Glasgow meningococcal septicemia prognostic score.
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Child, Preschool↗
Biomedical subjects
S F Evans
Publications and source records attributed to S F Evans.
Characterization of circulating pro-opiomelanocortin-related peptides in human septic shock.
The nature of circulating pro-opiomelanocortin (POMC)-related peptides was investigated in patients with a diagnosis of septic shock. Also, changes following administration of methylprednisolone were monitored using established chromatographic techniques and three radioimmunoassays directed towards the N-terminal, mid-portion and C-terminal regions of the precursor. Adrenocorticotrophin and beta-endorphin-like peptides were identified in the circulation. By 60 min after a pharmacological dose of methylprednisolone (30 mg/kg) concentrations of these peptides were reduced and continued to fall up to 180 min. beta-Lipotrophin and N-terminal POMC(1-76) were also detected by the beta-endorphin and gamma 3-MSH assays respectively. The concentrations of these peptides were noticeably reduced only after 180 min. The 31,000 Da MSH/ACTH/beta-endorphin (POMC) and the 22,000 Da MSH/ACTH precursors were also present in the circulation in septic shock and their concentrations increased following steroid treatment.
Adrenocorticotropic Hormone↗
Nitrous oxide inhalation does not influence plasma concentrations of beta-endorphin or Met-enkephalin-like immunoreactivity.
The possibility that nitrous oxide releases endogenous opioid peptides into the circulation has been tested in 10 pain-free, unstressed volunteers breathing 30% nitrous oxide in oxygen. Despite achieving plateau concentrations in venous blood, accompanied by subjective effects, there were no significant changes in plasma concentrations of immunoreactive beta-endorphin, methionine-enkephalin or ACTH. These results indicate that, in the absence of nociceptive input, the effects of the inhalation of nitrous oxide are unrelated to alterations in peripheral concentrations of these endogenous opioid peptides.
Adrenocorticotropic Hormone↗
Neuroendocrine and cardiovascular changes in septic shock and after cardiac surgery: effect of high-dose corticosteroid therapy.
Plasma levels of beta-endorphin-like immunoreactivity (BLI) were similarly elevated in patients with septic shock (group A) and in normotensive subjects recovering from cardiac surgery (group B) (1231 +/- 483 pg ml-1 and 1,240 +/- 355 pg ml-1, respectively). In neither group was cardiac output reduced, but total peripheral resistance index (TPRI) was low in group A and low or normal in group B. Intravenous methylprednisolone (MP) 30 mg kg-1 variably suppressed BLI by a mean of only 30% in group A, while in group B, BLI usually rose and then fell following MP. In group A percentage changes in BLI were positively correlated with percentage changes in cardiac index (CI) and mean arterial pressure (MAP) (r = .83, P less than .01, r = .59, P less than .05 respectively). No such correlations were found in group B. These findings suggest that increases in circulating beta-endorphin are unlikely to be responsible for myocardial depression or hypotension in septic shock. ACTH levels were in general normal in group A but were consistently elevated in group B, although plasma cortisol was similarly elevated in both groups. Furthermore there was a good correlation between percentage changes in ACTH and BLI following MP in group B (r = .87, P less than .01) but not in group A. Possible explanations for these findings are discussed.
Adrenocorticotropic Hormone↗
A secondary immune deficiency in the Fatty/Orl-op rat.
The response of T and B lymphocytes to the mitogens PHA and LPS was studied in the Fatty/Orl-op rat. Whereas T and B cells from op/op spleen showed no lack of responsiveness compared with that of normal (op/+) littermate rats, the response of thymic cells to the T cell mitogen was lower in op/op rats over 12 days of age compared with normal rats of the same age. Osteopetrotic rats of 10 days and younger did not show this T cell deficiency. The responsiveness of T cells from op/op lymph nodes to PHA was less than that of normal rats at 12 days and older. Thus, though splenic T and B cell populations were well maintained in the adult op/op rat despite the severe depletion of marrow cells in this mutant, the thymus and lymph node T cell populations were qualitatively or quantitatively deficient. Since osteopetrotic obliteration of the marrow cavities precedes the appearance of the immune deficiency we suggest that the immune deficiency may be caused by a failure of T cell supply to the thymus and lymph nodes.
Animals↗
Plasma levels and biochemical characterisation of circulating met-enkephalin in canine endotoxin shock.
