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

The influence of controlled ischemia on myocardial ultrastructure was investigated in isolated, metabolically supported canine hearts. Recovery of functionally normal tissue as indicated by the reversibility of morphological alterations was observed up to 60 minutes of anoxia. It was shown that prolonged reperfusion of the empty beating heart supports the recovery of normal cellular ultrastructure. Severe ischemic damage of mitochondria due to ischemia of 60 minutes was almost completely reversible after a reperfusion period of 50 minutes.
Thorac Cardiovasc Surg 1979 Feb
PMID:Recovery of the heart after normothermic ischemia. Part I: Ultrastructural findings during postischemic reperfusion. 44 56

Malperfusion due to increased coronary vascular resistance is presumably one of the factors responsible for incomplete functional recovery of the heart after aortic cross-clamping. Myocaridal blood flow (MBF, radioactive microspheres) was measured before and after 60 min of hypothermic ischemia in 16 dogs on cardiopulmonary bypass. After ischemia the hearts were reperfused for 30 min. MBF was measured in the empty beating heart and in the isovolumetrically contracting ventricle loaded with enddiastolic volumes (EDV) of 10, 20 and 30 ml (intraventricular latex balloon).
Thorac Cardiovasc Surg 1979 Apr
PMID:Regional myocardial blood flow after hypothermic arrest and cardioplegia. 45 86

The effects of 1 and 2 hours of hypothermic anoxic arrest and cardioplegia induced by Mg-lidocaine, K-Mg, or K on left ventricular mitochondrial respiratory function, blood flow, and edema were studied in 41 mongrel dogs. Mitochondrial respiration was assessed by the indices of oxidative phosphorylation. Myocardial temperature recorded in ventricular septum was kept at 20 degrees C during ischemic arrest and 10 minutes of reperfusion. Cardioplegic solutions did not influence noncoronary blood flow during cross-clamping of the aorta. Mitochondrial respiratory function remained at control levels after 1 hour of ischemia induced by hypothermic anoxic arrest or by Mg-lidocaine or K-Mg hypothermic cardioplegia. Mitochondrial state 3 respiration after 2 hours of anoxic arrest was significantly higher in Mg-lidocaine cardioplegia than in anoxic arrest (p less than 0.05), but myocardial edema was equivalent in both groups. Mg in the cardioplegic solution suppressed mitochondrial nonphosphorylating oxygen consumption. These data suggest that mitochondrial function after 1 hour of ischemic arrest at 20 degrees C and 10 minutes of reperfusion is not significantly depressed, but at 2 hours of ischemic arrest, mitochondrial respiration is significantly impaired. However, hypothermic Mg-lidocaine cardioplegia appears to be more effective in sustaining myocardial respiration than does simple hypothermic anoxic arrest when the anoxic period is extended to 2 hours.
J Thorac Cardiovasc Surg 1979 Aug
PMID:Myocardial respiration and edema following hypothermic cardioplegia and anoxic arrest. 45 28

Contraction and relaxation of the canine myocardium were examined during normothermic ischemia in an isolated heart model. Decrease in the development of tension depends on the duration of ischemia. Deficient functional recovery was observed after ischemic periods extending beyond 30 minutes, in spite of reperfusion periods of over 1 hour. A decrease in compliance was observed during the anoxic period, but a persistent defect of relaxation occurred only after 60 minutes of ischemia. After this period there was also a disturbance in the autoregulative mechanisms of coronary perfusion and an uncoupling of O2-consumption and mechanical efficiency. A prolonged reperfusion period of the heart beating empty allowed ultrastructural recovery of the damaged myocardium. In contrast, functional recovery of the myocardium, as determined by several parameters of contraction and relaxation, did not correlate with ultrastructural recovery and was not improved by prolonged reperfusion.
Thorac Cardiovasc Surg 1979 Jun
PMID:Recovery of the heart after normothermic ischemia. Part II: Myocardial function during postischemic reperfusion. 46 62

To determine the protective effects of different methods of cardioplegia, studies on ATP/lactate levels and ultrastructure were performed in human papillary muscles obtained during mitral valve replacement. In group I (n = 5), plain ischemic arrest in hypothermia (systemic venous temperature = 24 degrees C) was accomplished. In group II (n =12), the heart was arrested by injection cardioplegia using magnesium-aspartate-procaine at systemic venous and myocardial temperatures of 24 degrees C. In group III (n = 12) Bretschneider infusion cardioplegia at systemic venous and myocardial temperatures of 26 degrees C and 19 degrees C respectively was applied. With regard to ultrastructural changes there were no clearcut differences in the three methods of hypothermic cardiac arrest after 60 minutes of ischemia. Ischemic changes tended to be slightest in group III (infusion cardioplegia). ATP decay and lactate increase were significant in group I and moderate to minimal in groups II and III after the same period of time. It is concluded that for aortic cross-clamp times up to 60 minutes, body hypothermia and injection cardioplegia using magnesium-aspartate-procaine at a myocardial temperature of 24 degrees C provide adequate protection of the myocardium. For ischemia times beyond 70 minutes, profound myocardial hypothermia below 20 degrees C is preferred.
Thorac Cardiovasc Surg 1979 Aug
PMID:Ultrastructural and biochemical changes of human papillary heart muscle during different methods of induced cardiac arrest. 49 22

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
J Thorac Cardiovasc Surg 1979 Dec
PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

