Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renin activity and aldosterone concentration in plasma and excretion of sodium and potassium in urine were measured during a period of 24 hours in 12 patients undergoing hysterectomy under general anaesthesia or epidural analgesia. Analgesia extended from T4 to S5 and was effective throughout the study. The normal stress-induced increase in plasma renin activity and aldosterone was inhibited by epidural analgesia. Urinary excretion of potassium was significantly lower in the epidural group, but sodium and water retention showed no difference between groups. It is concluded that neurogenic stimuli from the surgical area are important release mechanisms of the renin-aldosterone response to surgery. The results suggest that post-operative sodium retention is caused by factors other than the mineralocorticoid system.
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PMID:Epidural analgesia inhibits the renin and aldosterone response to surgery. 48 83

The effect of a high epidural blockade on postoperative sodium (Na) retention has been studied in 8 patients undergoing cholecystectomy, with a further 8 patients, who received conventional anaesthesia and analgesia, acting as a control group. Preoperatively, all the patients received 90 mmol of Na per day and were in Na balance at the start of operation; this intake was continued for 48 h after the operation by intravenous infusion, and the epidural blockade was maintained with regular supplements of bupivacaine throughout. In addition to urine Na excretion and blood pressure changes, plasma levels of aldosterone, cortisol, renin activity and glucose were measured at appropriate intervals. The Na retention in both the epidural and control groups was the same (139 mmol and 135 mmol respectively at 48 h), but there were significant differences in the measurements of all the other factors. It is concluded that the epidural was providing effective blockade, but that the factors which cause Na retention were not affected by the epidural blockade. These results are at variance with another study of the effect of epidural blockade on postoperative Na retention (Bevan, 1971), and the possible reasons for this are discussed.
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PMID:The effect of epidural analgesia on postoperative sodium balance. 50 60

Intraspinally administered alpha 2-adrenergic agonists are being examined for postoperative analgesia, yet their effects on the hemodynamic response to acute hemorrhage have not been examined. In this study chronically prepared conscious sheep received thoracic intrathecal saline or clonidine 300 micrograms followed in 15 min by rapid removal of 1,000 ml blood. In saline-treated ewes blood pressure was maintained and heart rate steadily increased during hemorrhage of up to 700 ml blood, with further blood removal resulting in rapid decreases in both variables. In contrast, heart rate never increased and blood pressure was maintained only up to 400 ml blood loss in animals receiving intrathecal clonidine. Compared to saline controls, clonidine did not alter blood pressure or heart rate at the end of hemorrhage or during blood pressure restitution during the next hour. Clonidine inhibited the increase in plasma epinephrine at the end of hemorrhage without altering plasma norepinephrine, vasopressin, renin, or atrial natriuretic factor. Intrathecal idazoxan, a specific alpha 2-adrenergic antagonist, reversed clonidine's effect on blood pressure during hemorrhage. Intravenous DG-5128, a poorly lipid-soluble alpha 2-adrenergic antagonist, also reversed clonidine's effect and additionally completely blocked any reduction in blood pressure and heart rate during hemorrhage. These data suggest that intrathecal clonidine interferes with maintenance of blood pressure during hemorrhage, likely because of a spinal sympatholytic effect, but does not affect the ultimate decrease in blood pressure after rapid removal of 1,000 ml blood. This difference in effect during the two phases of hemorrhage can be explained by the relative importance of the sympathetic nervous system in each.
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PMID:Intrathecal clonidine and the response to hemorrhage. 135 38

1. The antinociceptive effect of compound 48/80 was reversed by the pretreatment with an angiotensin-converting enzyme (ACE) inhibitor, Hoe 498, in a dose-dependent manner and with a opiate receptor antagonist, naloxone (5.0 mg/kg, s.c.) in rats. 2. The increase of plasma beta-endorphin-like immunoreactivity produced through s.c. administration of compound 48/80 was attenuated by the pretreatment with Hoe 498 but not with naloxone. 3. The present data suggest the possible involvement of renin-angiotensin system in compound 48/80-induced analgesia in rats.
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PMID:The role of renin-angiotensin system in compound 48/80-induced analgesia in rats. 252 74

The effects of subcutaneous (s.c.) administration of compound 48/80 (a well known histamine liberator) on latency to thermoalgesic stimulus, hematocrit (Hct) and plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in male rats. The s.c. administration of compound 48/80 in doses ranging from 0.5 to 5.0 mg/kg into the rats produced significant analgesia in the hot plate test and increased Hct in a dose-dependent manner. Concomitant variation was observed between the analgesia and the increase of Hct. This analgesic effect, but not the increase of Hct, was diminished by pretreatment with the opiate receptor antagonist, naloxone (5 mg/kg, s.c.). A significant increase of plasma beta-END-LI was observed by s.c. injection of compound 48/80. Together with a previous finding that compound 48/80 induced-hypovolemia increases the renin release from kidney and then causes water intake in the rats, it is suggested that s.c. administration of compound 48/80 induced analgesia mediated through stimulation of an opioid system, may be closely related to stimulation of the renin-angiotensin system.
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PMID:Analgesia and plasma beta-endorphin-like immunoactivity in compound 48/80-induced hypovolemia of the rats. 296 94

The effects of halothane anaesthesia or epidural analgesia on the per- and postoperative change in blood concentrations of ACTH, beta-lipotropin, cortisol, dehydroepiandrosterone, aldosterone, glucose, lactate and free fatty acids were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with halothane and nitrous oxide was found to be associated with a significant increase in plasma ACTH levels and beta-LPH levels. Changes in plasma dehydroepiandrosterone were similar to those in plasma cortisol. The elevation of plasma aldosterone during major surgery could be explained as the effect of an increased renin secretion. However, simultaneous increase in plasma cortisol and plasma aldosterone during surgery reflect an additional effect of adrenocorticotropin upon aldosterone secretion.
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PMID:[Behavior of the hypophyseal-adrenal cortex system in inhalation and conduction anesthesia. A review with comparative study]. 299 12