Endogenous opioid peptides have been implicated in the pathophysiology of shock (1-5). In anaesthetised mongrel dogs, administration of E coli endotoxin caused a rise in plasma met-enkephalin-like immunoreactivity (MLI). Biochemical characterisation of MLI by gel filtration chromatography revealed various molecular forms: 31K, 8K, 3-5K and the native pentapeptide in approximately equal amounts. After enzymatic treatment of column fractions the 31K form predominated (90.7%). This is the first demonstration of elevated MLI in endotoxin shock.
Animals↗
A new canine model of endotoxin shock.
A new canine model of endotoxin shock has been developed in which spontaneous recovery of cardiovascular function is largely prevented, the haemodynamic effects of anaesthesia are minimized and intravascular volume replacement is given. This model has been evaluated using two groups of five adult mongrel dogs anaesthetized with alpha-chloralose and breathing spontaneously. Animals in one group were anaesthetized, instrumented and given Escherichia coli (E. coli) endotoxin intravenously, whilst those in the control group were subjected only to anaesthesia and instrumentation. E. coli endotoxin was given to dogs in the shock group as a bolus dose of 5 mg kg-1 followed by a continuous infusion at 2 mg kg-1 h-1. This produced immediate, severe, cardiovascular depression, with precipitous falls in mean arterial pressure (MAP), cardiac index (CI), stroke index (SI) and left ventricular (LV) dp/dt max. There were associated increases in systemic and pulmonary vascular resistances. Arterio-venous oxygen content difference (C(a-v)O2) increased after induction of shock, and animals developed a progressive metabolic acidosis. Increasing haemoconcentration occurred, as evidenced by a rising haematocrit (PCV). Hypovolaemia was reflected by a concurrent fall in pulmonary capillary wedge pressure (PCWP). One hour after induction of shock, intravascular volume replacement was given in the form of a colloidal gelatin solution, as a bolus dose of 10 ml kg-1, followed by a continuous infusion at 10 ml kg-1 h-1. Volume replacement reversed haemoconcentration, restored PCWP and produced some haemodynamic improvement, although in general, severe cardiovascular depression persisted throughout a three hour observation period. This severe endotoxin shock model has proved to be stable, reproducible and economical. It provides a useful preliminary test for new methods of treatment in hypodynamic endotoxin shock, as well as allowing investigation of acute metabolic and physiological changes.
Acid-Base Equilibrium↗
Effects of intravascular volume expansion on the cardiovascular response to naloxone in a canine model of severe endotoxin shock.
The specific opiate receptor antagonist, naloxone, can produce haemodynamic improvement and increased survival in experimental shock. The efficacy of naloxone therapy in a canine model of endotoxin shock has been evaluated both with and without intravascular volume replacement. Animals were anaesthetized with alpha-chloralose and allowed to breathe spontaneously. A large bolus dose of endotoxin was followed by a continuous infusion and treatment was instituted one hour after the endotoxin bolus. In the absence of volume replacement, naloxone caused only limited and transient increases in mean arterial pressure (MAP) and left ventricular (LV) dp/dt max, with little effect on cardiac index (CI). Total peripheral resistance index (TPRI) tended to rise in both control and naloxone-treated dogs. In volume-replaced animals, naloxone produced substantial and sustained increases in the MAP and LV dp/dt max with an associated rise in the CI. TPRI rose initially in this series and then fell progressively. Further analysis of the improvements in the CI showed an increase in stroke index with a tendency for heart rate to fall. These findings suggest a myocardial action of naloxone in endotoxin shock, which is augmented by volume replacement. An initial, transient vasoconstrictor effect cannot, however, be excluded. Further work is required to determine the mechanism of the effects described.
Animals↗
Effect of dobutamine on insulin requirement in diabetic ketoacidosis.
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Catecholamines↗
Efficacy of intravaginal misoprostol in second-trimester pregnancy termination: a randomized controlled trial.
