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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight kinds of neuropeptides and four kinds of neuropeptide receptors were examined in the right and left hemispheres of mongolian gerbils after unilateral carotid ligation-induced stroke and in normal controls. Five hours after ligation of the right common carotid artery, beta-endorphin concentration in the right hemisphere (ischemic side) of the stroke group was significantly increased compared with that in the contralateral hemisphere (non-ischemic side), but there were no differences between sides in other neuropeptides either with or without stroke. Furthermore, although there were no differences in [3H]naloxone binding, [3H]thyrotropin-releasing hormone binding or 125I-vasoactive intestinal polypeptide binding in the brain in this model of stroke, [3H]enkephalin binding was significantly lower on the ischemic side than on the non-ischemic side in the stroke group. These results suggest that increased activity in the beta-endorphinergic system in the brain might be partly caused by ischemic brain failure.
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PMID:Changes of neuropeptides and their receptors in experimental stroke gerbil brains. 132 Jun 63

We observed the effects of a new thyrotropin-releasing hormone derivative, YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]-L-histidyl-L-prolinamide dihydrate), on behavioral changes in rats for 3 weeks after focal cerebral ischemia. Under halothane anesthesia, the left middle cerebral artery was occluded via a transretro-orbital approach. YM-14673 was administered just after the operation and once a day for 3 weeks. Neurologic deficits, including hemiplegia and abnormal posture, and disturbance of passive avoidance learning were present in solvent-treated control rats for the entire 3 weeks. YM-14673 at 0.1 or 0.3 mg/kg i.p. or 1 mg/kg p.o. significantly accelerated the recovery of neurologic deficits and ameliorated cognitive disturbance compared with the solvent-treated controls although the drug at 0.1 and 0.3 mg/kg i.p. did not influence the size of the ischemic infarct. YM-14673 mitigated the behavioral disturbances in this model of chronic focal cerebral ischemia. We also discuss the suitability of this model for the evaluation of drugs.
Stroke 1989 Mar
PMID:Effects of a new thyrotropin-releasing hormone derivative on behavioral changes after focal cerebral ischemia in rats. 249 90

Although loss of normal pituitary function may be silent and asymptomatic, sudden loss of gland function (pituitary apoplexy) typically results in characteristic presentations. Sheehan's syndrome is the development of hypopituitarism after postpartum hemorrhage or shock. Patients with Sheehan's syndrome may have typical or atypical presentations based on the extent of pituitary gland destruction. Patients with typical symptoms fail to lactate after giving birth; subsequently these patients also develop symptoms and signs of hypopituitarism. Measuring the serum prolactin level after giving thyrotropin-releasing hormone is a reasonable first step in the diagnosis of this condition in patients who fail to lactate after giving birth. The diagnosis of hypopituitarism is delayed for up to 7 years in patients with atypical symptoms. Acute symptomatic failure of the pituitary gland (pituitary apoplexy) commonly occurs in patients who have asymptomatic pituitary tumors. Many patients with pituitary tumors do not have signs of abnormal endocrine gland secretion and have a normal appearance. Most patients have the following signs or symptoms: headache; acute disturbances in visual acuity or visual fields; ophthalmoplegia, and changes in the level of consciousness. The syndrome of pituitary apoplexy usually evolves over hours to days. Subarachnoid hemorrhage and acute bacterial meningitis are the two most important mimics of pituitary apoplexy. Intravenous steroids and prompt neurosurgical consultation are mandatory in cases of pituitary apoplexy since both steroids and surgery can improve vision. Testings for acute or chronic hypopituitarism is challenging in the Emergency Department setting; however, carefully chosen tests will aid in the subsequent early correct diagnosis after initial Emergency Department management.
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PMID:Adrenal and pituitary emergencies. 268 Apr 71

We observed the effects of a new thyrotropin-releasing hormone analogue, YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]-L-histidyl-L-prolinamide dihydrate) on behavioral changes in 26 rats subjected to middle cerebral artery occlusion. The administration of 0.1 mg/kg i.p. YM-14673 was started 1 week after occlusion and was repeated daily for 2 weeks. YM-14673 significantly accelerated the recovery of neurologic deficits and ameliorated the disturbance of passive avoidance learning. Thus, YM-14673 improved behavioral response in a model of chronic focal cerebral ischemia. The availability of a chronic middle cerebral artery occlusion model for the evaluation of drugs is also discussed.
Stroke 1989 Aug
PMID:Effects of a new thyrotropin-releasing hormone analogue administered in rats 1 week after middle cerebral artery occlusion. 275 41

Cardiovascular and regional hemodynamic effects of the intrathecal (i.t.) administration of a thyrotropin-releasing hormone (TRH) analog, MK-771 (L-pyro-2-aminoadipyl-histidyl-thiazolidine-4-carboxamide), were studied in rats. MK-771 (0.01-5.0 micrograms i.t.) caused dose-related increases in mean arterial pressure (MAP) and heart rate (HR). TRH (10 micrograms i.t.), but not TRH-free acid, produced similar cardiovascular effects. The MAP response to MK-771 (i.t.) remained primarily intact after cervical spinal cord transection, whereas the HR response was attenuated (37% of control). The MAP response to MK-771 was blocked by peripheral administration of pentolinium or phentolamine, and was partially attenuated by adrenalectomy. The HR response was reduced by pentolinium or atropine. Assessment of changes in regional blood flow and vascular resistance with the radioactive microsphere technique showed that MK-771 increased total peripheral resistance and vasoconstricted cutaneous, skeletal muscle, adrenal, renal and intestinal vascular beds. Cardiac output and stroke volume were not altered. MK-771 had no effect on vascular resistance locally or in other central nervous system structures. However, blood flow was elevated by MK-771 in spinal cord and brain. These data show that TRH receptor activation in the thoracic spinal cord, presumably in the intermediolateral cell column, elevated MAP by increased sympathetic activity to the peripheral vasculature and the adrenals. However, the HR response to TRH receptor activation required a supra-spinal component and was mediated in part by vagal inhibition.
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PMID:Thyrotropin-releasing hormone receptor activation in the spinal cord increases blood pressure and sympathetic tone to the vasculature and the adrenals. 283 44

