Biomedical subjects

N Welsh

Publications and source records attributed to N Welsh.

At least 91 records · Page 5Linked to original sources

PubMed1989

Effects of protein kinase C activation on the regulation of the stimulus-secretion coupling in pancreatic beta-cells.

Effects of protein kinase C (PKC) activation on the insulin-secretory process were investigated, by using beta-cell-rich suspensions obtained from pancreatic islets of obese-hyperglycaemic mice. The phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), which is known to activate PKC directly, the muscarinic-receptor agonist carbamoylcholine and high glucose concentration enhanced the phosphorylation of a specific 80 kDa PKC substrate in the beta-cells. At a non-stimulatory glucose concentration, 10 nM-TPA increased insulin release, although there were no changes in either the cytoplasmic free Ca2+ concentration ([Ca2+]i) or membrane potential, as measured with the fluorescent indicators quin-2 and bisoxonol respectively. At a stimulatory glucose concentration TPA caused a lowering in [Ca2+]i, whereas membrane potential was unaffected. Despite the decrease in [Ca2+]i, there was a large stimulation of insulin release. Addition of TPA lowered [Ca2+]i also in beta-cells stimulated by tolbutamide or high K+, although to a lesser extent than in those stimulated by glucose. There was no effect of TPA on either Ca2+ buffering or the ability of Ins(1,4,5)P3 to release Ca2+ in permeabilized beta-cells. However, the phorbol ester inhibited the rise in [Ca2+]i in response to carbamoylcholine, which stimulates the formation of InsP3, in intact beta-cells. Down-regulation of PKC influenced neither glucose-induced insulin release nor the increase in [Ca2+]i. Hence, although PKC activation is of no major importance in glucose-stimulated insulin release, this enzyme can serve as a modulator of the glucose-induced insulin-secretory response. Such a modulation involves mechanisms promoting both amplification of the secretory response and lowering of [Ca2+]i.

Animals↗

PubMed1989

Transfection of insulin-producing cells with a transforming c-Ha-ras oncogene stimulates phospholipase C activity.

Pancreatic islet beta-cells and insulin-producing RINm5F cells were electroporated in the presence of the c-Ha-ras oncogene, to assess the possible involvement of the encoded product in coupling extracellular receptors to phospholipase C. After two days the c-Ha-ras-transfected cells increased their expression of c-Ha-ras mRNA. These cells were also found to contain more [3H]InsP3, suggesting an increased basal (non-ligand-activated) phospholipase C activity. In addition, the transfected cells were unable to respond to ligand (bombesin) activation of phospholipase C. The ras-transfected insulin-producing cells showed enhanced phosphorylation of a 200 kDa substrate crossreacting with an antibody to an 80 kDa protein kinase C substrate. The phorbol ester 12-O-tetradecanoyl 13-acetate and bombesin also induced phosphorylation of the 200 kDa substrate. All of these changes occurred without changes in the rates of [3H]thymidine incorporation. The results suggest that the mutated c-Ha-ras oncogene directly or indirectly stimulates the basal phospholipase C activity of these cells.

Animals↗

PubMed1989

Decreased cell replication and polyamine content in insulin-producing cells after exposure to human interleukin 1 beta.

Interleukin 1 (IL-1) has been suggested to cause the islet B cell destruction occurring during the development of insulin-dependent diabetes mellitus. One mechanism by which B cell loss can be compensated for is via de novo formation of new cells through replication. In the present study the replicatory activity of cells in isolated rat pancreatic islets and in the insulin-producing cell line RINm5F has been assessed by [3H]thymidine incorporation methods after exposure to 1-25 U/ml of human recombinant IL-1 beta (rIL-1 beta). In the rat islets [3H]thymidine incorporation was decreased by 20% 5 h after exposure to 25 U/ml rIL-1 beta. A similar inhibition was also observed in islets exposed to 2.5 and 12.5 U/ml rIL-1 beta. In the RINm5F cells there was a dose-dependent inhibition of the cell replication to approximately 50% of the controls in cells exposed to 25 U/ml rIL-1 beta for 48 h. This was also accompanied by an increased cell death, as measured by trypan blue inclusion (controls 13% and rIL-1 beta treated cells 25%). The insulin content of the RINm5F cells was reduced by about 40% after a 48-h exposure to 25 U/ml rIL-1 beta. When the exposure of the RINm5F cells to rIL-1 beta was decreased to 24 h there was no increased cell death, but a reduced replicatory activity was still observed. rIL-1 beta decreased the cellular content of the polyamines spermidine and spermine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Failure of glucose to elicit a normal secretory response in fetal pancreatic beta cells results from glucose insensitivity of the ATP-regulated K+ channels.

