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

This study was intended to investigate the effect of high arterial oxygen tension on the peripheral circulation between normal and hypoxic area by using twelve dogs. For this purpose, acute temporary ischemia was produced at the right hindlimb by an occlusion of the right external iliac artery for 1 and 2 hours, and the left hind-limb was let alone as a control. The peripheral vascular resistance and the arterio-venous difference in oxygen tension between the right and the left hind-limb were measured continuously during 1 hour from immediately after reopening of the blood flow of the right external iliac artery. They were compared between at the condition of breathing room air at 1 ATA and pure oxygen at 2 ATA. The high arterial oxygen tension causes vasoconstriction. When there exists hypoxia in the peripheral tissue, however, it does not act on as a vasoconstrictive factor until the oxygen deficit is improved.
J Cardiovasc Surg (Torino)
PMID:Effect of increased oxygen on peripheral circulation in acute, temporary limb hypoxia. 65 92

The experimental and clinical studies on the protective effect of Betamethasone upon the myocardium particularly on the prevention of the subendocardial ischemia after the cardiopulmonary bypass was investigated on the ultrastructural alterations of the epicardium and the endocardium obtained by the transmural left ventricular myocardial biopsy. Pretreatment of Betamethasone, 5 mg/Kg, with single intravenous injection a half to one hour before cardiopulmonary bypass was effective to preserve the myocardial ultrastructure after the anoxic arrest and in the recovery period after restoring the coronary circulation. The intramyocardial gradient of the ultrastructure was diminished by Betamethasone hardly demonstrating the no-reflow phenomenon. Hemodynamic and metabolic changes did not show the significant effectiveness of Betamethasone. It was suspected that Betamethasone stabilized the cell membrane and lysosome and suppressed the interstitial edema in the myocardium during and after anoxic arrest.
J Cardiovasc Surg (Torino)
PMID:Protective effect of betamethasone on the subendocardial ischemia after the cardiopulmonary bypass. 65 3

The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.
J Thorac Cardiovasc Surg 1978 Jun
PMID:Effects of procaine-induced cardioplegia on myocardial ischemia, myocardial edema, and postarrest ventricular function. A comparison with potassium-induced cardioplegia and hypothermia. 66 57

Dealing with lower limbs arteriopathies with combined aorto iliac and superficial femoral occlusive diease and when ischemia leads to operation should an extension bypass to the popliteal or tibial artery be associated every time it is possible? The authors have investigated the results of revascularizing operation above the profunda femoris on 35 limbs (27 patients). On 19 limbs only, has the revascularization been sufficient to cure the distal ischemia. On the other 16 limbs, a second operation was necessary 7 times an extension bypass to the popliteal or tibial artery, once an above knee amputation, twic a below knee amputation. From the comparison of these results with the degree of ischemia and the arteriographic aspect of the profunda femoris, the author's conclusion is that revascularization must extent below the profunda femoris unless the profunda is in good condition and there is no rest ischemia.
J Cardiovasc Surg (Torino)
PMID:When can revascularization be limited to the profunda femoris alone? 68 38

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.
Cardiovasc Res 1978 Jun
PMID:Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs. 69 89

The effects of intra-aortic balloon pumping (IABP) on myocardial flow distribution were studied in 50 dogs. Cardiac output was controlled by right heart bypass. In each dog the following parameters were measured with and without IABP during normal coronary perfusion and after regional ischemia was induced by anterior descending coronary vein flow by timed collection, and endocardial/epicardial flow ratios by a previously reported thermal washout technique. In nonischemic myocardium, IABP significantly (p less than 0.05) increased mean coronary sinus flow 11.5 percent +/- 5.8 percent (S.D.) and the mean endocardial/epicardial ratio, 17.3 percent +/- 0.28 percent. In the regionally ischemic myocardium, IABP significantly (p less than 0.05) increased mean segmental coronary vein flow 13.9 percent +/- 1.23 percent but decreased the endocardial/epicardial ratio 29.9 percent +/- 1.1 percent. We conclude that in the dog, IABP enhances subendocardial blood flow in perfused but not in ischemic myocardium. Contrary to common suppositions, the increase in collateral blood flow with IABP preferentially supplies epicardial layers in segmental ischemic zones, but may be shunted from the subendocardium.
J Thorac Cardiovasc Surg 1978 Oct
PMID:Effect of intra-aortic balloon pumping on nutrient coronary flow in normal and ischemic myocardium. 70 60