A prospective randomized, double-blind, controlled clinical trial to compare the clinical efficacy and side effects of intravaginal misoprostol with the traditional prostaglandin, gemeprost, in second-trimester pregnancy interruption was conducted. A sample size of 100 women was calculated to demonstrate that misoprostol was as effective as gemeprost in achieving delivery within 24 hours (alpha = 0.1, 80% power). Women were recruited with fetal death in utero, severe fetal anomaly, or psychosocial pregnancy termination between 14 and 28 weeks gestation and randomized to receive either 1 mg gemeprost 3 hourly for 5 doses, or 200 mcg misoprostol 6 hourly for 4 doses, intravaginally. The therapeutic regimens were repeated if undelivered by 24 hours. Those undelivered after 48 hours received an extra-amniotic PGF2 alpha infusion. The median gestation at recruitment was identical: gemeprost 19 weeks (IQ 17-22 weeks) vs. misoprostol 19 weeks (IQ 17-21 weeks), P = 0.887. Delivery within 24 hours occurred in 75.1% of women receiving gemeprost and 74.9% receiving misoprostol (P = 1.0). The median time from prostaglandin commencement to delivery was similar: gemeprost 13.7 hours (IQ 9.0-23.5 hours) vs. misoprostol 16.9 hours (IQ 10.3-23.5 hours), P = 0.769. A significant reduction in the incidence of vomiting in women randomized to misoprostol occurred (34% vs. 13.2%, P = 0.017). There was no significant difference in the incidence of maternal fever > 37.5 degrees C, nausea, diarrhea, or placental retention. A 200-fold pharmaceutical cost advantage was observed with the use of misoprostol compared with gemeprost. Intravaginal misoprostol performs as effectively as gemeprost in achieving delivery in the second trimester without increase in adverse effects and displaying a significant cost advantage.
Abortifacient Agents, Nonsteroidal↗
Maternal, but not fetal, administration of corticosteroids restricts fetal growth.
OBJECTIVE: Previous studies have shown that repeated doses of corticosteroids given to pregnant sheep improve postnatal lung function, but restrict fetal growth. Repeated administration of corticosteroids directly to the fetus also enhances postnatal lung function. The purpose of the present study was to investigate and characterize the relative effects on growth of repeated maternal and fetal treatments by study of body, organ, and placental weights. METHODS: Date-bred pregnant sheep were given intramuscular betamethasone or saline to either the mother or fetus on three occasions at weekly intervals commencing at 104 days gestation, followed by cesarean section at 125 days. Twenty-two animals which had received three doses of betamethasone were compared with 21 which had received a single dose at 104 days and with 12 saline-treated controls. RESULTS: Repeated maternal doses of betamethasone resulted in reductions in birthweight and weights of the placenta and major organs. Direct fetal injection did not affect birthweight, placental weight, placental/ birthweight ratio, or weights of the major organs with the exception of the liver. CONCLUSIONS: Administration of repeated doses of betamethasone directly to the sheep fetus does not produce the growth-restricting effects induced by maternal administration and does not affect the placental/birthweight ratio.
Adrenal Cortex Hormones↗
Patient-controlled epidural analgesia in labor: the addition of clonidine to bupivacaine-fentanyl.
BACKGROUND AND OBJECTIVES: Epidural clonidine has not been evaluated as a component of patient-controlled epidural analgesia (PCEA) solutions during labor. A randomized, double-blind trial was conducted to investigate the efficacy and side effects of PCEA using bupivacaine and fentanyl, with or without clonidine. METHODS: Seventy-five healthy parturients in active labor were assigned to a PCEA solution of 0.0625% bupivacaine and fentanyl 2 microg/mL (4 mL demand bolus, 15 min lockout), with or without clonidine 4.5 microg/mL. The primary outcome measure was parturient rating of analgesia; others assessments included pain scores, drug utilization, supplementation and side effects. RESULTS: Thirty-one parturients received clonidine (group BFC) and 38 received control solution (group BF). Eight (6 group BF, 2 group BFC, P = .28) failed to achieve satisfactory epidural analgesia. There was a trend for parturient ratings of pain relief to be higher in group BFC, with significantly more reporting excellent first-stage analgesia (81% v. 57%, P<.05). Pain scores were similar. Clonidine (median dose, 28 microg/h) reduced total bupivacaine and fentanyl use (P<.01), and reduced supplementation (P<.01). Maternal blood pressure (BP) and recordings of systolic BP below 100 mm Hg did not differ. Group BFC had higher sedation scores (P<.01), but no one appeared oversedated. Shivering was reduced in group BFC (P<.01). CONCLUSIONS: The addition of clonidine to epidural bupivacaine and fentanyl for PCEA in labor improved analgesia, reduced the supplementation rate, and reduced shivering. Increased sedation and lower BP were not clinically important.
Adjuvants, Anesthesia↗