Fetal pancreatic beta cells demonstrate a deficient insulin release in response to glucose, but the underlying mechanism at the cellular level is unknown. By using beta cells from 21-day fetal rats we made an attempt to clarify the mechanism(s) behind this reduced glucose response. In addition to measuring insulin release, glucose metabolism, and cellular ATP content, ATP-regulated K+ channels (G channels) and voltage-activated Ca2+ currents were investigated with the patch-clamp technique. It was thus demonstrated that the ATP-regulated K+ channels in fetal beta cells were not sensitive to glucose but otherwise had similar characteristics as those of adult beta cells. Also, the characteristics of the voltage-activated Ca2+ currents were similar in adult and fetal beta cells. However, as judged from measurements of both glucose oxidation and glucose utilization, glucose metabolism was impaired in fetal beta cells. In addition, there was no increase in the ATP content, even when the cells were stimulated for 30 min. It is therefore concluded that the attenuated glucose-induced insulin release in fetal pancreatic beta cells is due to an immature glucose metabolism resulting in impaired regulation of the ATP-sensitive K+ channels. These findings may be relevant to the understanding of the deficient stimulus-secretion coupling associated with non-insulin-dependent diabetes.

Adenosine Triphosphate↗

PubMed1989

Studies on the mechanisms causing inhibition of insulin secretion in rat pancreatic islets exposed to human interleukin-1 beta indicate a perturbation in the mitochondrial function.

This study aimed at a more detailed characterization of the mechanisms by which interleukin 1 (IL-1) inhibits insulin secretion. For this purpose, isolated rat pancreatic islets were kept in tissue culture for 5 days in medium RPMI 1640 plus 10% calf serum. The islets were subsequently transferred to the same culture medium containing various test substances plus 1% human serum with or without 25 U/ml human recombinant IL-1 beta. After a culture period of 48 h the islet structure was examined in the electron microscope and the islet function studied in short term incubations in the absence of IL-1. Islets exposed to IL-1 showed ultrastructural signs of degeneration in 10-20% of the B cells while such changes were not found in other types of islet cells. An increased number of secondary lysosomes and occasional myelin figures were observed in the B cells exposed to IL-1. These ultrastructural alterations were, however, reversed in islets cultured in cytokine-free medium for 6 days after the IL-1 treatment. In islets cultured in the presence of 11.1 mM glucose only, or 11.1 mM glucose plus 10 mM nicotinamide, 61 mM dimethyl area, 2 micrograms/ml indomethacin, 10 microM 4-bromophenacyl bromide or 10 microM nordihydroguaiaretic acid, 10 microM phenantroline, and 0.1 or 1.0 microgram/ml cyclosporin A, IL-1 reduced the insulin release by 64-85%. Culture at 5.6 mM glucose did not modify the IL-1-induced inhibition of insulin release, whereas a significant protective effect was observed at 28 or 56 mM glucose. The DNA content in IL-1-exposed islets cultured at 11.1 mM glucose was decreased by about 20% but not in islets cultured at other glucose concentrations. The D-[5-3H]glucose utilization at 16.7 mM glucose was unaffected by IL-1, whereas the oxidation of D-[6-14C]glucose was reduced by 50%. The present results suggest that IL-1-induced inhibition of insulin secretion is related to a disturbed mitochondrial function. This effect is not counteracted by a poly(ADP-ribose) synthetase inhibitor, a hydroxyl radical scavenger, an iron chelator, a T lymphocyte-specific immunosuppressive drug, or inhibitors of phospholipase A2 or inhibitors of prostaglandin and leukotriene synthesis. Thus, IL-1-induced inhibition of insulin secretion seems not to be mediated by the same mechanisms as those causing alloxan- or streptozotocin-induced damage of B cells. Furthermore, the action of IL-1 does not appear to be mediated via arachidonic acid metabolism. Glucose affords some protection, probably by enhancing the B cell mitochondrial function.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetophenones↗

PubMed1989

Human interleukin 1 beta stimulates islet insulin release by a mechanism not dependent on changes in phospholipase C and protein kinase C activities or Ca2+ handling.

