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

Postextrasystolic potentiation after a single closely coupled extrasystole may identify residual ventricular contractile performance in acutely ischemic myocardium without producing sustained secondary ischemic depression of myocardial function. Postextrasystolic potentiation was systematically used in eight open chest dogs to assess the progression of regional contraction abnormalities during a 10 minute occlusion of the left anterior descending coronary artery. Segment function was determined from pressure-length loop areas inscribed during right ventricular pacing at 128 +/- 3 (mean +/- standard error of the mean) beats/min, and after single closely coupled (179 +/- 3 msec) extrasystoles. Despite a 50 percent decrease in border zone segment function, postextrasystolic potentiation consistently augmented mechanical performance to control levels throughout the ischemic period. Central ischemic zone segment function deteriorated more profoundly, with the development of holosystolic aneurysmal bulging within 30 seconds after occlusion. Nonetheless, postextrasystolic potentiation produced marked inotropic augmentation, but not to control levels, for up to 10 minutes of ischemia. These results suggest that latent viability and contractile reserve may exist during brief periods of coronary occlusion.
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PMID:Experimental myocardial infarction. XVI. The detection of inotropic contractile reserve with postextrasystolic potentiation in acutely ischemic canine myocardium. 7 88

Axonal transport of acetylcholinesterase (AChE) and choline acetyltransferase (ChAc) and ultrastructural degenerative changes were compared in isolated nerve segments of rabbit peroneal nerves kept in vivo for 22 h, either with preserved blood supply (control segments) or under conditions of ischemia (ischemic segments). Ischemia abolished the proximo-distal and disto-proximal axonal transport of AChE and the proximo-distal transport of ChAc which, in control segments, were revealed by accumulations of the enzymes at corresponding ends of the segments. Total activities of AChE and ChAc recovered in isolated segments with intact blood supply corresponded to the activities in normal nerves; in ischemic segments, 50% of ChAc activity was lost in 22 h, whereas all AChE activity was preserved. Ultrastructural changes were found in few fibres in control segments and in many fibres in ischemic segments 22 h after nerve interruption. The early changes in control segments correspond to those described in the literature for peripheral stump of severed nerves. The microtubules, neurofilaments and mitochondria were not affected. In ischemic segments, various stages of axoplasmic disintegration occurred in the myelinated and unmyelinated axons:flocculation and clumping of axoplasmic material, decomposition of neurofilaments and microtubules, swelling, formation of amorphous densities and breakdown of mitochondrial cristae. Swelling, amorphous densities, clumping of nuclear chromatin and necrotic mitochondrial changes appeared also in Schwann cells. It is concluded that ischemia blocks axonal transport and brings about, within 22 h, ultrastructural changes both in nerve fibres and in Schwann cells. Cytoplasmic ChAc is affected earlier by necrotic degeneration of the axons than membrane-bound AChE.
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PMID:Effect of ischemia on axonal transport of choline acetyltransferase and acetylcholinesterase and on ultrastructural changes of isolated segments of rabbit nerves in situ. 7 11

A case of right sided extradural neurinoma at the level of the foramen magnum is reported which presented as an intramedullary spinal cord syndrome. Ischemia of the anterior spinal artery or of the vertebral artery was considered to be an important pathogenic factor in the production of the neurological syndrome. The outer part of the spinothalamic tract, where sensory fibers carrying pain and thermal sensibility from the sacral segments are situated, escaped ischemia as that part is supplied by penetrating branches of the pial arterial plexus. The discrepancy between the level of neurological deficit (C5) and site of the tumor (C1-2) was due to distant ischemia. The lack of a history of root pain and the rapid recovery following removal of the tumor also favor a vascular origin for the neurological deficit.
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PMID:Intramedullary syndrome due to an extradural neurinoma near the foramen magnum. 7 75

A woman, aged 38, lost consciousness immediately after manipulation of the cervical spine and remained in coma for nearly 5 years in a combined decorticate and decerebrate state. Cerebral angiography revealed impaired circulation in the vertebrobasilar system. The EEG initially showed generalized cerebral dysrhythmia but tended, over the years, to become more normal with desynchronized fast activity of low voltage. Neuropathological examination postmortem revealed a large cystic lesion in the pressure equalization area of the carotid and basilar circulation in the upper pons, mesencephalon, posterior hypothalamus and basal thalamus. No definite stenosis or occlusion was seen in the cerebral vessels on angiography or at the postmortem examination. The mechanism of the lesion is considered to have been temporary interference with the blood flow in the vertebrobasilar system during manipulation of the cervical spine sufficient to cause ischemia and subsequent infarction of the brainstem. The pathogenesis of vascular lesions of the brain stem following manipulation of the cervical spine is discussed briefly.
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PMID:Brainstem lesion with coma for five years following manipulation of the cervical spine. 7 77