Popliteal artery injuries are followed, in many cases, by amputation of the leg. Results after re-construction depend on the time of ischemia. In this experimental work 12 dogs with injury of the popliteal artery had a direct end to end anastomosis or an anastomosis using saphenous vein graft. Blood flow was checked by an electromagnetic flowmeter or ultrasounds, blood samples for Hb, oxyhaemoglobin saturation, Hct and ph were taken before and after operation. Changes in these values depend on the time elapsing between injury and re-establishment of circulation. Operative angiography was done in all dogs. Except in two dogs, no early or late thrombosis occurred. Three dogs required amputation. The outcome of the operation is related to the time elapsing between injury and restoration of circulation.
J Cardiovasc Surg (Torino)
PMID:Experimental remarks on leg ischemia following popliteal artery injuries. 71 21

107 patients presenting Raynaud's phenomenon attacks were studied. It has been demonstrated by means of arteriographies that in pallid phase of Raynaud's phenomenon attacks not only the digital but also the radial ulnar and interosseous arteries are in spasm. In the cyanotic phase of Raynaud's phenomenon the natural arteriovenous anastomoses are widely open bringing about peripheral skin ischemia. On the assumption that the opening of arteriovenous anastomoses in Raynaud's phenomenon attacks is due to injury of that part of the peripheral nerve which lies in contact with the cervical vertebral column all 107 studied patients were submitted to detailed cervical vertebral column X-ray examinations. In 103 patients i.e. in 96.3% characteristic degenerative changes of cervical vertebrae were recognised. In 100 controls who never had neither Raynaud's phenomenon attacks nor cervico-brachial neuritis the same type of degenerative changes were found in 10% only. The authors presume that the Raynaud's phenomenon attacks are due to peripheral mixed nerve or their roots injury. The blue phase of Raynaud's phenomenon attacks is due to opening of arteriovenous anastomoses.
J Cardiovasc Surg (Torino)
PMID:The origin of Raynaud's phenomenon. 73 33

The persistent high mortality from power failure resulting from myocardial infarction has stimulated an intensive search for methods of reducing infarct size, which has been shown to relate directly to the occurrence of power failure. By analyzing the time course of myocardial injury during ischemia, the reversibility of lesions with reperfusion, and the characteristics of reversibly injured tissues along the border zone of ischemic areas, concepts have been formulated regarding the possibility of salvaging marginally injured cells. Measures designed to diminish myocardial oxygen consumption, to increase blood flow or oxygen supply to ischemic areas, to increase substrate availability, or to change the degree of swelling and autolysis of injured cells have all been tested in experimental animals with some success. These methods are just beginning to be tested in the clinical setting, and, if successful, will no doubt usher in a new era in medical therapy for acute myocardial infarction.
Cardiovasc Clin 1975
PMID:Modification of infarct size. 81 57

This study compares the effects of normothermic and hypothermic spontaneous fibrillation at perfusion pressures of 100 and 50 mm. Hg on the adequacy and distribution of coronary blood flow. During normothermia (37 degrees C.), subendocardial oxygen delivery decreased 45 per cent ( p less than 0.01) and left ventricular flow became redistributed away from the subendocardium (endo-epi flow ratio fell from 1.2 to 0.8) when perfusion pressure was lowered to 50 mm. Hg; abnormal glycolysis (lactate washout) became evident when perfusion pressure was raised to 100 mm. Hg and ischemia was demonstrated by histochemical stains. Hypothermia (28 degrees C) reduced myocardial oxygen uptake 52 per cent (p less than 0.01) at 100 mm. Hg perfusion pressure; left ventricular flow, distribution, and metabolism did not change from control values. Lowering perfusion 50 mm Hg caused a pronounced reduction in subendocardial oxygen delivery (63 per cent, p less than 0.01); abnormal glycolysis developed and histochemical ischemia was seen. These studies show that lowering perfusion pressure in normothermic fibrillating hearts impairs oxygen delivery to the left ventricular subendocardium. While hypothermia significantly reduces left ventricular oxygen requirements, the ventricle is not protected against subendocardial ischemia if perfusion pressure falls to levels frequently used during clinical open-heart surgery.
J Thorac Cardiovasc Surg 1977 Jan
PMID:Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. III. Effects of temperature, time, and perfusion pressure in fibrillating hearts. 83 Sep 99


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