Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
 ...
PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

A rare case is presented of a woman with spontaneous recovery from hypopituitarism following postpartum hemorrhage. One month after delivery, serum thyroid hormone, TSH, LH and FSH levels were low, and their secretion from the pituitary gland responded poorly to the TRH and LH-RH tests. Pituitary TSH response was normal 3 months after delivery. In the LH-RH test, pituitary LH and FSH response returned to normal at 2 months. Pituitary GH secretion and serum cortisol levels induced by ITT already responded normally one month postpartum. Excessive secretion of pituitary PRL was observed 3 months after delivery and improved gradually thereafter. These results indicate that the secretion of pituitary tropic hormones was sensitive to pituitary ischemia in the following order: TSH, gonadotropin, GH and ACTH. The disturbance of these hormones also persisted in the same order.
 ...
PMID:Spontaneous recovery from hypopituitarism due to postpartum hemorrhage. 250 17

Eleven patients with Korean (epidemic) hemorrhagic fever were each studied three times with high-resolution CT in order to demonstrate necrosis of the pituitary gland and to correlate the CT findings with the patients' pituitary function and visual fields. Seven of the 11 patients showed varying degrees of progressive decrease in the height of the pituitary gland: one severe, two moderate, and four mild. The visual fields of all the patients were checked at the time of the third (last) follow-up CT. Six of the 11 patients had bitemporal superior quadrantanopsia. In five patients, the decreased height (atrophic change) of the pituitary gland and the visual-field defect were coincidental. The visual-field defects in those patients were not improved on follow-up examination 5 weeks later. Two patients in whom a 1-year follow-up examination was performed showed no interval changes in the defects. Pituitary function tests were performed in nine of the 11 patients (six with atrophic pituitary glands and three without atrophic changes) at the time of the third CT. Five of the six patients with atrophy showed decreased pituitary reserve function for follicle-stimulating hormone, cortisol, or human growth hormone, while only one patient showed decreased reserve function for cortisol among the three patients without atrophic change. The pituitary atrophic changes observed on follow-up sellar CT are thought to be the result of the ischemic necrosis of the gland. The high probability (five of seven) of visual-field defects in those patients with atrophic glands suggests optochiasmatic and pituitary ischemia as the basic pathogenesis.
 ...
PMID:Pituitary atrophy in Korean (epidemic) hemorrhagic fever: CT correlation with pituitary function and visual field. 287 38

A 52-year-old woman with secondary amenorrhea presented with ophthalmoplegia, subarachnoidal bleeding. Pituitary function tests showed mild hyperprolactinemia and deficiencies of other functions of adenohypophysis. X-ray films of the skull showed enlarged sella turcica, and CT scan was interpreted as demonstrating pituitary tumour. Carotid arteriography led to diagnosis of intrasellar aneurysm of the right internal carotid, without any pituitary tumour. After embolisation of the aneurysm, followed, by a temporo-sylvian anastomosis, endocrine functions did not improve. The mechanism of hyperprolactinemia is discussed, probably due to pituitary ischemia. This case provides evidence of interest of further investigations before a transsphenoidal surgery in pituitary tumours, in particular if subarachnoidal bleeding occurs.
 ...
PMID:[Intrasellar carotid aneurysm simulating prolactin adenoma]. 383 39

Pituitary adenylate cyclase-activating polypeptides and PAC1-R are expressed during early embryogenesis and PACAP's neurotrophic action supports a role in neuronal development. In the adult brain PACAP functions as a neuroprotective factor that attenuates the neuronal damage resulting from various insults. The tumor suppressor gene p53 and the new zinc finger protein Zac regulate apoptosis and cell cycle arrest through unrelated pathways and both genes are up-regulated under cerebral ischemia. We report here that p53 and Zac induce expression of the PAC1-R gene. By this mechanism p53 and Zac could fine-tune the balance between death promoting and protective signals and may thus fulfil a dual role in ischemia.
 ...
PMID:Induction of the PAC1-R (PACAP-type I receptor) gene by p53 and Zac. 1036 51

This study was designed to determine the role of altered cAMP and K(+) channel-dependent mechanisms in impaired pial artery dilation to the newly described opioid, nociceptin/orphanin FQ (NOC/oFQ) following hypoxia/ischemia in newborn pigs equipped with a closed cranial window. Recent studies have observed that NOC/oFQ elicits pial dilation via release of cAMP, which, in turn, activates the calcium sensitive (K(ca)) and the ATP-dependent K(+) (K(ATP)) channel. Global cerebral ischemia (20 min) was induced via elevation of intracranial pressure, while hypoxia (10 min) decreased pO(2) to 35+/-3 mm Hg with unchanged pCO(2). Topical NOC/oFQ (10(-8), 10(-6) M) induced vasodilation was attenuated by ischemia/reperfusion (I+R) and reversed to vasoconstriction by hypoxia/ischemia/reperfusion (H+I+R) at 1 h of reperfusion (control, 9+/-1 and 16+/-1%; I+R, 3+/-1 and 6+/-1%; H+I+R, -7+/-1 and -12+/-1%). Such altered dilation returned to control values within 4 h in I+R animals and within 12 h in H+I+R animals. NOC/oFQ dilation was associated with elevated CSF cAMP in control animals but such biochemical changes were attenuated in I+R animals and reversed to decreases in cAMP concentration in H+I+R animals (control, 1037+/-58 and 1919+/-209 fmol/ml; I+R, 1068+/-33 and 1289+/-30 fmol/ml; H+I+R, 976+/-36 and 772+/-27 fmol/ml for absence and presence of NOC/oFQ 10(-6) M, respectively). Topical 8-Bromo cAMP (10(-8), 10(-6) M) pial dilation was unchanged by I+R but blunted by H+I+R (control, 10+/-1 and 20+/-1%; I+R, 11+/-1 and 20+/-2%; H+I+R, 0+/-1 and 0+/-2%). Pituitary adenylate cyclase activating polypeptide and cromakalim, adenylate cyclase and K(ATP) channel activators, respectively, elicited dilation that was blunted by both I+R and H+I+R while NS1619, a K(ca) channel activator, elicited dilation that was unchanged by I+R but blunted by H+I+R. These data indicate that impaired NOC/oFQ dilation following I+R results form altered adenylate cyclase and K(ATP) channel-dependent mechanisms. These data further indicate that impaired NOC/oFQ dilation following H+I+R results not only from altered adenylate cyclase and K(ATP) channel but also from altered cAMP and K(ca) channel-dependent mechanisms.
 ...
PMID:Role of cAMP and K(+) channel-dependent mechanisms in piglet hypoxic/ischemic impaired nociceptin/orphanin FQ-induced cerebrovasodilation. 1108 86

