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

Adenohypophyses of adult male rats have been investigated by light microscopy, immunocytology and electron microscopy 30 minutes, 1, 2, 4, 6 and 24 hours following electrolyte destruction of the pituitary stalk. Light microscopy revealed massive ischemic infarction of the adenohypophysis. Immunoreactive growth hormone, prolactin, TSH, FSH and LH were demonstrated up to 24 hours after surgery in necrotic adenohypophysial cells by the immunoperoxidase technique. Fine structural abnormalities were already noticeable 30 minutes following stalk lesion. The changes rapidly progressed and within 2 hours unmistakable signs of cellular necrosis became evident. Mitochondria, especially those of growth hormone cells, seemed to be affected at an early stage, whereas alterations in rough-surfaced endoplasmic reticulum membranes developed later. Nuclear changes, formation of cytoplasmic vacuoles and disruption of cell membranes were conspicuous findings. No evidence, indicating the participation of lysosomes in the development of cellular damage, was obtained. Secretory granules were prominent and well preserved even in cells which showed advanced necrosis. The failure of discharge and degradation of secretory granules in the necrotic cells suggest that factors accounting for their intracellular migration and extrusion are very sensitive to ischemia and are paralyzed at an early phase.
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PMID:Adenohypophysial necrosis in rats following destruction of the pituitary stalk. A histologic, immunocytologic and fine structural study. 33 35

Recent studies have shown that the principal component of the senile plaque in Alzheimer's disease (AD), beta-amyloid protein (beta AP) can exert direct and indirect neurotoxicity in vitro. Because of the studies that demonstrated potentiation of excitatory amino acid toxicity by beta AP, we decided to test whether beta AP was able to potentiate damage in an in vivo model where excitotoxic damage is thought to be important. The present study evaluated the in vivo effects of beta AP implants in the brain of rats before and after being subjected to 10 min of transient global forebrain ischemia by 4-vessel occlusion (4-VO). Implants of either synthetic beta AP or prolactin (PRL), which was used as a control protein, were made into the striatum and the hippocampus of either the left (beta AP) or the right (PRL) cerebral hemisphere. The implants were made in a lipophilic, non-toxic vehicle so as to try and achieve sustained beta AP exposure. One group of animals was evaluated for direct in vivo effects within 1 week following implantation; the other group was subjected to 4-VO 3-4 days post-implantation for evaluation of potential indirect effects. This latter group was compared to the histopathology of animals subjected to 4-VO without prior implantation. In the group of animals evaluated for direct effects, no evidence of neurotoxicity was observed. Bielschowsky silver staining and immunostaining for ubiquitin were unremarkable in all lesions. beta AP was detected by immunocytochemistry in the parenchymal tissue that received beta AP implants. Marked glial activation was observed to be associated with experimental and control implants. Under the experimental conditions employed in this study, significant protection from ischemia rather than potentiation of damage was observed. These results suggest that beta AP may not be neurotoxic in rodents in vivo and that the lesions and/or trauma produced by the implantation procedure 3-4 days prior to 4-VO may have induced factors that were protective against ischemia-induced damage.
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PMID:In vivo effects of beta-amyloid implants in rodents: lack of potentiation of damage associated with transient global forebrain ischemia. 152 Nov 57

A 27-year-old woman with amenorrhea following cessation of birth control pills was found to have a pituitary tumor which was secreting large amounts of prolactin. Many tumor cells had large mitochondria, the diameter of which ranged between 7 and 12 mu. Some tumor cells also displayed oncocytic transformation, and a few were definite oncocytes. The pathogenesis of mitochondrial swelling in pituitary tumors is discussed and the possible roles of prolonged intake of steroids and/or ischemia are suggested.
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PMID:Large mitochondria in a pituitary adenoma with hyperprolactinemia. 624 83