In normothermic anesthetized cats complete cerebral circulatory arrest for one h was produced and followed by blood recirculation of the brain for 30 min to 4 h. Total and local blood flow of the brain, kidney, heart and liver were measured before and after ischemia using radioactive labelled microspheres. Before ischemia blood flow of the brain was 39.1 +/- 2.3 ml/100 g/min, of the kidney 307.2 +/- 28.3 ml/100 g/min, of the heart 241.1 +/- 32.5 ml/100 g/mmin and of the liver 87.8 +/- 25.6 ml/100 g/min (means +/- SEM). Regional flow rates within the brain varied between 35 and 51 ml/100 g/min. Reactive hyperemia was present in the brain 30 min after the beginning of recirculation following ischemia for 1 h. Local cerebral flow rates increased three to five times above the control flow, depending on the respective region. Mean cerebral blood flow returned to or slightly below normal, 2 to 4 h after ischemia, but there was considerable redistribution of flow rates within the brain. The filter capacity of the brain for microspheres of 15 mu and 50 mu diameter did not change after ischemia indicating that postischemic blood recirculation was not accompanied by an opening of arteriovenous shunts.
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PMID:Microsphere analysis of local cerebral and extracerebral blood flow after complete ischemia of the cat brain for one hour. 8 Dec 76

The middle cerebral artery (MCA) of cats was occluded permanently for 24h to study the influence of arterial hypertension during the early phase of focal ischemia upon the development of endema and changes of the blood-brain barrier (BBB). In normotensive animals MCA occlusion results in a hemispheric weight increase of about 8% and marked water and electrolyte alterations in both the grey and white matter of the MCA territory. The RISA space increases mainly in the grey matter. Hypertension aggravates these changes significantly, whereby water and electrolyte changes in the grey matter are predominantly concerned, while there is a preferential increase of the RISA space in the white matter. It is suggested that arterial hypertension aggravates the ischemic edema and enhances a vasogenic type of edema in the white matter.
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PMID:The effect of arterial hypertension of focal ischemic edema. An experimental study. 8 57

Changes of morphological and neurophysiological characteristics of pyramidal neurons in response to complete ischemia have been studied by means of vital microscopy of cat and rabbit cortex neurons in addition to some other cytological methods. These responses were found to be complex involving phasic changes in the neuron size, membrane potential and redox potential. Neurons of particular types responded to normo- and hypothermic ischemia differently. Pyramidal neurons retained their vital ability for the whole prolonged period of the complete ischemia (up to 40--60 min).
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PMID:[Reaction of the cerebral cortical neurons to complete ischemia]. 8 19

During intestinal ischemia in rabbits histamine concentration and diamine oxidase activity were altered in the intestinal wall and in the perfusate of mesenteric vessels. The results were interpreted as a histamine release and an increased catabolism of diamine oxidase. Thus, the combination of release of vasoactive histamine and partial elimination of a protective enzyme may contribute to the fatal outcome after mesenteric ischemia.
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PMID:[Histamine concentration and diamine oxidase activity in the small intestine in superior mesenteric artery occlusion]. 8 94

Two adult brains with small ischemic lesions in the hippocampus, due to impairment of the supply from the posterior cerebral artery, are presented. The first case corresponds to what is described in the literature as "incisural sclerosis" and shows no difference in vulnerability between the Sommer and the Spielmeyer sector. In the second case the hippocampal lesion is due to an embolic occlusion of the posterior cerebral artery and consists of selective necrosis of the subiculum, the Sommer sector and part of the endfolium of the pyramidal layer, the Spielmeyer sector remaining noninfarcted. The postmortem angiograms of 12l hippocampi of adults, as well as full term born and premature infants, show that the h1 and h2 sectors and part of the h3 sector of the hippocampus are supplied by the same "sulcus" arteries. Although there is a selective vulnerability to ischemia in some sectors of the hippocampus, which is typical for Ammon's horn sclerosis, this cannot be explained by a difference of arterial supply or by compression of arteries during the process of birth.
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PMID:Ischemic lesions of the hippocampus and their relation to Ammon's horn sclerosis. A neuropathological study of two cases and a comparison to the vascular anatomy. 8 8

When keratome-sliced pig epidermis was floated on Hank's balanced salt solution, we observed a rapid decrease in the intracellular level of cyclic GMP. A portion of the lost cyclic GMP was detected in the incubation medium. When the epidermis was kept in air at room temperature, the cyclic GMP level also decreased rapidly but to a lesser degree. Incubating the epidermal slice at 37 degrees C in Hank's balanced salt solution with the addition of 3-isobutyl-1-methyl xanthine (IBMX) prevented the decrease. Also, after the cyclic GMP level had fallen, it could be raised to be the in vitro level by the addition of IBMX. Increased amounts of cyclic GMP were detectable in the medium in this case. These data indicate that the decrease in cyclic GMP in ischemic epidermis is due to sudden activation of epidermal cyclic GMP-phosphodiesterase and also in part due to leakage of cyclic GMP extracellularly. In contrast to the rapid decline in the cyclic GMP level, ischemia caused a rapid and transient increase in epidermal cyclic AMP. This confirms previous data by ourselves and by others (Br J Dermatol 92: 249-254, 1975; J Invest Dermatol 68:125-127, 1977). These "ischemic effects" must be avoided in order to measure the "in vivo level" of cyclic nucleotides in epidermis.
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PMID:Cyclic GMP System in epidermis: I. Effect of ischemia. 8 73


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