Seven active tetrapeptide amides characterized by a C-terminal phenylalanyl aminoadamantane (PheNHAd) sequence, were identified by selective testing for human renin inhibitory activity among compounds with adjacent hydrophobic groups and molecular size equivalent to 3-5 amino acid residues. The new inhibitors were compared with known renin inhibitors (RIP, pepstatin, H-77) and opioid analgesic agents (Met-enkephalin, morphine), with the following results: The new inhibitors were active against human renin (IC50 approximately 10-5M), but inactive against rat renin and pepsin. Although active in opiate receptor binding studies (IC50 approximately 10(-7)M), they were, with few exceptions, inactive in the mouse writhing and hot plate tests for analgesia. SAR studies suggested a separation of the renin inhibitory from the analgesic activity of enkephalin analogs. Preliminary experiments with sodium-depleted rhesus monkeys indicated hypotensive activity for three of the new inhibitors at 3 mg/kg i.v., and RIP at 1 mg/kg. The recently reported clinical hypotensive properties of RIP (Zusman et al., Trans. Assoc. Am. Physicians 96:365, 1983) along with the present comparative studies suggest that the new inhibitors may lead to clinically useful agents.
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PMID:New class of inhibitors specific for human renin. 300 Jun 56

The influence of halothane-nitrous oxide anaesthesia and normotensive epidural analgesia (level of sensory block T8-T10), respectively, on the plasma concentrations of adrenocorticotrophic hormone (ACTH), beta-lipotropin (beta-LPH), cortisol, dehydroepiandrosterone (DHA) and aldosterone as well as on the metabolites glucose, lactate and free fatty acids (FFA) was studied in 20 healthy patients who underwent elective orthopaedic procedures on the lower limbs. ACTH and beta-LPH concentrations in plasma rose significantly (P less than 0.001) during halothane-nitrous oxide anaesthesia. DHA secretion closely followed the secretory profile of cortisol. Increased renin levels and increased ACTH release seemed to be responsible for increased aldosterone secretion, intra-operatively. The hormonally induced rise of glycogenolysis and lipolysis did not produce important intra-operative increases in metabolite concentrations in the blood. In normotensive epidural analgesia no significant increase in stress response could be demonstrated, even with low levels of sensory block.
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PMID:A comparison of two types of anaesthesia on the endocrine and metabolic responses to anaesthesia and surgery. 302 43

The role of variation of venous return on baroreflex control of heart rate during lumbar epidural anesthesia was investigated in 12 unpremedicated patients. Group 1 patients (n = 6) received 8 ml of 0.5% plain bupivacaine in the epidural space (L3-4) (mean upper level of analgesia at T10). Group 2 patients (n = 6) received 8 ml of saline at the same level in the epidural space. Following the epidural injection, phenylephrine (PHE) and nitroglycerin (NTG) were employed to alter the stimulation of baroreceptor sites before and during application of lower body positive pressure (LBPP). Plasma bupivacaine, catecholamines, renin activity, and vasopressin were assayed. In contrast to saline, epidural bupivacaine induced a decrease in systolic arterial and right atrial pressures (-11 +/- 4 and -3.2 +/- 0.7 mmHg, respectively, mean +/- SEM) without change in heart rate, an increase in baroreflex slopes during PHE and NTG injections (+5.9 +/- 1.6 ms/mmHg and +2.8 +/- 0.9 ms/mmHg, respectively), and a decrease in plasma norepinephrine (-248 +/- 89 pg/ml). The application of LBPP restored hemodynamic and reflex variables to preepidural analgesia values, whereas plasma catecholamines decreased further. Plasma renin activity and vasopressin were not modified at any time in either groups. This study indicates that lumbar epidural anesthesia enhances cardiac vagal tone mainly through a decrease in venous return.
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PMID:Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans. 308 Sep 22

It has been suggested that stimulation of adrenoreceptors could be responsible for some of the haemodynamic effects of isoflurane. But there are no solid data demonstrating the role of sympatho-adrenal stimulation induced by pain during isoflurane administration. The impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension has been investigated in 28 patients (47-76 years), scheduled for total hip arthroplasty. After premedication with morphine hydrochloride (0.1 mg/kg), patients were randomly assigned to receive either no fentanyl (control group) or fentanyl (5 micrograms/kg before tracheal intubation, 5 micrograms/kg before skin incision, and 2 micrograms/kg each 15 min during the 1st hour). Isoflurane was given to maintain mean arterial blood pressure in the range 6.7-8 kPa in both groups. Haemodynamic data and blood samples for determination of plasma renin activity (PRA) and epinephrine (E) and norepinephrine (NE) levels were collected before and during hypotension. The fentanyl group and the control group differed significantly during hypotension: heart rate, cardiac index, oxygen consumption and E, NE and PRA were lower (P less than 0.01) in the fentanyl group than in control group. Fentanyl lowered the required concentration of isoflurane to achieve the same degree of hypotension (end-tidal concentration: 0.8 +/- 0.2% in the fentanyl group and 1.4 +/- 0.15% in the control group; P less than 0.001). Our results demonstrate that the cardiovascular effects of higher isoflurane concentrations in the absence of narcotic analgesia are counterbalanced by adrenergic stress stimulation of released epinephrine and norepinephrine. Among the likely reasons for catecholamine release during isoflurane administration, inadequate analgesia may be considered.
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PMID:Impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension. 328 71


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