Isolated islets from adult rats or obese hyperglycemic (ob/ob) mice were incubated with human recombinant interleukin 1 beta in order to study whether the acute effects of the cytokine on islet insulin release are associated with changes in islet phospholipase C activity, Ca2+ handling or protein phosphorylation. The cytokine stimulated insulin release both at low and high glucose concentrations during one hour incubations. In short-term incubations (less than 1 min) interleukin 1 beta did not affect the production of inositoltrisphosphate. Addition of interleukin 1 beta affected neither the cytoplasmic free Ca2+ concentration at rest nor that observed subsequent to stimulation with a high concentration of glucose. Furthermore, the endogenous protein kinase C activity, as visualized by immunoprecipitation of a 32P-labelled substrate for this enzyme, was not altered by interleukin 1 beta. Separation of 32P-labelled proteins by means of 2-dimensional gel electrophoresis failed to reveal any specific effects of the cytokine on the total protein phosphorylation activity. These results suggest that the stimulatory effects on insulin release exerted by interleukin 1 beta are not caused by acute activation of phospholipase C and protein kinase C or by an alteration of islet Ca2+ handling of the B-cells.

Animals↗

PubMed1989

Content of adenine nucleotide translocator mRNA in insulin-producing cells of different functional states.

This study was undertaken to characterize the expression of the gene coding for the adenine nucleotide translocator (ANT) in the insulin-producing beta-cell and to study any possible relationship between its expression and the functional state of the beta-cell. Adult and fetal rat pancreatic islets were prepared and cultured under different conditions in vitro. The total RNA from these islets and from the insulin-producing RINm5F cells was isolated and analyzed by the Northern blot technique via a cDNA clone (pAAC-9) coding for the bovine ANT. We found that a 1600-base pair (bp) mRNA hybridizing to the pAAC-9 clone could be detected in RINm5F cells, and a 1450-bp mRNA was similarly observed in the islets. These sizes correspond well to previously reported forms of mRNA for the ANT observed in other tissues. When comparing the intensities of the pAAC-9 hybridizing bands of the different islet groups, it was observed that fetal islets contained less of this mRNA than adult islets. Furthermore, the content of the ANT mRNA in adult islets cultured at a high glucose concentration was increased compared with islets cultured at a low glucose concentration. Finally, streptozocin-treated islets, which display an impaired glucose-sensitive insulin release after 6 days in culture, also contained less of this mRNA than the control islets. We conclude that pancreatic islet cells express an mRNA that appears to be highly homologous to the bovine ANT and that the contents of this mRNA increases with the functional status of the beta-cell. It is furthermore suggested that defects in the expression of this gene may be associated with impaired glucose sensitivity.

Animals↗

PubMed1989

Personal adjustments and regimen compliance 1 year after myocardial infarction.

The relationship of attitudes and perceived beliefs of others to regimen compliance and personal psychologic and social adjustments of patients with myocardial infarction was investigated 1 year after the infarction. Eighty-one patients (39 in the experimental group, 42 in the control group) who participated in a prior study on the effect of a nursing intervention on regimen compliance, completed scales that assessed attitudes toward regimen prescriptions (diet, medications, activity, smoking, and stress response), perceived beliefs of others concerning compliance, personal adjustments, and regimen compliance. At 1 year, no differences were found between experimental and control groups for regimen compliance or personal adjustments. There was a significant decrease in mean scores for all variables from the time the patient was in the hospital to 30 days afterward, but no change at 1 year from the 30- or 60-day visit. At 1 year, attitudes were predictive of compliance for all regimen prescriptions. Perceived beliefs of others were predictive of diet, activity, and medication prescriptions.

Adaptation, Psychological↗

PubMed1988

Polyamines and insulin production in isolated mouse pancreatic islets.

