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

During four years, the authors have observed ten lesions of the sub-clavian artery associated with a fracture of the clavicle. The clinical picture in one case out of two was that of an acute ischemia of the upper limb. The surgical repair has been performed in 8 cases. The thoracic approach was necessary three times. The clavicle was resected in most cases. The prognosis of these lesions depends on the rapidity of their recognition, and of their treatment, and on the fact whether the brachial plexus is involved or not
J Cardiovasc Surg (Torino)
PMID:Fractures of the clavicle and injuries of the sub-clavian artery. Report of 10 cases. 110 36

Intracoronary injection of 14 mcg. of tetrodotoxin into the ischemic isolated rat heart resulted in immediate cessation of mechanical activity. Upon reperfusion with oxygenated, modified Krebs-Henseleit bicarbonate buffer in a modified Langendorff apparatus, all hearts recovered normal rate, rtythm, and contractile vigor after up to 60 minutes of ischemia. In contrast, all hearts not administered tetrodotoxin showed bradycardia, irregular rhythm, and weak contraction upon reperfusion after 30 and 45 minutes of ischemia; after 60 minutes, no mechanical activity was evident. The improved cardiac function following ischemia in the tetrodotoxin-treated hearts was associated with persistence of normal adenosine triphosphate (ATP) levels after up to 30 minutes of ischemia and normal or elevated creatine phosphate (CP) levels after up to 60 minutes of ischemia. On the other hand, ATP and CP levels progressively declined to reach 50 per cent of normal values after 30 minutes in the ischemic hearts without tetrodotoxin. These findings indicate that postarrest ATP and CP levels play an important role in myocardial recovery after ischemic arrest.
J Thorac Cardiovasc Surg 1975 Feb
PMID:The mechanism of myocardial protection from ischemic arrest by intracoronary tetrodotoxin administration. 111 37

An intact, working swine heart preparation with controlled coronary perfusion is described. In this model, hemodynamic and metabolic functions were correlated in control and ischemic myocardium. A closed-loop, extracorporeal coronary perfusion circuit in series with a perfusion pump and oxygenator was designed to return reoxygenated coronary venous blood at controlled flow rates to the left and right coronary arteries. In 9 swine at normal flows (232 plus or minus 17 ml. per minute), the preparation maintained stable hemodynamic performance and oxygen consumption for a 1 hour period, after which ischemia was induced by reducing coronary flow by 50 per cent. As a result, left ventricular end-diastolic pressure (LVEDP) rose by 227 per cent, whereas heart rate (-17 per cent), aortic pressure (-9 per cent), pressure time/minute (PTM) (-28 per cent), left ventricular work (-47 per cent), and oxygen consumption (-39 per cent) all decreased. The ischemic myocardium shifted from lactate extraction to production. With this model, we can define, over a period of time, several mechanical and metabolic collations as a function of total coronary blood flow in an intact, large animal. We can also test interventions during the acute phases of ischemia in an effort to reduce myocardial damage.
J Thorac Cardiovasc Surg 1975 Feb
PMID:An experimental model for studying myocardial ischemia. Correlation of hemodynamic performance and metabolism in the working swine heart. 111 38

To determine the hemodynamic characteristics of critical stenosis of coronary arteries, mean left circumflex coronary artery (LCCA) flow, myocardial peak reactive hyperemic response (PRHR), myocardial PO2 and PCO2 electrocardiograms, and aortic pressure were monitored at precise degrees of LCCA stenosis in 18 dogs. Stepwise LCCA constriction by a specially designed occluder resulted in a gradual drop in PRHR but little change in other variables. When PRHR was reduced 96 per cent, critical stenosis was achieved, and further constriction caused pronounced and sudden changes in all parameters. When critical stenosis occurred, LCCA diameter had been reduced by 74 plus or minus 2 per cent. Mean LCCA flow was reduced from a base-line level of 42 plus or minus 2 to 34 plus or minus 2 c.c. per minute. PO2 in the myocardium was reduced from 24 plus or minus 1.5 to 16 plus or minus 1.6 mm. Hg. PCO2 increased from 43 plus or minus 5 to 55 plus or minus mm. Hg. T waves in Lead II because isoelectric. The myocardium was well perfused and able to regulate flow through an artery narrowed up to 74 per cent. Beyond this point of critical stenosis, the vascular bed was maximally dilated and further narrowing caused ischemia. These findings indicate that PRHR may be useful at operation to determiine whether all significant lesions are bypassed and whether graft flow is adequate.
J Thorac Cardiovasc Surg 1975 Feb
PMID:Hemodynamic characteristics of critical stenosis in canine coronary arteries. 111 39