Ischemic pain was produced by a blood pressure cuff placed to the arm of healthy human subjects for 15 min which produced a mean pain score of 59% (visual analogue scale). Ischemia induced a significant dental pain threshold elevation (mean 67%) and 2 mg of naloxone did not reduce it. Thermal sensitivity of the upper lip had a tendency to reduction during ischemia and 2 mg of naloxone reduced this effect. Tactile thresholds in the forehead or in the contralateral arm were not markedly elevated. Neither ACTH nor prolactin level in the plasma was related to the dental pain threshold elevation during ischemia. The findings of the present study suggest that ischemic pain nonsegmentally produces a predominant inhibition of responses to thin afferents. Endogenous opioids may markedly contribute to the reduction of thermal sensitivity induced by ischemia, but their contribution to dental pain threshold elevations seems to be less important. Stress or other adenohypophyseal mechanisms involving the release of ACTH or prolactin do not explain the effects of ischemia found in the present study.
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PMID:Ischemic pain nonsegmentally produces a predominant reduction of pain and thermal sensitivity in man: a selective role for endogenous opioids. 629 48

alpha-Lipoic acid, which plays an essential role in mitochondrial dehydrogenase reactions, has recently gained considerable attention as an antioxidant. Lipoate, or its reduced form, dihydrolipoate, reacts with reactive oxygen species such as superoxide radicals, hydroxyl radicals, hypochlorous acid, peroxyl radicals, and singlet oxygen. It also protects membranes by interacting with vitamin C and glutathione, which may in turn recycle vitamin E. In addition to its antioxidant activities, dihydrolipoate may exert prooxidant actions through reduction of iron. alpha-Lipoic acid administration has been shown to be beneficial in a number of oxidative stress models such as ischemia-reperfusion injury, diabetes (both alpha-lipoic acid and dihydrolipoic acid exhibit hydrophobic binding to proteins such as albumin, which can prevent glycation reactions), cataract formation, HIV activation, neurodegeneration, and radiation injury. Furthermore, lipoate can function as a redox regulator of proteins such as myoglobin, prolactin, thioredoxin and NF-kappa B transcription factor. We review the properties of lipoate in terms of (1) reactions with reactive oxygen species; (2) interactions with other antioxidants; (3) beneficial effects in oxidative stress models or clinical conditions.
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PMID:alpha-Lipoic acid as a biological antioxidant. 764 94

ATP-sensitive potassium channels are found in a number of different tissues where they undertake distinct physiologic functions. In endocrine cells they regulate the secretion of hormones such as insulin, prolactin, and growth hormone. They influence the excitability of cardiac, skeletal, and vascular smooth muscle. They are of particular importance during ischemia in both the heart and the brain, where they intervene to reduce or delay cell death. Both electrophysiologic and pharmacologic evidence points toward ATP-sensitive potassium channels making up a class of ion channels with tissue-specific as well as functional differences. There is therefore considerable scope for the development of specific products to either enhance or inhibit the action of these ion channels under different pathologic conditions.
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PMID:ATP-sensitive potassium channels: an overview. 789 2

ATP-sensitive potassium channels are found in a number of different tissues where they play distinct physiological functions. In all these tissues they are blocked by antidiabetic sulfonylureas. In endocrine cells they regulate the secretion of hormones such as insulin, prolactin, and growth hormone. They influence the excitability of cardiac, skeletal, and vascular smooth muscle. They play an important role in connecting changes of extracellular glucose levels in the brain to changes of neurotransmitter release. They are of particular importance during hypoxia and ischemia in both the heart and the brain, where they intervene to reduce or delay cell death. Both electrophysiological and pharmacological evidence points towards ATP-sensitive potassium channels making up a class of ion channels with tissue-specific as well as functional differences. Particularly, these different classes of ATP-sensitive K+ channels have different sensitivities to antidiabetic sulfonylureas. There is probably considerable scope for the development of specific products to either enhance or inhibit the action of these ion channels in different tissues under different pathological conditions.
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PMID:Ion channel effects of antidiabetic sulfonylureas. 891 86

