Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to investigate the influences of halothane and isoflurane as well as different extubation techniques on the endocrine stress response during recovery from general anesthesia. Forty patients scheduled for herniorrhaphy and cholecystectomy were randomly allocated to 4 groups: 20 received halothane and 20 received isoflurane anesthesia. Within the halothane and isoflurane groups, 10 patients each were extubated during anesthesia (1/2 MAC) and a further 10 had awake extubation. Premedication, induction of anesthesia, and intraoperative anesthetic management were standardized in all groups. Plasma levels of endocrine stress parameters as well as mean arterial pressure (MAP), heart rate (HR), and arterial oxygen saturation (SaO2) were measured at nine time points up to 60 min after extubation. Biometric data and duration of operation and anesthesia were comparable in all groups. In the recovery period, epinephrine levels were higher in the isoflurane groups than in the halothane groups (P = 0.02). With respect to time course, earlier and more marked increases of epinephrine, norepinephrine, and antidiuretic hormone (ADH) levels were observed in the isoflurane groups compared to the halothane groups (P less than 0.01), representing the more rapid elimination of isoflurane. The sympathoadrenergic stress response was more pronounced in patients with extubation during anesthesia than in those with awake extubation: epinephrine levels were slightly higher and group levels of norepinephrine were significantly increased (P = 0.02). No influence of the extubation techniques was observed on ADH, ACTH, and cortisol levels or on MAP, HR, or SaO2. In summary, extubation during anesthesia did not reduce the endocrine stress response. It is concluded that awake extubation should be preferred unless the operation or the patient's condition requires extubation during anesthesia.
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PMID:[The stress reaction in the recovery phase from halothane and isoflurane anesthesia]. 195 37

Few studies have used the vasopressin test to evaluate urine concentrating ability after sevoflurane anaesthesia. We performed a vasopressin test on the first day after operation to compare the effect of prolonged sevoflurane anaesthesia for orthopaedic procedures (n = 11) with that of isoflurane (n = 10). Mean doses of sevoflurane and isoflurane were 10.6 (SE 0.9) and 8.5 (1.5) MAC-h, respectively. Mean peak serum fluoride concentration in patients anaesthetized with sevoflurane was 41.9 (2.5 mumol litre-1 and exceeded 20 mumol litre-1 for approximately 20 h. Each group showed similar responses to vasopressin. There was no evidence of subclinical nephrotoxicity in patients given prolonged sevoflurane anaesthesia.
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PMID:Urine concentrating ability after prolonged sevoflurane anaesthesia. 791 43

Ornipressin (OR), a synthetic derivative of natural vasopressin, is widely used in combination with local anaesthetics in order to reduce surgical bleeding and systemic absorption of the local anaesthetic. As shown previously in experimental studies, OR causes severe coronary vasoconstriction. The myocardial oxygen balance is compromised by an increase in myocardial oxygen demand due to hypertension and impaired oxygen delivery following coronary vasoconstriction. We describe the case of a 19-year-old male who was admitted to the hospital for elective tonsillectomy. There was no evidence of systemic or cardiovascular disease (ASA I). Following the induction of anaesthesia with thiopentone 4 mg/kg and ventilation with N2O/O2 (FiO2:0.25), vecuronium was administered to facilitate orotracheal intubation. Anaesthesia was maintained with N2O/O2 (FiO2:0.33) and 2 MAC isoflurane. After reaching an anaesthetic steady state with stable haemodynamic conditions, peritonsillar infiltration with a prilocaine solution containing a total of 0.8 IU OR (0.1 IU/ml) produced marked tachycardia and hypertension. Concomitantly, distinct ST-segment-depression was observed in a lead II ECG. Hypertension and tachycardia occurred within 3 min after the local infiltration with prilocaine/OR. Maximum ST-segment depression and haemodynamic changes were recorded 11 min after infiltration, with an increase in heart rate from 58 to 136 min and a rise in blood pressure from 115/50 to 217/130 mmHg. Considering experimental results, the ECG changes in this case show clear evidence that even in healthy humans OR-induced systemic haemodynamic changes may be complicated by severe myocardial ischaemia due to coronary vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Signs of a severe myocardial ischemia following peritonsillar infiltration with ornipressin (POR 8)]. 831 91

Rifabutin is increasingly critical for treatment of atypical mycobacterial infections. One of its serious adverse effects is leukopenia. When encountering rifabutin-induced leukopenia, clinicians are faced with the dilemma of whether to lower the dosage of rifabutin or discontinue it because existing literature does not indicate whether rifabutin-induced leukopenia is dose related or idiosyncratic. We report the first established case of idiosyncratic rifabutin-induced leukopenia in an immunocompetent man treated for pulmonary Mycobacterium avium complex infection. The patient also developed rifabutin-induced syndrome of inappropriate antidiuretic hormone (SIADH), which also has not been previously reported.
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PMID:Idiosyncratic rifabutin-induced leukopenia and SIADH: case report and review. 1131 May 23

Volatile anesthetics such as isoflurane have been shown to offer anti-inflammatory effects during experimental endotoxemia whereas the alpha-adrenergic vasopressor norepinephrine exhibits proinflammatory properties on systemic cytokine release under the same conditions. However, during major surgery and in patients with systemic inflammatory response syndrome or sepsis both agents are frequently administered concurrently. We therefore aimed to investigate the influence of preexisting i.v. administration of noradrenaline or vasopressin on the anti-inflammatory effects of isoflurane during experimental endotoxemia. Anesthetized, ventilated Sprague-Dawley rats (n=7 per group) were randomly treated. In the LPS-only group, animals received lipopolysaccharide (LPS, 5 mg/kg, i.v.) with no further specific treatment. In the LPS-isoflurane group, isoflurane inhalation at 1 MAC was initiated simultaneously with induction of endotoxemia (LPS 5 mg/kg, i.v.). Animals in the LPS-isoflurane-norepinephrine group received norepinephrine infusion at 50 microg/kg/h 10 min prior to injection of LPS and inhalation of isoflurane. In the LPS-isoflurane-vasopressin group, vasopressin was administered at 0.5 IE/kg/h 10 min prior to LPS and isoflurane. In the LPS-norepinephrine and the LPS-vasopressin groups the infusion of each vasopressor was started prior to LPS injection without any application of isoflurane. A Sham group served as the control. After 4 h of endotoxemia, plasma levels of TNFalpha, IL-1beta and IL-10 were measured. Alveolar macrophages (AM) were cultured ex vivo for nitrite assay. Induction of endotoxemia resulted in a significant rise in measured plasma cytokines and nitrite production from cultured AM. Inhalation of isoflurane significantly attenuated plasma levels of TNFalpha (-65%) and IL-1beta (-53%) compared to the LPS-only group whereas it had no effect on nitrite production from cultured AM. Preexisting infusions of norepinephrine or vasopressin abolished the anti-inflammatory effects of isoflurane. The data demonstrate that the administration of norepinephrine or vasopressin both counteracted the anti-inflammatory effects of inhaled isoflurane on proinflammatory cytokine release during experimental endotoxemia in rats.
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PMID:Norepinephrine and vasopressin counteract anti-inflammatory effects of isoflurane in endotoxemic rats. 1778 93