The aim of the present study was to evaluate the role of polyamines in the metabolism and insulin production of pancreatic-islet cells. For this purpose islets were prepared from adult mice and used either immediately or after tissue culture. There was a significant decrease in the islet content of spermidine during culture, although the effect was less pronounced in a high glucose concentration. Furthermore, a stimulatory effect of a high glucose concentration, as compared with low guclose, on the content of spermine was observed. To elucidate further the role of polyamaines in beta-cell physiology, the ornithine decarboxylase inhibitors difuoromethylornithine (DFMO) and methylacetylenic putrescine (MAP) and the S-adenosylmethionine decarboxylase inhibitor ethylglyoxal bis(guanylhydrazone) (EGBG) were added to the culture media. Addition of DFMO together with MAP decreased the cellular contents of putrescine and spermidine, whereas the content of sperimine was unaffected. When EGBG was added in combination with DFMO and MAP, there was a decrease in the content of spermine also. Cell viability in the islets depleted of their polyamine contents was not impaired, as assessed by determinations of oxygen-uptake rates and ATP contents. Depletion of putescine plus spermidine by addition of DFMO+MAP was associated with decreased biosynthesis of (pro)insulin and total protein. When the content of spermine was decreased also by the further addition of EGBG, the decrease in (pro) insulin biosynthesis was more pronounced and was paralleled by a decrease in the insulin-mRNA content. Under these conditions, the glucose-stimulated insulin release, the insulin content and the rates of islet DNA synthesis were also decreased. It is concluded that putrescine and spermidine are necessary for the maintenance of normal insulin and protein biosynthesis, whereas spermine may exert a role in some other cellular processes, such as DNA replication, RNA transcription and glucose-stimulated insulin release.

Adenosine Triphosphate↗

PubMed1988

Stimulation of pancreatic islet beta-cell replication by oncogenes.

Although the growth potential of the pancreatic islet beta cells is limited, glucose, cAMP, and certain polypeptide growth factors have been reported by other workers to exert modest stimulatory effects on beta-cell replication. To further assess means through which beta-cell growth can be stimulated, selected oncogene constructs linked to a rat insulin promoter were introduced by means of electroporation into free islet cells prepared from fetal rats and adult hyperglycemic obese (ob/ob) mice. The uptake and expression of the added oncogenes were sufficiently efficient to exert effects on beta-cell physiology in short-term experiments (less than or equal to 4 days). Stimulation of islet cell [3H]thymidine incorporation was observed after transfection with src alone or the combination of myc and ras. The effect observed in the fetal islet cells with src was more pronounced than any effect previously reported. Transfection with the src oncogene resulted in phosphorylation of lipocortin I and was paralleled by an increased immunofluorescence against src-like immunoreactivity in a majority of the electroporated cells. It is concluded that electroporation can induce sufficiently efficient expression of added oncogene constructs to study their effects on cells that are not readily transformable into continuously growing cell lines. Furthermore, the results suggest that beta-cell replication might be manipulated extrinsically by inserting appropriate growth-promoting genes into these cells.

Animals↗

PubMed1988

Preferential reduction of insulin production in mouse pancreatic islets maintained in culture after streptozotocin exposure.

The ability of the pancreatic beta-cell to repair itself after a cytotoxic injury and reassume its functional activities may be a key issue in affording protection from insulin-dependent diabetes mellitus. The molecular mechanisms behind the functional responses of the beta-cell after cytotoxic damage are still largely unknown. The present study in an attempt to elucidate this issue. Mouse pancreatic islets were isolated with collagenase and, after overnight culture, exposed for 30 min at 37 C to 2.2 mM streptozotocin (SZ) or vehicle alone (controls). The islets were subsequently cultured for 6 days in medium RPMI-1640 plus 10% calf serum. After the culture they were subjected to light microscopical examinations or different functional tests during short term incubations. The SZ-treated islets showed markedly diminished insulin release after stimulation with the beta-cell nutrients glucose and leucine plus glutamine. Compounds known to increase intracellular cAMP [theophylline and (Bu)2-cAMP] were able to partially counteract the SZ-induced reduction of insulin release. Stimulation with arginine could also slightly restore the impaired insulin release. Glucose-stimulated oxygen uptake, proinsulin biosynthesis, and insulin and insulin mRNA contents were also decreased, with values at about 50% of the controls. However, the cellular contents of DNA and RNA and total protein biosynthesis rates were essentially normal. Besides mild degranulation in some islets, the morphological appearance of the SZ-treated islets did not reveal any obvious differences compared to the control islets. The present observations suggest that after a toxic injury there remains a population of partially damaged beta-cells, which are able to maintain most of their basal metabolic functions, but fail to maintain adequate insulin biosynthesis and release.