Estrogen administration has a number of favorable cardiovascular effects, and recent evidence suggests that these include an increase in arterial distensibility. Whether this is also the case for the physiological changes in estrogen production during the menstrual cycle has never been determined, however. In 21 premenopausal healthy women, we continuously measured radial artery diameter and blood pressure by an echo-tracking device and a beat-to-beat finger device, respectively. Arterial distensibility was calculated as distensibility/blood pressure curve. The measurements were made during the follicular, ovulatory, and luteal phases of the menstrual cycle. As expected, compared with the follicular phase, plasma estradiol, follicle-stimulating hormone, luteinizing hormone, and prolactin were increased in the ovulatory phase, whereas progesterone was increased in the luteal phase, together with antidiuretic hormone. Radial artery distensibility was increased in the ovulatory and reduced in the luteal phase, the changes being independent of the small, concomitant blood pressure changes. The arterial wall stiffening seen in the luteal phase was associated with a reduction in the flow-dependent endothelial dilatation of the radial artery as assessed by the hyperemia after short-term ischemia of the hand. Thus, the natural menstrual cycle is characterized by alterations in radial artery distensibility. The mechanisms responsible for this phenomenon remain to be clarified. It is possible, however, that the greater arterial distensibility of the ovulatory phase is due to an estrogen-dependent reduction in vascular smooth muscle tone, whereas the arterial stiffening of the luteal phase depends on vascular smooth muscle contraction due to more complex hormonal phenomena, ie, an endothelial impairment due to estrogen reduction but also to an increase in progesterone and antidiuretic hormone levels.
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PMID:Fluctuations of radial artery distensibility throughout the menstrual cycle. 1044 72

L-Arginine (Arg) is the substrate for the synthesis of nitric oxide (NO), the endothelium-derived relaxing factor essential for regulating vascular tone and hemodynamics. NO stimulates angiogenesis, but inhibits endothelin-1 release, leukocyte adhesion, platelet aggregation, superoxide generation, the expression of vascular cell adhesion molecules and monocyte chemotactic peptides, and smooth muscle cell proliferation. Arg exerts its vascular actions also through NO-independent effects, including membrane depolarization, syntheses of creatine, proline and polyamines, secretion of insulin, growth hormone, glucagon and prolactin, plasmin generation and fibrinogenolysis, superoxide scavenging and inhibition of leukocyte adhesion to nonendothelial matrix. Compelling evidence shows that enteral or parenteral administration of Arg reverses endothelial dysfunction associated with major cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes, obesity/insulin resistance and aging) and ameliorates many common cardiovascular disorders (coronary and peripheral arterial disease, ischemia/reperfusion injury, and heart failure). Dietary Arg supplementation may represent a potentially novel nutritional strategy for preventing and treating cardiovascular disease.
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PMID:Arginine nutrition and cardiovascular function. 1105 97

Hypopituitarism is a disease complex with variable clinical manifestations. Recent studies have improved our understanding of its pathophysiology, particularly in patients with pituitary adenomas. In that setting, hypopituitarism was previously considered a permanent and irreversible process, requiring life-long hormone replacement therapy. While this could be true in some instances, recent data demonstrated recovery of pituitary function in a large number of patients with hypopituitarism following surgical decompression. Mechanical compression of portal vessels and the pituitary stalk, by the expanding adenoma was postulated to be the predominant mechanism causing hypopituitarism in this setting. Since portal vessels also provide blood supply to the anterior lobe, ischemic necrosis of portions of the pituitary can occur as a result of increased and prolonged compression by the expanding adenoma. Recent data demonstrated increases in intrasellar pressure (ISP) in patients with pituitary macroadenomas, particularly those with hypopituitarism. The data showed that ISP measurements correlated positively with the serum prolactin levels but not with tumor sizes. It is postulated that increased ISP has predominant role in the pathogenesis of hypopituitarism in patients with pituitary adenomas while. The increase in ISP results in decreased blood flow through the portal vessels and the pituitary stalk. The latter will result in diminished delivery of hypothalamic hormones to the anterior pituitary and may also cause ischemia and/or necrosis in some portions of the normal gland. Recovery of pituitary function can thus be anticipated after surgical decompression, in patients who have viable pituitary cells. Understanding the pathophysiology of hypopituitarism and recognizing the probability for recovery of function should be emphasized in the management of patients with this disease. An important aspect of the management is patients' education about their disease, including the use of medic alert identification. The managing physician should appreciate the variable clinical manifestations of the disease and the possible occurrence of other associated neuroendocrine, neurological and neuro-ophthalmologic signs and symptoms. Treatment of hypopituitarism should not be rigid but instead, always individualized. Management should take into consideration the patients' age, sex, education, original disease process and clinical history.
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PMID:Medical management of hypopituitarism in patients with pituitary adenomas. 1267 8


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