In our previous work thyroidectomy significantly improved survival in canine hemorrhagic shock. This finding, coupled with the reported beneficial hemodynamic effects of thyrotropin-releasing hormone (TRH) in circulatory collapse, led to the present study. Anesthetized, heparinized dogs were bled rapidly into a reservoir until MAP = 40 mm Hg. After 60 min of hypotension (E60) the reservoir line was clamped for 30 min (E90). In 10 dogs three doses of TRH (2 mg/kg) were administered iv at 10-min intervals during clamping. In 11 other animals equivalent volumes of saline were given. At E90 the reservoir line was unclamped, and shed blood was reinfused over 30 min. After 1 hr of monitoring (E180) the dogs were returned to the kennel and observed for at least 3 days. Among 11 control dogs, 6 died. In the TRH group only 1 of 10 dogs died (P less than 0.05). During uncompensated shock (E60-E90), TRH-treated dogs had significantly higher mean arterial pressure, cardiac index, stroke index, and right and left ventricular stroke work indexes, and arterial pH than control animals. At the conclusion of the acute experiment (E180) there were few intergroup hemodynamic-metabolic differences. The significant enhancement of 3-day survival by TRH in canine hemorrhagic shock might be related to hemodynamic improvement at a critical stage of circulatory collapse (E60-E90). Direct or indirect neuromodulatory actions of TRH on the CNS could also explain our results. These findings lend further support to the potentially key role of hypothalamic-pituitary-thyroid interrelationships in shock.
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PMID:Thyrotropin-releasing hormone increases survival in canine hemorrhagic shock. 307 47

A thyrotropin-releasing hormone (TRH) test with serum thyroid-stimulating hormone (TSH) assays was performed in 22 euthyroid stroke patients without thyroid disease and the results were compared with those in 17 age-matched euthyroid controls. Basal and maximum TSH levels after TRH injection were significantly lower in the stroke group without elevation of basal serum thyroid hormone levels. There was a tendency towards an inverse relationship between TSH levels and the degree of pareses of the extremities. The test was repeated in 7 stroke patients 3-4 months after the onset of stroke with essentially the same results. The abnormal TSH parameters in stroke patients seem to be the result of the brain lesion per se.
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PMID:Serum thyroid-stimulating hormone in cerebrovascular disease. 308 6

Serum total thyroxine, triiodothyronine, and thyrotropin response to thyrotropin-releasing hormone (TRH-TSH test) were measured in 126 consecutive patients admitted with atrial fibrillation: 33 patients with an acute arterial limb embolism (Group I), 31 patients with an acute embolic stroke (Group II), and 62 patients without any arterial occlusion (Group III). A blunted TRH-TSH test, suggestive of thyrotoxicosis, was found in 5 patients in Group I, 8 patients in Group II, and 2 patients in Group III. The diagnosis of hyperthyroidism was confirmed in 8 patients (by repeated TRH-TSH test and scintigraphy): 4 patients in Group I (12.1%) and 4 patients in Group II (12.9%). All of them had a nonvalvular atrial fibrillation. Thyrotoxicosis should not be recognized in 6 of them if TRH-TSH test was not performed, because peripheral hormone levels were normal. Five of these 8 patients with thyrotoxicosis had reversion to sinus rhythm after treatment with carbimazole, either spontaneously or after cardioversion. This outcome prevented prolongation of anticoagulant therapy for an indefinite time.
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PMID:Occult thyrotoxicosis in patients with atrial fibrillation and an acute arterial embolism. 317 63

The gerbil model for stroke, using permanent unilateral carotid artery occlusion and restriction of the contralateral artery, was used to assess exogenous thyrotropin-releasing hormone (TRH, 10 mg/kg, i.p.) effect on cerebral ischemia. TRH immediately post-occlusion, compared to saline controls, significantly increased mortality (P = 0.025). This was supported by worsening reflected in the stroke index and time to death. Thyrotropin (0.1 IU, i.p.) in the same model was without effect. These surprising results were unexpected due to the beneficial response to the pharmacologically related naloxone.
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PMID:Thyrotropin-releasing hormone (TRH) increases morbidity and mortality in the gerbil stroke model. 681 91

Pituitary apoplexy often occurs spontaneously in adenomas. A few cases have been reported after testing anterior pituitary function by means of intravenous injections of a mixture of gonadotropin-releasing hormone and thyrotropin-releasing hormone, or gonadotropin-releasing hormone alone. In these cases the development of visual field defects has necessitated surgical intervention, which confirmed pituitary apoplexy. We describe a patient with a pituitary macroadenoma. He developed symptoms and signs of pituitary apoplexy immediately after intravenous injection of a mixture of hypothalamic releasing hormones. His visual fields remained normal, and he recovered spontaneously.
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PMID:[Pituitary apoplexy after injection of pituitary-hormone releasing hormones]. 807 63


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