Animals↗

PubMed1988

Use of liposomes to introduce substances into pancreatic islet cells.

The liposome technique is widely used to transport substances that cannot normally traverse the plasma membrane into the cell. The interactions of liposomes with the plasma membrane of pancreatic islet cells have not previously been studied. We evaluate the suitability of the liposome technique for introducing substances into the pancreatic beta-cell to which the cell membrane is impermeable. Liposomes were synthesized with an ether-injection method, and the cell-liposomal interactions were investigated by means of radioactive labeling and the fluorescent aqueous space marker 6-carboxyfluorescein. Experiments were performed on freshly isolated mouse pancreatic islets and on free islet cell preparations. With fluorescence microscopy, liposomes were observed to fuse spontaneously with islet cells, and the corresponding internalized volumes were quantified with spectrofluorometric measurements. The liposome association with islets and islet cell suspensions, as assessed by radioactive labeling, was found to increase with the liposome concentration. The effects of liposome membrane lipid composition on the fusion rate were found to be decreased in the presence of glucolipid. In addition, polyethylene glycol failed to affect the liposomal uptake. Freshly isolated islets incubated with liposomes containing glucose 6-phosphate were observed to release slightly more insulin than islets incubated with "empty" liposomes. In conclusion, liposomes fuse spontaneously with islet cells in vitro, and the uptake of liposomes is regulated by the lipid composition of the liposomal bilayer and the amount of liposomes present. The function of the beta-cell can be altered with the liposome technique, e.g., by addition of biologically active molecules such as glucose 6-phosphate.

Animals↗

PubMed1988

Insulin production and glucose metabolism in isolated pancreatic islets of rats with NIDDM.

Rats with non-insulin-dependent diabetes mellitus (NIDDM) induced by neonatal injection of streptozocin are known to have a deficient insulin response to glucose. To evaluate to what extent this glucose insensitivity can be attributed to a perturbation of the islet glucose metabolism, we estimated the rates of glucose phosphorylation, glucose utilization, oxygen consumption, and glucose oxidation in islets isolated from normal and NIDDM rats and compared these values with rates of islet insulin biosynthesis and release in vitro. The data confirm that islets from rats with NIDDM display a deficient response to glucose of both insulin biosynthesis and release that is still present after an overnight culture of the islets at 5.5 mM glucose. Furthermore, they show that islets of these rats have 1) normal low- and high-Km glucose-phosphorylating activities and no major alteration of the glucose utilization rate, 2) decreased insulin release in response to glyceraldehyde, 3) decreased rates of basal respiration and glucose oxidation and a markedly reduced stimulation by glucose of both islet oxygen consumption and glucose oxidation, and 4) decreased glucose-stimulated net 45Ca uptake. We conclude that the relative unresponsiveness to glucose of islets from NIDDM rats is associated with, and perhaps due to, a deficient islet glucose metabolism. This defect is not due to gross alterations in the glycolytic pathway but probably reflects alteration in the islet mitochondria function.

Animals↗

PubMed1987

Mechanisms of leucine- and theophylline-stimulated insulin biosynthesis in isolated rat pancreatic islets.

To extend previous observations on the mechanisms of translational regulation of insulin biosynthesis [Welsh, Scherberg, Gilmore & Steiner (1986) Biochem. J. 235, 459-467], we have now compared the intracellular distributions of insulin mRNA after stimulation of insulin biosynthesis by glucose, leucine or theophylline. In comparison with low glucose (3.3 mM) only, the presence of 10 mM-leucine + 3.3 mM-glucose resulted in the transfer of insulin mRNA from the pool of the uninitiated mRNA to the free polysome/monosome fraction and an increase in the amount of insulin mRNA associated with the microsomal fraction. Islets exposed to 5 mM-theophylline + 3.3 mM-glucose also showed a decreased content of uninitiated insulin mRNA in the cytosol, but these islets showed no increase in insulin mRNA in the microsomal fraction. These results suggest that leucine, a nutrient stimulant of insulin biosynthesis, acts essentially by the same mechanisms as those of glucose, whereas theophylline acts only to stimulate initiation rates.

