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

The evolution and continuous improvement of the ultrasonic diagnostic devices allows an hemodynamic and morphological exploration of the deep abdominal vessels that until now seemed to be precluded to non invasive diagnostic techniques. For example, the angiodynography today advantageously substitutes classical urographic investigation during the initial screening of the hypertensive patients suspected of stenotic lesions of the renal arteries. In fact the ecocolordopplersonography allows not only a morphological evaluation of the parenchyma and of the renal vascular tree, but also supplies a quantitative measurement of the blood flow through the renal artery. Still more important are the possibilities offered by these devices in the study of the acute or chronic intestinal ischemia, in which until now a sure diagnosis was only possible using invasive techniques. Performing a study of the mesenteric vascularization urgently, sometimes is possible a decisive demonstration of an ischemic pathology where the clinical abdominal picture provides only uncertain diagnostic elements.
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PMID:New diagnostic and screening possibilities in the stenobliterative lesions of the deep visceral vessels. 209 Sep 88

We have given an overview of the management of the acute myocardial infarction patient utilizing the aggressive reperfusion techniques available today. Anatomic reperfusion rates have been over 95% with the combined methods described. The remaining problems technically are those of earlier reperfusion, methods to enhance myocardial recovery after ischemia, and prevention of restenosis or reocclusion. The use of laser methodology, coronary sinus retroperfusion, partial left heart bypass, and other innovative strategies may improve these results. The introduction of tissue plasminogen activator will affect our approach and will profoundly alter society's expectations of therapeutic success. Still, patients will die from acute myocardial infarction and its complications. The search for a prevention must, therefore, not be overshadowed by our current enthusiasm for reperfusion techniques. Hopefully, our current approach will become a historical footnote as breakthroughs in preventive strategies occur.
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PMID:Newer emergency reperfusion techniques in acute myocardial infarction. 328 52

In most reviews of arterial embolism or thrombosis the source of emboli or the cause of thrombosis can reasonably be established in over 90% of patients. Still about 10% remain without demonstrable cardiac or intraarterial sources. Although hypercoagulability induced by malignancy has been alluded to as a cause of unexplained intravascular thrombosis reports of arterial thromboembolism with such association are rare. Seven patients with unequivocal thromboembolism are presented. Two distinct clinical patterns are observed, one with in situ thrombosis of small arteries and the other with occlusion of large arteries causing limb ischemia or fatal organ infarction. The various pathogenetic mechanisms of arterial thrombosis or embolism in malignancy include sustained spasm of arteries, precipitation of cryoglobulins or other abnormal proteins in small arteries, direct tumor invasion of arteries, fragmentation and embolization of intracardiac or intraarterial metastases and spontaneous arterial thrombosis due to hypercoagulability. The hypercoagulable state can be recognized by the observation of shortened bleeding and clotting times, partial thromboplastin and prothrombin times, elevation of coagulation factors, platelets and yield stress index and resistance to anticoagulation. Patients presenting with arterial thromboembolic events with out demonstrable source should be investigated for malignancy. Conversely patients with malignancy should be searched for evidence of hypercoagulability in an attempt to prevent arterial thromboembolic complications.
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PMID:Arterial thrombosis and embolism in malignancy. 403 Aug 80

The beneficial effect of chronic beta-blockade in patients with congestive heart failure has been repeatedly shown since its introduction into treatment for this condition in 1975. Still this kind of therapy remains controversial, it is sometimes regarded as a therapeutic paradox, and its use is mainly limited to specialist centers. Various favorable effects of beta-blockers in patients with heart failure due to idiopathic dilated cardiomyopathy and ischemic heart disease have been demonstrated, the principal among them being reduction in energy requirements and ischemia, antiarrhythmogenic effect, improvement of diastolic function, protection of myocytes against catecholamine overload, centrally mediated increase in vagal tone, upregulation of beta-adrenergic receptors, and possible blockade of autoantibodies against beta 1-receptors. Although most of the studies used metoprolol, these effects may be relevant to certain other beta-blockers. Despite very solid pathophysiological and pharmacological rationales for the use of beta-blockade, a major obstacle for a general acceptance of this therapeutic concept is the striking contrast between hemodynamic changes during the acute effect and long-term treatment. When titrated carefully from very low doses and used with a true commitment to long-term treatment, beta-blockers have been shown to prevent further deterioration of heart failure and to improve hemodynamics, exercise tolerance, quality of life, and prognosis.
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PMID:Use of beta-adrenoceptor blockers in patients with congestive heart failure. 766 94

