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

A new colloid hyperosmolar solution with high concentrations of proteins, potassium, and glucose has been favorably compared with a crystalloid, intracellular, and hyperosmolar solution (Sacks II) for 24-hr hypothermic storage of ischemic and nonischemic canine kidneys. Sixty minutes of warm ischemia was overcome by all kidneys flushed with the colloid hyperosmolar solution. In four of six ischemic kidneys flushed with Sacks' solution the function returned to normal limits. Hypothermic storage (24 hr) without warm ischemia did not cause any deleterious effects on either one of the flushed group of kidneys. Thirty minutes of warm ischemia followed by 24-hr hypothermic storage was tolerated by most of the kidneys (83%) flushed with the colloid hyperosmolar solution and one-half of the kidneys flushed with the crystalloid hyperosmolar solution. Sixty minutes of warm ischemia and 24-hr hypothermic storage was detrimental to 50% of the kidneys flushed with the colloid hyperosmolar solution.
Transplantation 1978 Sep
PMID:Comparison of sacks and a new colloid hyperosmolar solution for hypothermic renal storage. 70 72

In advanced ischemia of the lower extremity, the deep femoral artery is rarely completely occluded, but may have a hemodynamically significant occluding plaque at its origin. Detection of this lesion requires biplanar arteriographic views. As indicated in this report, the related simple procedure of femoral artery profundaplasty may salvage limbs and lower amputation sites, and it is suitable for poor risk patients.
Am J Surg 1978 Sep
PMID:Femoral artery profundaplasty. 70 5

Obstructive lesions of the profunda femoris artery extending beyond the lateral circumflex branch were repaired in sixty-two limbs with superficial femoral occlusion and profound ischemia. The operation relieved rest pain in all thirty-four limbs with this symptom. Of twenty-eight limbs with tissue loss, twenty-two were salvaged without further reconstructive surgery. This experience illustrates that in diffuse profunda disease, extended profundaplasty is a useful alternative to femoropopliteal by pass, particularly for the relief of rest pain, and does not preclude more distal arterial reconstruction.
Am J Surg 1978 Sep
PMID:The use of extended profundaplasty in limb salvage. 70 6

The influence of an instantaneous increase in afterload on the hemodynamics and regional myocardial function was studied in five anesthetized dogs before and after occlusion of the left anterior descending coronary artery. By inflation of an intaaortic balloon during single ejections, an instantaneous increase in afterload was obtained. From biplane cineventriculograms, the following parameters were calculated: left ventricular volumes (EDV, ESV), stroke volume (SV), ejection fraction (EF). Mean circumferential fiber shortening (V CF) was calculated in three ventricular diameters in the RAO projection. Simultaneously PLV, PLVED, PAo, and LV dp/dt were obtained. In the control ventriculograms, an increased afterload (delta PLV 16.4 +/- 8 mm Hg) caused only a minor decrease of SV (2.6 +/- 2.5 ml), EF (4.2 +/- 2.4%), and V CF (0.20 circ . s -1). After coronary occlusion (delta PLV 14.5 +/- 6.7 mm Hg),the reduction of SV (5.9 +/- 2.7 ml) and EF (8.2 +/- 2.6%) was more pronounced. This was caused mainly by a significant reduction of V CF in the center of ischemia (delta V CF -93%). For the evaluation of regional myocardial function by ventriculography, the marked influence of afterload in ischemic areas must be taken into consideration. This is of special interest in comparative ventriculograms, such as those before and after coronary bypass surgery.
Z Kardiol 1978 Sep
PMID:[The influence of afterload on the normal and ischemic myocardium in the dog]. 71 34

Gliosis is increased in the respiratory control area of the brainstem in victims of sudden infant death syndrome (SIDS), as it is in infants who have died of congenital heart disease. In the latter, the lesions appear to result from hypoxia or ischemia, and studies of the brainstem microvasculature of SIDS victims indicated a close relationship between the gliosis and adjacent vasculature. It is postulated that cerebral hypoperfusion may play a role in SIDS.
Ann Neurol 1978 Sep
PMID:Cerebral hypoperfusion in the sudden infant death syndrome? Brainstem gliosis and vasculature. 71 38

