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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of ergotamine and dihydroergotamine on the cerebral circulation was studied in the dog, anaesthetized with chloralose, by recording the intracranial venous pressure and the venous outflow from the superior cerebral vein. Under optimal experimental conditions, ergotamine (5 to 10 mug./kg.) and dihydroergotamine (100 mug./kg.) gave a marked and long-lasting cerebral vasoconstriction accompanied by a slight hypertension. The cerebral vasoconstriction provoked by ergotamine may be very small and was sometimes absent when the cerebral blood-flow was low. This vasoconstrictor effect is more pronounced the higher the initial intracranial venous pressure and hence the cerebral blood-flow. After the induction of a cerebral vasodilatation by 48/80 or strychnine, the vasoconstrictor action of ergotamine was more pronounced. The effect was not observed when CO(2) was employed to modify the intracranial venous pressure. Simultaneous registration of the cerebral, nasal cavity, and kidney vascular responses demonstrated the relative specificity of the action of ergotamine on the cerebral vessels. The small doses of ergotamine used may weaken or abolish the vasoconstrictor action of adrenaline on cerebral vessels. The modification of the responses of the cerebral circulation which such factors as anaesthesia, respiratory acidosis, and operative trauma can produce have been confirmed and emphasized. The results support the view that the vasoconstrictor action of ergotamine on the cerebral vessels might account for the therapeutic value of this drug in migraine.
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PMID:The action of ergotamine on the intracranial venous pressure and on the cerebral venous outflow of the dog. 1344 79

Allopregnanolone (AP) is a potent modulator of the GABAA receptor. Brain AP concentrations increase in response to stress, which is thought to provide neuroprotection by reducing excitation in the adult brain. Umbilical cord occlusion (UCO) causes hypoxia and asphyxia in the fetus, which are major risk factors associated with poor neurological outcome for the neonate, and may lead to adverse sequelae such as cerebral palsy. The aims of this study were as follows: (i) to determine the effect of 10 min UCO on AP concentrations in the extracellular fluid of the fetal brain using microdialysis, and (ii) to compare the content of the steroidogenic enzymes P450scc and 5alpha-reductase type II (5alphaRII) with brain and CSF neurosteroid concentrations. UCO caused fetal asphyxia, hypertension, bradycardia and respiratory acidosis, which returned to normal levels after 1-2 h. AP concentrations in dialysate samples from probes implanted in grey and white matter of the parietal cortex were significantly increased 1 h after UCO from control levels of 10.4 +/- 0.4 and 12.4 +/- 0.3 to 26.0 +/- 5.1 and 27.6 +/- 6.4 nmol l(-1), respectively (P < 0.05), before returning to pre-occlusion levels by 3-4 h after UCO. When fetal brains were collected 1 h after a 10 min UCO, the relative increases of AP and pregnenolone content in the parietal cortex were similar to the increase observed in the extracellular (dialysate) fluid. AP, but not pregnenolone, was increased in CSF at this time. P450scc and 5alphaRII enzyme expression was significantly increased in the cerebral cortex in the UCO fetuses compared to control fetuses. These results suggest that the fetal brain is capable of transiently increasing neurosteroid production in response to asphyxia. The action of the increased neurosteroid content at GABAA receptors may serve to diminish the increased excitation due to excitotoxic amino acid release, and provide short-term protection to brain cells during such stress.
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PMID:Increased allopregnanolone levels in the fetal sheep brain following umbilical cord occlusion. 1533 82

