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)

A reduced duration of activity of local anesthetic drugs in patients with chronic renal failure has been described by several authors. Because surgical duration is not always predictable and these patients must be classified as high-risk patients (ASA physical status III-IV), reduced effectiveness may be a significant problem in clinical practice. Various reasons have been discussed as possible explanations for this phenomenon such as: (1) uremia-induced changes in acid-base status of blood and tissue, (2) alterations in protein-binding; and (3) changes in hemodynamic parameters. However, we have not been able to find any severe changes in electrolyte or acid-base status in patients with chronic renal failure after adequate hemodialysis. We wondered, therefore, whether changes in tissue pH might be one cause of the shorter duration of action of anesthetic drugs. We also examined some other pharmacokinetic parameters after administration of the anesthetic drug in order to find differences in comparison to healthy patients. Supraclavicular brachial blockade (3 mg/kg bupivacaine 0.5% + 0.1 IU vasopressin/ml) was performed in 11 patients with chronic renal failure requiring hemodialysis who were admitted to the hospital for a shunt operation in the forearm. The control group consisted of 11 healthy patients who were admitted for minor hand surgery. Preoperative blood samples were taken for measurement of blood urea nitrogen, serum creatinine, serum electrolytes, lactate, hemoglobin and hematocrit, and an arterial blood gas duration of action was defined as the time to full recovery of sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The action of bupivacaine-HCl following supraclavicular plexus block in patients with chronic kidney insufficiency]. 341 3

Using captopril (C), an angiotensin (ANG) I converting-enzyme inhibitor, to increase endogenous prostaglandins (PGs) and to decrease endogenous ANG II synthesis, we studied the relationship between endogenous ANG II, PG, and antidiuretic hormone (ADH) release in seven normal volunteers before (control study) and after inhibition of PG synthesis by a single dose of aspirin (ASA study). In the control study, following the administration of 100 mg of C, there was a significant increase of plasma PGE2, plasma-renin activity (PRA), and urinary PGE2 and 6-keto-PGF1 alpha and a decrease of plasma ADH. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were unaffected by C; urine output, fractional sodium excretion (FENa), and osmolal clearance (Cosmol) increased; and urinary osmolality (Uosmol) decreased significantly after C. In the ASA study PG were undetectable in plasma and significantly reduced in urine 1 h after aspirin and did not increase when C was added. Plasma ADH decreased and PRA increased, as in the control study, after C, whereas GFR, RPF, urine output, FENa, Cosmol, and Uosmol were unchanged. These results suggest that the effect of C on ADH release may be mediated, to a large extent, by a fall in endogenous circulating ANG II, since ADH decreased in the presence of both high or undetectable levels of PGE2. The results also suggest that the increase in PGE2 induced by C may precipitate the diuretic and natriuretic effects of acute C administration.
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PMID:Angiotensin II inhibition with captopril on plasma ADH, PG synthesis, and renal function in humans. 352 28

Type IIB von Willebrand's disease (vWD) is a distinct form of this disorder in which the largest multimers of the von Willebrand factor (vWF) are lacking in plasma but present in platelets. When the vasopressin analogue, 1-deamino-8-D-arginine vasopressin (DDAVP), is given to patients with type IIB vWD, an abnormal vWF is released to plasma. This vWF causes thrombocytopenia in vivo and platelet aggregation in vitro. Aggregation occurs in the plasma milieu and thus at physiological fibrinogen concentration. In this study we demonstrate that IIB post-DDAVP vWF aggregated only metabolically active platelets. The platelet aggregation was completely inhibited by EDTA and PGE1, and either inhibited or greatly weakened by ASA, demonstrating the role of divalent cations and thromboxane A2 formation. In spite of inhibiting platelet aggregation, EDTA, PGE1 and ASA did not prevent platelet binding of IIB post-DDAVP vWF. An antiserum against GP Ib made normal platelets less responsive to the IIB vWF although neither platelet aggregation nor vWF binding were completely prevented. The aggregation was fibrinogen-dependent and platelets from patients with Glanzmann's thrombasthenia were unresponsive. The studies provide evidence that IIB post-DDAVP vWF is bound to unstimulated platelets and that the interaction between vWF and platelets in type IIB vWD is different from ristocetin-induced as well as thrombin- and epinephrine-induced binding to platelets of normal vWF.
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PMID:Platelet--von Willebrand factor interactions in type IIB von Willebrand's disease. 387 38