Rats were subjected to a 30% body surface area full-thickness burn. Two hours after injury, 93% of animals had gastric mucosal erosions. At 5 hours this increased to 100%, but at 24 and 72 hours, lesions were fewer and less severe. Histologic study suggested that lesions noted at 24 and 72 hours represented erosions formed earlier. No mucosal abnormalities were noted in control rats. A causal relationship between mucosal ischemia and the development of erosions is suggested by the presence of A-V shunts at 2 and 5 hours only. Significant increases in H+ back-diffusion and protein leakage into the gastric lumen at 2 and 5 hours also implicated changed mucosal permeability in the etiology of erosions. The return of H+ back-diffusion to control values at 24 and 72 hours, when lesions were still present, appears to contradict the theory that permeability changes are secondary to erosion formation.
J Trauma 1978 Sep
PMID:Gastric mucosal lesions after burn injury: relationship to H+ back-diffusion and the microcirculation. 73 53

As a part of the series of studies on lipid metabolism in ischemic myocardium, the present study was attempted to analyse 29 infarcted hearts with acute or scar lesions by a routine histopathology and lipid histochemistry. The time after the onset of attack till death ranged from one day to years. Sixteen were of the acute form, less than 2 month-old, and 13 were of the chronic scarred form. Within the first day, fat deposition appeared in the survived muscle cells around the infarcts reaching the peak from 2 days to one week, but necrotized cells never contained fat droplets. Macrophages in granulation tissue in periphery of the infarcts tended to have significant fat droplets usually in 10 days to one month. Fat disappeared from the survived muscle cells and also from the scar later than 2 months. The survived cells around the infarcts might be degenerated with fat, probably triglyceride, which accumulated by a relative ischemia not severe enough to produce coagulation necrosis, and they bear some relationship with extension or limitation of size of infarcts.
Acta Pathol Jpn 1978 Sep
PMID:Histochemical study on lipid metabolism in acute myocardial infarction. 73 9

Unstable angina is a syndrome which comprises a spectrum of symptomatic manifestations of coronary artery disease which lies between stable angina pectoris and acute myocardial infarction. Patients fall into three groups: angina of recent onset (4 weeks), angina of changing pattern, and angina occurring at rest (longer than 15 minutes). The syndrome may presage acute myocardial infarction or sudden death, or may itself be the manifestation of a myocardial infarction. The pathophysiology may involve primary cardiac events or extracardiac precipitating factors, and does not appear to be the consequence of a particular anatomic pattern of coronary artery disease. Pain may occur as a result of regional reduction of coronary flow to pressure-dependent areas of myocardium during states of increased myocardial oxygen demand. Persisting ischemia leads to infarction via a series of events which may include myocardial edema formation, increased beta-sympathetic tone, and others which have been experimentally modified by interventions designed to limit infarct size. Although the incidence of acute myocardial infarction and death was high in early studies, in recent reports acute infarction occurs in under 15.5 per cent and death in under 2 per cent. Patients at high risk are those pain persists with bed rest, and those with preceding stable angina pectoris or myocardial infarction. Prognostic differences among Groups 1, 2, and 3 may exist but cannot be assessed from available studies. Studies of the management of unstable angina have generally been uncontrolled. Hospitalization, bed rest, and short- and long-acting nitrates are generally employed in Groups 2 and 3 patients and the marked reduction in myocardial infarction rates from early to recent studies tends to support these approaches. Anticoagulants are less used now than formerly. Propranolol can produce a significant reduction of myocardial oxygen consumption and may redirect coronary flow to ischemic areas. The drug has effectively controlled pain in several studies and is now widely used to manage unstable angina. Aortocoronary bypass surgery has been extensively employed but there is only one preliminary report of a controlled study available. The role of surgery is not yet defined. The optimal approach to therapy may eventually involve the use of medical therapy, including beta-blockade to stabilize patients, with delayed semielective coronary angiography and surgery in those who respond. Emergency angiography and surgery might then be reserved for the high-risk group of patients whose pain persists during optimal medical therapy.
Am Heart J 1976 Sep
PMID:Unstable angina pectoris. 78 21