The involvement of calcium ions in mechanisms of ischemic brain injury has been suggested for several years. Our understanding of the role of intracellular Ca2+ as a trigger of acute neurotoxicity and in the induction of long lasting processes leading to necrotic and/or apoptotic postischemic delayed neuronal death or of compensatory, neuroprotective mechanisms has increased considerably. Still many questions concerning the generation of Ca+ signal such as the nature of the main routes of ischemic Ca2+ influx to neurones, involvement of intracellular Ca2+ stores and Ca2+ buffers, spatial and temporal relations between ischemia-induced increases in intracellular Ca2+ concentration and neurotoxicity remain open. Some conclusions from experiments in cultured neurones concerning glutamate-evoked destabilization of Ca2+ homeostasis and neurotoxicity may be not relevant to in vivo ischemic conditions. This review, apart from emphasising generally proposed mechanisms of Ca2+ transients and toxicity in ischemic neurones, will discuss some of these controversial issues.
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PMID:Calcium transients in brain ischemia: role in neuronal injury. 878 90

Ischemia-reperfusion injury is one of the major problems in reconstructive microsurgery. The ischemic insult may be due to an occlusion of either the artery or the vein. Clinical observations have suggested that flap survival is more sensitive to venous stasis than to arterial ischemia. The current study evaluated the viability of the myocutaneous rectus abdominis flap following secondary arterial or venous occlusion and its possible dependency on tissue metabolites and length of the preceding reperfusion period. Forty-eight bilateral 5 X 10 cm myocutaneous rectus abdominis flaps were elevated in 24 pigs and exposed to consecutive periods of primary ischemia (2 hours), reperfusion (1, 4, 8, and 12 hours), and secondary pedicle occlusion (6, 8, 10, 12, 14, or 16 hours) of arterial or venous origin. Muscle adenosine triphosphate (ATP) and glucose-6-phosphate (G6P) were assessed immediately after flap elevation, at the end of primary ischemia, after reperfusion, and at the end of secondary ischemia. Flap viability was assessed 5 days after the operation. Secondary venous occlusion resulted in reduced survival rates as compared with arterial occlusion (9 of 24 versus 20 of 24; p < 0.01), although the average ATP content was higher in flaps subjected to venous stasis [median (25 to 75) percentiles, 3.7 (1.7 to 7.1) micromol/gm protein] than in those subjected to arterial ischemia 1.2 (0.8 to 1.8 micromol/gm protein) (p < 0.01). During reperfusion, muscle ATP decreased from 28.5 (17.9 to 36.6) micromol/gm protein to 15.4 (7.4 to 24.9) micromol/gm protein (p < 0.01) and glucose-6-phosphate from 7.6 (4.1 to 11.6) micromol/gm protein to 1.0 (0.5 to 4.1) micromol/gm protein (p < 0.01). Still, flap survival following secondary arterial ischemia was improved by increasing the reperfusion time from 1 to 8 hours (p < 0.05). No effect of reperfusion time was seen on viability after venous stasis. In conclusion, despite poorer flap survival, venous stasis was less detrimental to tissue ATP level, suggesting that the continued inflow may have supplied substrates for glycolysis. Furthermore, the larger blood volume may have accumulated the glycolytic waste products. After reperfusion, the recovery of aerobic metabolism was far from complete, and cellular glycolytic substrates were nearly exhausted. However, prolongation of the reperfusion time preceding secondary arterial ischemia improved flap survival.
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PMID:Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels. 904 3

Affinity of hemoglobin (Hb) for O2 determines in part the rate of O2 diffusion from capillaries to myocytes by altering capillary PO2. We hypothesized that a decrease in Hb O2 affinity (increased P50) would increase capillary and tissue PO2 (PtiO2) and improve O2 consumption during ischemia. To test this hypothesis, blood flow to the pump-perfused left hindlimb of 18 anesthetized and paralyzed dogs was progressively decreased over 90 min while hindlimb O2 consumption and O2 delivery (QO2) and PtiO2 were measured at the muscle surface. Arterial PO2 was maintained at 150 +/- 10 Torr in all dogs. We increased P50 by 12.3 +/- 0.9 (SE) Torr in nine dogs with RSR-13, an allosteric modifier of Hb. This decreased arterial O2 saturation to 90-92% but increased mean PtiO2 from 35.5 +/- 11.6 to 44.1 +/- 15.2 (SD) Torr (P < 0.05) with no change in controls (n = 9). O2 extraction ratio at critical QO2 was 74 +/- 2% in controls and 79 +/- 1% in RSR-13-treated dogs (P = not significant). PtiO2 was 30-40% higher in the RSR-13-treated group at any QO2 above critical but did not differ between groups below critical QO2. Perfusion heterogeneity and convergence of the dissociation curves near critical QO2 may have mitigated any effect of increased P50 on O2 diffusion. Still, increasing P50 by 12 Torr with RSR-13 significantly increased PtiO2 at QO2 values above critical.
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PMID:Raising P50 increases tissue PO2 in canine skeletal muscle but does not affect critical O2 extraction ratio. 937 39