The influence of the nervous system on the response of the coronary vessels to ischemia was evaluated by observing the reactive hyperemia subsequent to a 10 second occlusion of the left circumflex coronary artery in 19 awake dogs. Sympathectomy produced by pretreatment with 6-hydroxydopamine, chronic total surgical cardiac denervation, beta-adrenergic blockade with propranolol, and alpha blockade with phentolamine did not significantly after the reactive hyperemic response. Thus cardiac denervation did not impair the ability of the coronary vasculature to respond to a brief ischemic stimulus.
J Thorac Cardiovasc Surg 1975 Mar
PMID:Neurogenic influences on the coronary vascular response to ischemia in the awake dog. 111 33

In the USSR, like in other countries, aorto-arteritis is no rarity. Onehundred and twentysix patients with aorto-arteritis have been studied at the A.N. Bakulev Institute for Cardio-Vascular surgery during the past 13 years (81 women and 45 men from 8 to 49 years of age). Morphologic changes consisted in inflammatory infiltration of the adventitia and, to a lesser degree, of the media as well as in reactive hyperplasia of the intima. The predominant features in the chronic stage were those of sclerosis and fibrosis of the adventitia and the media which in combination with the intimal hyperplasia resulted in stenosis or occlusion of the aorta and its main branches. The clinical picture and symptpmatology depend largely on the localization, form, and severity of the lesions. In aorto-arteritis ischemia of various organs and hypertension can be eliminated only by radical reconstructive surgery of the aorta and its branches. The most adequate restoration of the blood flow in the major vessels is provided by resection combined with replacement. It is not quite clear yet whether endarterectomy is possible and justified. Radical surgery was performed in 80 patients. In addition, different palliative and explorative operations were performed in 10 patients. The majority of patients had resection with replacement of the brachiocephalic arteries, descending thoracic aorta, abdominal aorta, renal and visceral arteries. Blood flow in the major vessels was restored in 69 patients. Early postoperative thrombosis of the prosthesis occurred in 7 patients. Immediate postoperative mortality was 13.3 percent. Sixtytwo patients were followed up from 1 to 9 years after radical surgery. Persistent normalization or significant improvement of the systemic and regional hemodynamics was found in 53 patients. Late thrombosis of the aorto-renal branch or aorto-femoral prosthesis occurred in 4 patients. There were three late deaths.
J Cardiovasc Surg (Torino)
PMID:Nonspecific aorto-arteries. 112 4

Myocardial protection, in two parallel series of 100 consecutive valvular patients operated upon between June 1972 and July 1973 in Broussais Hospital, was afforded in two different ways: one withh hypothermic ischemia (H.I.) as it was advocated by N. Shumway, the other with coronary perfusion (C.P.) of a beating heart with consecutive ischemic periods limited to 20 minutes. Three parameters were used to evaluate the quality of protection: death with primary cardiogenic shock, post-operative myocardial infarction and acute cardiac insufficiency making it necessary to use post-operative inotropic support. Death was 1% (H.I.) and 5% (C.P.). Infarctions were 5% (H.I.) and 8% (C.P.). Acute cardiac insufficiency was: with cardiogenic shock 0% (H.I.) and 4% (C.P.), without cardiogenic shock 8% (H.I.) and 2% (C.P.). Peculiar aspects of myocardial infarction in each series are analyzed, and apparent absence of correlation between aortic cross-clamp time and ischemic complications is discussed. A "myocardial intrinsic factor" seems to be part of each valvular group and appears also to be an important factor in producing ischemic complications.
J Cardiovasc Surg (Torino)
PMID:Selective cardiac hypothermia versus coronary perfusion. A study of ischemic complications in two series of 100 consecutive valvular patients. 115 Jul 30