We can summarize the results of our studies as follows (Fig. 15). The critical cellular factors involved in the loss of reversibility following ischemia appear to be the mechanisms involved in the membrane function of energy transduction. Irreversibility appears to correlate with an irrepairable defect in energy transduction. This could involve both the mitochondrial energy transduction functions and those in the plasma membrane. The mechanisms involved in this transition are not presently clear but they are associated with increased leakiness or permeability of these membranes accompanied by changes in lipid content, alterations in membrane proteins, and presumably in lipid-protein interactions. There are two prominent theories to explain energy transduction. These are the "proton pump" hypothesis of Mitchell (1972) and the "paired moving charge" hypothesis of Blondin and Green (1975). Both of these hypotheses require integrated function of membrane components, i.e., lipid and protein. The hypothesis of Blondin and Green, however, can work even with discontinuous membrane sheets because it involves the concept of ribbons of protein embedded in the protein-lipid membrane matrix. The characteristic finding of our studies following ischemic injury, namely, the continuous electron flow well into the irreversible phase while the energy transduction is impaired, could be explained by both hypotheses. What do these observations have to say about theories of energy conservation? We have observed that the vectorial nature of the proton separation is stopped. Charge separation may not occur at this time across the membrane since proton gradient and possible membrane potential are abolished. Electron transport, however, continues indicating the generation of protons. Since the decline of P/O ratio, decline of proton gradient and the cellular "point-of-no-return" coincide, these observations point toward the important membrane defects acquired at that particular time. The "paired moving charge" model which involves moving ions encapsulated in endogenous ionophores such as lecithin and maintenance of magnesium is favpred by the observation that phosphatidyl choline and phosphatidyl ethanolamine are lost in correlation with irreversibility. Furthermore, the decrease in magnesium content of cells is closely associated with the loss of viability following ischemia. The "paired moving charge" hypothesis has the attractive feature in that it involves antagonistic effects of calcium and magnesium. During reflow, calcium may inhibit magnesium mediated transport of inorganic phosphate by lecithin. Also, according to this theory fatty acids or their cyclic anions which act as uncouplers may foster the loss of phosphorylation capacity.
Beitr Pathol 1976 Sep
PMID:Recent studies on the pathophysiology of ischemic cell injury. 79 Dec 45

Vascular-circulatory derangements affecting the function of the central nervous system may result in parenchymal lesions that are hemorrhagic, ischemic, or mixed. Most nontraumatic intraparenchymal brain hemorrhages are found in asssociation with cerebral arteriolar sclerosis and other stigmata of hypertensive disease, such as hypertrophy of the left cardiac ventricle and granular kidneys. Global temporary ischemia, the type that exists during severe and transient hypotension, results in a wide variety of parenchymal lesions that may be bilateral, hypotension, results in a wide variety of parenchymal lesions that may be bilateral, unilateral, supratenorial, or infratentorial. The cerebral and cerebellar cortices, white matter, basal ganglia, brain stem, and spinal cord may be involved simulatenously or there may be isolated, focal lesions that are confined occasionally to any one of these areas. Regions ischemia, the type induced through the occlusion of a major intracranial artery, evolves through a stage of acute encephalomalacia, during which the morphologic change consists of alternating cellular swelling and shrinkage. This is followed by leukocytic inflammation at three to four days and the beginning of resolution at about the tenth day after arterial occlusion. In the evolution of this form of abnormal circulation, after a few minutes, some neurons in the most distal arterial territories show the first recognizable changes. In these neurons the mitochondria swell massively. Astrocytes and neurites in the same foci are selectively swollen, whereas oligodendrocytes and capillaries remain structurally unchanged during the initial stages of ischemic injury.
Hum Pathol 1975 Sep
PMID:The neuropathology of stroke. 80 42


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