The role of prostaglandins in the development of aminoglycoside-induced acute renal failure was studied in CD-COBS rats (200 to 250 g). The animals were treated with gentamicin (80 mg/kg), acetylsalicylic acid (ASA, 100 or 200 mg/kg), or both drugs or saline for 5 or 10 days. Renal function was studied measuring creatinine clearance, blood urea nitrogen (BUN), and serum electrolytes, urine osmolality, and maximal urinary concentrating capacity after water deprivation and vasopressin administration. Gentamicin toxicity on the proximal tubule was evaluated by measuring urinary excretion of the lysosomal enzyme N-acetylglucosaminidase (NAG). Renal prostaglandin (PG) production was evaluated measuring the concentration of PGE2, PGD2, PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2 (TXB2) in whole renal homogenate after a 15-min incubation at 37 degrees C using gas chromatography-mass spectrometry. Gentamicin alone reduced the glomerular filtration rate (GFR) 20 to 30% after 5 and 10 days of treatment. Combination with ASA potentiated the toxic effect of the aminoglycoside after 10 but not after 5 days of treatment. Similarly, gentamicin reduced the urinary concentrating capacity and addition of ASA worsened the effects. Gentamicin markedly increased NAG excretion but this effect was reduced by ASA, probably as a result of lysosomal stabilization. ASA alone inhibited the production of prostaglandins in renal tissue by 70 to 90% after single or multiple doses. The animals treated with gentamicin alone presented a significant, specific increase in PGE2 production after 10 days of treatment but this increase did not occur when the two compounds were given together. Since PGE2 has a vasodilatory effect in the kidney these results suggest that it may play a specific role in maintaining normal renal blood flow and GFR during the development of aminoglycoside nephrotoxicity. The inhibition of prostaglandin production by nonsteroid anti-inflammatory drugs prevents this compensatory mechanism and worsens the renal damage.
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PMID:Prostaglandins and aminoglycoside nephrotoxicity. 404 89

This prospective, randomised study compared total intravenous anaesthesia (TIVA) and inhalation anaesthesia with respect to endocrine stress response, haemodynamic reactions, and recovery. METHODS. The investigation included two groups of 20 ASA I-II patients 18-60 years of age scheduled for orthopaedic surgery. For premedication of both groups, 0.1 mg/kg midazolam was injected IM. Patients in the propofol group received TIVA (CPPV, PEEP 5 mbar, air with oxygen FiO2 33%) with propofol (2 mg/kg for induction followed by an infusion of 12-6 mg/kg.h) and fentanyl (0.1 mg before intubation, total dose 0.005 mg/kg before surgery, repetition doses 0.1 mg). For induction of patients in the isoflurane-group, 5 mg/kg thiopentone and 0.1 mg fentanyl was administered. Inhalation anaesthesia was maintained with 1.2-2.4 vol.% isoflurane in nitrous oxide and oxygen at a ratio of 2:1 (CPPV, PEEP 5 mbar). For intubation of both groups, 2 mg vecuronium and 1.5 mg/kg suxamethonium were injected, followed by a total dose of 0.1 mg/kg vecuronium. Blood samples were taken through a central venous line at eight time points from before induction until 60 min after extubation for analysis of adrenaline, noradrenaline (by HPLC/ECD), antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH), and cortisol (by RIA). In addition, systolic arterial pressure (SAP) heart rate (HR), arterial oxygen saturation (SpO2), and recovery from anaesthesia were observed. RESULTS. Group mean values are reported; biometric data from both collectives were comparable (Table 1). Plasma levels of adrenaline (52 vs. 79 pg/ml), noradrenaline 146 vs. 217 pg/ml), and cortisol (82 vs. 165 ng/ml) were significantly lower in the propofol group (Table 2, Figs. 1 and 3). Plasma levels of ADH (4.8 vs. 6.1 pg/ml) and ACTH (20 vs. 28 pg/ml) did not differ between the groups (Table 2, Figs 2 and 3). SAP (128 vs. 131 mmHg) was comparable in both groups, HR (68/min vs. 83/min) was significantly lower in the propofol group, and SpO2 (97.1 vs 97.4%) showed no significant difference (Table 3). Recovery from anaesthesia was slightly faster in the propofol group (following of simple orders 1.9 vs. 2.4 min, orientation with respect to person 2.4 vs. 3.4 min, orientation with respect to time and space 2.8 vs. 3.7 min), but differences failed to reach statistical significance. CONCLUSIONS. When compared with isoflurane inhalation anaesthesia, moderation of the endocrine stress response was significantly improved during and after TIVA with propofol and fentanyl. Slightly shorter recovery times did not lead to an increased stress response. With respect to intra- and postoperative stress reduction, significant attenuation of sympatho-adrenergic reaction comparable SAP and reduced HR, sympatholytic and hypodynamic anaesthesia with propofol and fentanyl seems to be advantageous for patients with cardiovascular and metabolic disorders. For this aim, careful induction and application of individual doses is essential.
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PMID:[Endocrine stress reaction, hemodynamics and recovery in total intravenous and inhalation anesthesia. Propofol versus isoflurane]. 766 38

