible for functional changes of these organelles during ischemia/reperfusion.
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PMID:Ischemia/reperfusion impairs mitochondrial energy conservation and triggers O2.- release as a byproduct of respiration. 831 23

Miniature swine were used to study the effect of cervical fracture on femoral head blood flow. Laser Doppler flowmetry was used to evaluate femoral head blood flow before and after the fracture, after internal fixation with or without compression, and 8 weeks post-fracture. Fluorescent bone-labeling was performed at 2, 4 and 6 weeks post-fracture. Femoral head blood flow decreased to 40 percent of baseline following fracture, partly from the disruption of venous drainage. Histologically, all femoral heads showed some degree of trabecular thinning, microfracture, and neovascularization when compared with controls. Analyses of the laser Doppler flowmetry data, fluorescent label histology, microradiography and bone densitometry indicated that late (4-6 weeks) revascularization produces severe trabecular mechanical weakening and resultant femoral head collapse. Femoral head ischemia following fracture probably falls along a continuum, with only the more severe cases proceeding to mechanical collapse. Femoral neck fractures in the minipig produce femoral head necrosis of a severity and incidence which closely parallels that of the human population; thus, the minipig is a useful model for further study of complications following femoral neck fracture in humans.
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PMID:The effect of fracture on femoral head blood flow. Osteonecrosis and revascularization studied in miniature swine. 849 86


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