1. In thoracic outlet-syndrome arterial lesions--such as poststenotic aneurysm with or without peripheral arterial emboli--are mostly caused by permanent compression of the vessel. In 48% of cases arterial emboli show to be the first clinical manifestation of a subclavian artery lesion. 2. Venous lesions usually classified as "spontaneous axillar vein thrombosis" are probably initiated by intimal lesions of the axillary vein caused by compressionof this vessel in the costoclavicular space. 3. Unilateral ischemia of fingers or hand--especially in young patients--should be considered first of all as a peripheral manifestation of a cervical rib-syndrome. Surgical correction should include besides rib resection, lumen control of the poststenotic dilated artery, disobliteration of occluded main arteries and thoracic sympathectomy in cases with several distal arterial embolic occlusions. 4. Venous thrombectomy for acute thrombosis of the axillary and subclavian vein should be combined with the resection of the first rib in order to prevent any further compression to the vein in the costoclavicular space. The use of a temporary a.v.-fistula may be used as an additional mens for keeping the disobliterated vein patent. 5. In the thoracic outlet-syndrome neurological signs and complaints caused by intermittent or permanent mechanical nerve irritation represent the most frequent clinical findings (i.e. 90%). On the other hand in two thirds of patients with arterial or venous complications neurological signs are missed and therefore do no help for diagnosis.
J Cardiovasc Surg (Torino)
PMID:Thoracic outlet-syndrome with vascular complications. 51 18

Infected aneurysms involve the aorta, visceral and peripheral arteries and are associated with a high morbidity and mortality. Prompt confirmation of the suspicion of infection, resection of all infected tissue, and prolonged antibiotic therapy based on appropriate sensitivity studies are crucial to successful management. Patients whose aortic aneurysms grew Gram negative organisms were more likely to suffer early rupture of an aortic aneurysm, and had a higher mortality. Superior mesenteric aneurysms are preferably treated by resection. Upper extremity aneurysms can often be excised without distal ischemia. Lower extremity aneurysms were more likely to require reconstruction which can be accomplished through non-infected tissue planes, preferably with autogenous tissue.
J Cardiovasc Surg (Torino)
PMID:The management of infected arterial aneurysms. 57 24

The effect of pulsatile cardiopulmonary bypass on intramyocardial gas tensions and regional myocardial blood flow was studied in 10 mongrel dogs. Following application of a critical stenosis to the circumflex coronary artery (CIRC), animals were placed on total bypass with vented, fibrillating hearts. During three 45 minute periods of perfusion, animals alternately received pulsatile or linear flow with perfusion pressure carefully maintained at 80 mm. Hg. In myocardium supplied by the stenosed CIRC, intramyocardial oxygen tension (PO2) rose from 13 +/- 3 to 19 +/- 5 mm. Hg when a period of linear flow was followed by a period of pulsatile flow (p less than 0.025). Similarly in the CIRC-supplied area, intramyocardial carbon dioxide (PCO2) decreased from 128 +/- 12 to 99 +/- 12 mm. Hg (p less than 0.005) with conversion from linear to pulsatile flow. Myocardial blood flow (microsphere technique) to endocardial and epicardial layers of the CIRC-supplied area was significantly greater (p less than 0.05) during pulsatile than during linear perfusion. In contrast, when periods of pulsatile bypass were followed by periods of linear perfusion, myocardial PO2 fell from 25 +/- 6 to 9 +/- 3 (less than 0.02) and myocardial PCO2 rose from 82 +/- 12 to 154 +/- 12 mm. Hg (p less than 0.001). These data suggest that (1) fibrillation-induced regional ischemia distal to a critical coronary stenosis can be reduced by pulsatile perfusion during bypass and (2) the mechanism for the reduction in regional ischemia is improved myocardial blood flow.
J Thorac Cardiovasc Surg 1978 Feb
PMID:Comparison of regional myocardial blood flow and metabolism distal to a critical coronary stenosis in the fibrillating heart during alternate periods of pulsatile and nonpulsatile perfusion. 62 24

The patterns of regional contractile function were examined with ultrasonic crystals in "open-chest" anesthetized dogs. In normal myocardium, the base-line end-diastolic segment length (EDL) was 1.63 +/- 0.12 cm. and the mean systolic length (MSL) was 1.47 +/- 0.17 cm. Mean velocity of shortening over the first one third of systole (V1/3) was 15.9 +/- 2.3 mm. per second. Coronary occlusion induced regional ischemia with segmental dyskinesia (MSL = 1.84 +/- 0.12 cm). Reperfusion after 5 or 10 minutes of occlusion induced rapid recovery of contractile function that was independent of catecholamine release, as demonstrated in animals pretreated with 6-OH dopamine. After initial recovery, however, contractile function deteriorated. There were an increase in EDL (from 1.73 +/- 0.11 to 1.78 +/- 0.11; p less than 0.001) and the appearance of early systolic dyskinesia. V1/3 diminished from 5.6 +/- 4.6 to -6.6 +/- 2.5 mm. per second (p less than 0.005). Thus reperfusion damage, defined as late deterioration after recovery from brief periods of ischemia, may be partly distinct from ischemic damage per se. It is possible that the deterioration of myocardial function which accompanies reperfusion of previously ischemic myocardium may be a contributing factor in the transient myocardial dysfunction that is occasionally seen following cardiopulmonary bypass.
J Thorac Cardiovasc Surg 1978 Mar
PMID:Contractile damage from reperfusion after transient ischemia in the dog. 63 43


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