Cardiac biopsies were taken from the hearts of 40 patients undergoing open heart surgery for acquired and congenital disease. Tissue samples were taken prior to aortic cross-clamping, at the end of the ischemic period, and 20 minutes after reperfusion. Cardiac arrest was induced with Kirsch's cardioplegic solution at mild hypothermia (28-30 degrees C). Electron-microscopy of these tissue samples showed that cardioplegic arrest allows safe recovery with a tolerable degree of cellular alterations following ischemic periods of approximately 45 minutes. This period of reversible ischemia agreed well with similar studies in dogs that were completed by metabolic studies. ATP4-time in these dogs was 60 minutes under conditions closely resembling those at operationmin spite of the similarity between ischemia tolerance times, marked discrepancies existed on the ultrastructural level. Human hearts showed, generally, a much more marked degree of cellular alterations. The good correlation between ultrastructural alterations and the metabolic status of the canine heart can, therefore, not be used to predict levels of metabolites from human electron-micrographies.
J Cardiovasc Surg (Torino)
PMID:Ischemia-tolerance following cardioplegic arrest in human patients and in experimental animals. 115 Jul 32

Our clinical experiences with ischemic tolerance of the human heart under the condition of ECC during the last 15 years allow us to state the following points: 1. The healthy human myocardium can be exposed to ischemia without danger on the basis of 15 min and a myocardial temperature of 35 degrees C. This time can be prolonged following the described value of Q10=2. 2. The previous damaged human myocardium is usually not able to cover this range. Frequently ischemic load within these limits causes functional deterioration. So, in such cases ischemic tolerance has to be applied on a distinct lower base. 3. Occasional transgressions of the described ischemic tolerance time without a fatal result do not allow us in our clinic to leave the effective principles in daily routine.
J Cardiovasc Surg (Torino)
PMID:Ischemic tolerance of the human heart during extracorporeal circulation: clinical experience. 115 Jul 34

The pulmonary artery of anesthetized dogs was constricted until right ventricular failure occurred (decreased cardiac output and aortic blood pressure; elevated right ventricular end-diastolic pressure). Coronary blood flow distribution was measured by means of an electromagnetic flowmeter and radioactive microspheres. With moderate levels of pulmonary stenosis (right ventricular pressure to 60 per cent of systemic pressure), right ventricular coronary flow increased (30 per cent, p smaller than 0.01) despite a significant fall in right ventricular driving pressure (aorto-right atrial pressure). Right ventricular failure occurred when right ventricular coronary flow did not increase sufficiently to meet raised oxygen requirements. Opening a pulmonary-systemic shunt during right ventricular failure increased pulmonary blood flow but lowered coronary driving pressure further, as blood was diverted into the lungs through the low-resistance fistula. Consequently, right ventricular coronary flow fell 50 per cent (p smaller than 0.01) and right ventricular failure with pulmonary stenosis resulted in a 362 per cent (p smaller than 0.01) increase in right coronary flow plus improved cardiac output. We made the following conclusions: (1) Right ventricular failure with pulmonary stenosis and intact ventricular septum is due to inadequate right ventricular blood flow to meet raised oxygen demands; (2) opening a pulmonary-systemic shunt may potentiate this failure and exaggerate ischemia by lowering coronary driving pressure and reducing right ventricular coronary flow.
J Thorac Cardiovasc Surg 1975 Jul
PMID:Effects of systemic-pulmonary shunts on regional myocardial blood flow in experimental pulmonary stenosis. 115 98


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