Pituitary adenylate cyclase activating polypeptide (PACAP) modulates neurotransmission in the central and peripheral nervous systems. In vitro and in vivo studies have shown the protective effects of PACAP against neuronal damage induced by ischemia and agonists of NMDA-type glutamate receptors. Here, we demonstrated that PACAP also protected against neuronal toxicity induced by beta-amyloid (Abeta) peptide, aggregation of which is a causative factor for Alzheimer's disease. PACAP (10(-9)M) rescued 80% of decreased cell viability and 50% of elevated caspase-3 activity that resulted from exposure of PC12 cells to Abeta. PACAP was at least 10(4)-fold more effective than other neuropeptides including vasoactive intestinal peptide (VIP) and humanin, which correlated with the level of cAMP accumulation. Thus, our results suggested that PACAP attenuates Abeta-induced cell death in PC12 cells through an increase in cAMP and that caspase-3 deactivation by PACAP is involved in the signaling pathway for this neuroprotection.
 ...
PMID:The neuropeptide PACAP attenuates beta-amyloid (1-42)-induced toxicity in PC12 cells. 1218 49

Postpartum hemorrhage (PPH) is a frequent complication of pregnancy in India. Sheehan's description of postpartum hypopituitarism promoted the belief that PPH leads to necrosis of the enlarged pituitary gland of pregnancy and hypopituitarism. However, slow clinical progression suggests factors other than ischemia in its pathogenesis. Tissue necrosis could release sequestered antigens, triggering autoimmunity of the pituitary and delayed hypopituitarism in Sheehan's syndrome. Twenty-six consecutive patients with postpartum hypopituitarism were studied, 19 with Sheehan's syndrome based on a history of PPH and hormone profile suggesting pituitary failure [mean (SD) age 32.7 +/- 6.4 yr, duration of illness 5.5 +/- 3.1 yr], and seven patients with no history of PPH, categorized as "Other." Pituitary imaging and basal T(4), TSH, cortisol, LH, FSH, 17beta-estradiol, and autoantibodies against pituitary (PitAb) and thyroid (TMA) were evaluated. Controls included 28 healthy females without prior conception (22 +/- 5 yr) and 28 with prior conception (26 +/- 5 yr). Twelve of 19 (63.1%) patients with Sheehan's syndrome and one of seven in the Other group had PitAb against the 49-kDa autoantigen; neuron-specific enolase. Four of 28 (14.2%) controls without prior conception and 5 of 28 (17.8%) controls with prior conception had PitAb positivity (P < 0.001 and <0.01 vs. Sheehan's syndrome, respectively). There was no significant difference in the mean serum hormone values and TMA positivity between patients with Sheehan's syndrome and the Other group as well as patients with or without PitAb positivity. Pituitary autoimmunity may play a role in the cause of hypopituitarism following PPH.
 ...
PMID:Pituitary autoimmunity in patients with Sheehan's syndrome. 1221 61

Pituitary adenylate cyclase activating polypeptide (PACAP) has neurotrophic and neuroprotective effects against various cytotoxic agents in vitro, and ischemia in vivo. Anoxia tolerance is most highly developed in some species of turtles. Recently, we have demonstrated high levels of PACAP38 in the turtle brain, exceeding those in corresponding rat and human brain areas by 10- to 100-fold. The aim of the present study was to investigate with electrophysiological methods the protective effects of PACAP in anoxia-induced neuronal damage of turtle retinal horizontal cells. Adult turtles (Pseudemys scripta elegans) were used for the experiments. After decapitation, half of the isolated eyecup slices were placed into a non-oxygenated Ringer solution, the other half into 0.165 microM PACAP solution. Intracellular recordings were obtained from horizontal cells 18, 22, 42 and 46 h after removal of the eyes. The amplitudes of light responses with the exception of the 0-h measurement, were larger at all time-points in PACAP-incubated slices than in control retinal slices. After both 18 and 22 h, the response amplitudes of PACAP-treated cells exceeded those taken from control horizontal cells by 1.2-fold. At later times, this difference became larger than 2-fold. In summary, the present results provide evidence that PACAP has neuroprotective effects on the anoxic retinal cells in the turtle.
 ...
PMID:PACAP inhibits anoxia-induced changes in physiological responses in horizontal cells in the turtle retina. 1240 17

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.
Pituitary 2002
PMID:Medical management of hypopituitarism in patients with pituitary adenomas. 1267 8


1 2 3 4 Next >>