Each year, thousands of peoples die, suffering from an anatomical or functional loss of their intestine; these patients would benefit from bowel transplantation; the difficulties of bowel transplantation are as follows: 1. the physiological characteristics of the small bowel, and the fact that denervation, lymphatics interruption and ischemia, independently from rejection, may disturb its function; 2. secondly, the organ is septic; thus, its transplantation causes major infectious problems; 3. at last, the immunological characteristics of the intestinal allograft. Bowel transplantation causes a two-way immunological conflict, not only a standard rejection response, but also a graft-versus-host disease, similar to that observed after bone marrow transplantation; this reaction is caused by the lymphoid tissue conveyed within the bowel graft. The introduction of a new immunosuppressive molecule, FK 506, in combination with profound antibiotic prophylactic regimens, decontamination protocols and vigorous anti-viral protection (against cytomegalovirus and Epstein-Barr), have significantly improved the results. Bowel transplantation has recently reached clinical application. The one-year survival rate of intestinal grafts reaches now 70%. Still, there is no doubt that, due to its microbiological and immunological characteristics, the small bowel will remain the most challenging abdominal organ to transplant.
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PMID:[Intestinal transplantation: a clinical reality in 1998]. 976 Jul 59

The introduction of open-heart surgery more than 4 decades ago signaled a new era in medicine. For the 1st time, previously untreatable cardiac anomalies became amenable to surgical therapy. The use of the heart-lung machine seemed to grant the surgeon unlimited time in which to operate inside the heart. Still frustrated by poor operating conditions and the threat of air embolism, Denis Melrose introduced elective cardiac arrest in 1955. His use of a potassium citrate solution seemed to offer a safe method to effect a quiet, bloodless field. However, a few years after its inception, numerous reports began to question the safety of this approach, and the Melrose technique was abandoned in the early 1960s. Nearly 15 years elapsed before potassium-based cardioplegia regained popularity. During this period, topical hypothermia, coronary perfusion with intermittent aortic occlusion, and normothermic ischemia were evaluated and discarded. A few European investigators like Hoelscher, Bretschneider, and Kirsch had maintained their interest in chemical cardioplegia, and it was through their efforts that future researchers like Hearse and Gay spearheaded the return to potassium-based cardioplegia, which today forms the core of the cardiac surgeon's myocardial protective armamentarium and has contributed towards lowering operative mortality rates.
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PMID:Myocardial protection: the rebirth of potassium-based cardioplegia. 1021 72

Dobutamine-atropine stress echocardiography (DASE) is an established method and has been shown to be accurate for the detection of coronary artery disease. Still, there are few large clinical studies that analyze the safety of DASE in general or the safety of performing it on an ambulatory basis. Most studies use a target heart rate as the primary end point regardless of whether asymptomatic ischemia occurs. Such studies have shown a serious cardiac event rate of approximately 0.3%. We prospectively studied 4,033 consecutive patients on an ambulatory basis and in the hospital with the use of DASE from July 1991 to December 1998. All tests were performed by an experienced physician, and all clinical and DASE data were stored in a large database organized at the beginning of the study. Dobutamine was infused in scalar doses of 5, 10, 20, 30, and 40 microg/kg per minute in 3-minute stages. Development of a new wall motion abnormality, achievement of 85% of target heart, and end of the DASE infusion protocol were used as an end point. If 85% of the target heart rate was not achieved, atropine was infused up to 1 mg in the absence of myocardial ischemia, which was used in 1,280 studies. There were 3,645 diagnostic tests, and 388 (10%) were found to be nondiagnostic. This result was due to poor image quality in 115 (3%), end of protocol in negative-submaximal examinations in 124 (3%), and limiting side effects in 149 (4%). Thirty-seven percent of the tests showed positive results for myocardial ischemia. Major test-related cardiac complications occurred in 10 (0.25%) patients and included 1 ventricular fibrillation, 1 case of myocardial infarction, and 8 cases of sustained ventricular tachycardia. Atropine poisoning was observed in 5 (0.12%) patients. No deaths occurred as a direct or indirect consequence of DASE. We conclude that dobutamine-atropine stress echocardiography is a reasonably safe method for detection of coronary artery disease in the hospital or in an ambulatory basis. The use of new wall motion abnormality as 1 of the end points may prevent further ischemia-related complications.
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PMID:Safety of dobutamine-atropine stress echocardiography: A prospective experience of 4,033 consecutive studies. 1051 46


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