This study was undertaken to investigate in a prospective randomized way the influence of the benzodiazepine antagonist flumazenil on endocrine stress response and haemodynamic parameters after modified neuroleptanaesthesia. A total of 24 patients (ASA scores I or II) aged between 18 and 60 who were scheduled for major gynaecological surgery, were investigated. For modified neuroleptanaesthesia, midazolam, fentanyl and vecuronium were administered in standardized doses. After extubation, patients of the flumazenil group received initial injections of 0.2 mg flumazenil to antagonize the residual effect of midazolam and additional doses of 0.1 mg per minute until the desired level of vigilance was reached (awareness of person, time and place). In the control group no flumazenil was used. Endocrine stress parameters and haemodynamic parameters were measured at 7 different times, from before induction of anaesthesia up to 60 minutes after the operation. In both groups, a marked increase in endocrine stress response was observed. Adrenaline, noradrenaline, antidiuretic hormone, adrenocorticotropic hormone, cortisol, glucose and lactate, however, were not additionally influenced by the antagonism. No influence of flumazenil on mean arterial pressure, heart rate and arterial oxygen saturation was observed. After modified neuroleptanaesthesia, a careful antagonism of midazolam with small doses of flumazenil is not disadvantageous with respect of endocrine stress response and haemodynamic reactions.
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PMID:[The effect of flumazenil on the endocrine stress reaction following modified neuroleptanesthesia]. 824 Jun 40

This study was undertaken to investigate the influence of the opiate-antagonist naloxone on the endocrine stress response and haemodynamic parameters after modified neuroleptanaesthesia in a randomized, prospective design. A total number of 22 patients (ASA-scores I or II) between 18 and 60 years scheduled for major gynaecologic surgery were included. For modified neuroleptanaesthesia, midazolam, fentanyl and vecuronium were administered in standardized doses. After extubation, patients of the naloxone-group received injections of 2 x 0.1 mg naloxone; in controls, no naloxone was used. Endocrine stress parameters and haemodynamic parameters were measured 7 times before induction of anaesthesia and up to 60 minutes after the operation. In both groups, remarkable increases in adrenaline, noradrenaline, antidiuretic hormone, adrenocorticotropic hormone, cortisol, glucose and lactate took place in the postoperative period. This stress response was comparable in both groups and not increased by naloxone. No significant influence of naloxone on mean arterial pressure, heart rate and arterial oxygen saturation was observed. After neuroleptanaesthesia, a careful opiate antagonism with small doses of naloxone is not disadvantageous with respect to endocrine stress response and haemodynamic reactions.
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PMID:[Endocrine and hemodynamic effects of naloxone following modified neuroleptanesthesia]. 829 47

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

The initiation of cardiopulmonary bypass creates significant derangements in cardiovascular volume status and both endocrine and autonomic nervous system function. To examine whether such derangements might differ in patients with different pre-operative physical status scores, we measured the plasma concentrations of calcitonin gene-related peptide, atrial natriuretic peptide and brain natriuretic peptide, catecholamines and antidiuretic hormone, as well as haemodynamic variables, during and after cardiopulmonary bypass in 27 consecutive patients undergoing coronary artery bypass grafting. The pre-operative levels of atrial natriuretic peptide and brain natriuretic peptide differed significantly between ASA II patients and III and IV patients [mean (SD) brain natriuretic peptide levels = 14 (8.2) vs. 129 (51) pg.ml-1]. Plasma calcitonin gene-related peptide increased significantly in both groups after the initiation of cardiopulmonary bypass, and remained increased throughout cardiopulmonary bypass. The changes in plasma epinephrine, norepinephrine and antidiuretic hormone were similar to those reported previously. The changes in plasma calcitonin gene-related peptide, atrial natriuretic peptide and brain natriuretic peptide did not correlate with any changes in haemodynamic variables before or after cardiopulmonary bypass. Measurement of plasma brain natriuretic peptide might usefully be included in the pre-operative evaluation of patients with cardiac disease.
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PMID:Changes in calcitonin gene-related peptide, atrial natriuretic peptide and brain natriuretic peptide in patients undergoing coronary artery bypass grafting. 1260 52

That endogenous vasopressin levels in successfully resuscitated human patients were significantly higher than in patients who died pointed to the possible benefit of administering vasopressin during cardiopulmonary resuscitation (CPR). Several CPR studies in pigs showed that vasopressin improved blood flow to vital organs, cerebral oxygen delivery, resuscitability and neurological outcome when compared with epinephrine. In a small clinical study, vasopressin significantly improved short-term survival when compared with epinephrine indicating its potential as an alternative pressor to epinephrine during CPR in human beings. As there was little clinical data available at that time, its recommended use was limited to adult human beings with shock-refractory ventricular fibrillation. In this report, we present the case of a dog in which the successful management of intraoperative asystolic cardiac arrest involved vasopressin. Unexpected cardiac arrest occurred during anaesthesia for the surgical removal of multiple mammary adenocarcinomata in a 11-year-old Yorkshire terrier. Despite an ASA physical status assignation of III, the dog was successfully resuscitated with external chest compressions, intermittent positive pressure ventilation and vasopressin (2 doses of 0.8 IU kg(-1)) and was discharged 3 days later without signs of neurological injury. We believe vasopressin contributed to restoring spontaneous circulation. It may prove increasingly useful in perioperative resuscitation in dogs.
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PMID:Cardiopulmonary resuscitation with vasopressin in a dog. 1576 17


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