Acute respiratory distress syndrome (ARDS) is a clinical-radiological diagnosis. Clinical diagnosis comprises severe hypoxemia assessed by arterial oxygen tension/fraction of inspired oxygen ratio of less than 200 and bilateral infiltrate on a chest radiograph in the absence of left atrial hypertension. The sensitivity and specificity of the clinical diagnosis vary based on the underlying etiology for ARDS. Except for presence of bilateral infiltrate on chest radiograph and severe hypoxemia on arterial blood gas, most diagnostic studies are used to exclude mimics of ARDS and potentially modify treatment. Computerized tomography of the chest is helpful in understanding the extent of the disease and is more sensitive in identifying pneumomediastinum and pneumothoraces seen frequently in patients with ARDS, which can be missed on a chest radiograph, especially if they are small in size. Measurements of alveolar dead space ventilation fraction can be helpful in determining the prognosis in individuals with ARDS. Bronchoalveolar lavage, transbronchial lung biopsy, and open lung biopsies can be safely performed in patients with ARDS. Bronchoalveolar lavage fluid in patients with ARDS shows neutrophil predominance with increased edema fluid to serum protein ratio. Diffuse alveolar damage, a pathognomic of ARDS, is seen on histopathology on transbronchial lung biopsy or open lung biopsy. Most common complications of these procedures include transient hypoxemia, respiratory acidosis, and pneumothorax with occasional persistent air leak. The potential risk of diagnostic studies should be balanced against the possible foreseeable benefits of the diagnostic studies.
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PMID:Diagnostic studies in patients with acute respiratory distress syndrome. 1676 46

Propafenone is a membrane-stabilizing agent belonging to a subgroup of the Vaughan Williams class I antidysrhythmic agents, structurally resembling propranolol and characterized by weaker beta-blocking activity. Despite respiratory complications having been reported as examples of side effects, very few reports have been published in the literature.We describe the case of an elderly woman with a history of hypertension and allergy to Parietaria, grass, olive, mites, and with periodic asthmatic manifestations, for whom the administration of oral propafenone for recurrent supraventricular dysrhythmia was associated with the sudden onset of severe bronchostenosis.A 78-year-old woman was frequently admitted to the Emergency Department for a recurrent supraventricular tachycardia, which was treated initially with veramapil and thereafter with ivabradin. During her last visit to the cardiologist, she was prescribed propafenone (150 mg, 3 times a day) in place of ivabradin. After the administration of the second dose on the first day of the therapy, the patient began to complain of the onset of progressively severe dyspnea at rest. In the Emergency Department, respiratory auscultation showed diffuse rhonchi, wheezing, and rales; and arterial pressure was 200/100 mm Hg. Hemogasanalysis revealed hypoxemia, respiratory acidosis with 83% of O2-saturation. Emergency treatment with O2 therapy, methylprednisolone intravenous, furosemide, and then salbutamol was also started; the electrocardiogram only showed sinusal tachycardia. Results of laboratory examinations, including a white cell count and cardiac enzymes, were within the normal range. The patient achieved good respiratory function, after a period of 3 days.This report describes that even a relatively small dose of oral propafenone after commencing treatment can have a severe effect in exacerbating the obstruction of the airways in a susceptible subject. The likely mechanisms are an allergic reaction or a direct bronchospastic effect. Considering the recognized asthmogenicity of propafenone due to beta-blocker activity, we suggest that the cardiologist always refer to the patient's medical history before prescribing this drug, which is capable of producing notable side effects in predisposed individuals, beginning the eventual administration in the hospital setting. The use of bronchial provocation test allows the selection of inclined patients, thus reducing the risk of bronchospasm.
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PMID:Severe Brochostenosis by Oral Propafenone Immediately After Commencing Treatment. 2124 22

Acute pancreatitis is one of the main causes of intra-abdominal hypertension (IAH). IAH contributes to multiple physiologic alterations and leads to the development of abdominal compartment syndrome (ACS) that induces multiorgan failure. We report a case of ACS in a patient with severe acute pancreatitis. A 44-year-old man who was admitted in a drunk state was found to have severe acute pancreatitis. During management with fluid resuscitation in an intensive care unit, drowsy mentality, respiratory acidosis, shock requiring inotropes, and oliguria developed in the patient, with his abdomen tensely distended. With a presumptive diagnosis of ACS, abdominal decompression through percutaneous catheter drainage was performed immediately. The intraperitoneal pressure measured with a drainage catheter was 31 mm Hg. After abdominal decompression, the multiorgan failure was reversed. We present a case of ACS managed with percutaneous catheter decompression.
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PMID:Abdominal compartment syndrome in severe acute pancreatitis treated with percutaneous catheter drainage. 2532 11


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