Animals↗

PubMed1986

Regulation of RNA metabolism in relation to insulin production and oxidative metabolism in mouse pancreatic islets in vitro.

This study was undertaken to investigate the long-term effects of different substrates, in particular glucose, on the regulation of islet RNA metabolism and the relationship of this regulation to the metabolism and insulin production of the islet B-cell. For this purpose collagenase-isolated mouse islets were used either in the fresh state or after culture for 2 or 5 days in RPMI 1640 plus 10% calf serum supplemented with various test compounds. Islets cultured with 16.7 mM glucose contained more RNA than those cultured with 3.3 mM glucose. Culture of islets in glucose at low concentrations inhibited glucose-stimulated RNA synthesis and this inhibitory effect was reversed by prolonged exposure to high glucose concentrations. Culture with 10 mM leucine and 3.3 mM glucose or with 10 mM 2-ketoisocaproate and 3.3 mM glucose increased the total RNA content of islets as compared to that of islets cultured with 3.3 mM glucose alone. Islets cultured with 5 mM theophylline maintained a high RNA content in the presence of 3.3 mM glucose. Theophylline also increased the islet RNA content when added together with 16.7 mM glucose, as compared to 16.7 mM glucose alone. Theophylline probably exerted this effect by decreasing the rate of RNA degradation. Changes in islet RNA metabolism showed a close correlation to changes in islet total protein biosynthesis, whereas islet (pro)insulin biosynthesis and insulin release exhibited different glucose-dependency patterns. The response of islet oxygen uptake to glucose was similar to that of islet RNA and protein biosynthesis. It is concluded that the RNA content of the pancreatic islets is controlled at the levels of both synthesis and degradation. Glucose stimulates the RNA synthesis and inhibits its degradation. Moreover, the results suggest that regulation of RNA synthesis may be mediated through islet metabolic fluxes and the cAMP system.

Animals↗

PubMed1985

Mechanisms of pancreatic B-cell degeneration during the course of insulin-dependent diabetes mellitus.

This paper presents a review of different mechanisms possibly responsible for the degeneration of the pancreatic B-cell in insulin-dependent diabetes mellitus. The genetic dependence probably located in the HLA DR-locus of the sixth chromosome and its role in an autoimmune reaction against antigenically altered pancreatic B-cells is discussed. The actions of alloxan and streptozotocin in the induction of experimental diabetes, as models for postulated human B-cytotoxins, are described.

Alloxan↗

PubMed1984

Effects of atracurium on intraocular pressure.

The effects of atracurium on intraocular pressure (IOP) were compared with those of pancuronium in 20 patients less than 45 years-of-age requiring surgery for trauma of one eye. After a standard premedication and the application of topical analgesia to the upper airway, anaesthesia was induced with thiopentone i.v. and the trachea was intubated without the use of neuromuscular blockade. Following 20 min of steady state anaesthesia during which measurements of IOP, arterial pressure, heart rate, FIO2, FE'CO2 and CVP were recorded, one group of patients received atracurium 0.45 mg kg-1 and the other pancuronium 0.1 mg kg-1. The observations were repeated for a further 15 min before surgery commenced. Neither atracurium nor pancuronium produced any change in IOP. Atracurium was associated with greater cardiovascular stability than pancuronium.

Adolescent↗

PubMed1982

Anaesthesia and intra-ocular pressure: a comparative of total intravenous anaesthesia using etomidate with conventional inhalation anaesthesia.

Intra-ocular pressure (IOP) was measured in two comparable groups of anaesthetised patients under standardised conditions. Group 1 received etomidate 0.3 mg/kg fentanyl 100 micrograms and droperidol 5 mg. with etomidate 20 microgram/kg/minute for maintenance. Group 2 received thiopentone 3.5 mg/kg and were maintained with halothane 0.5% in nitrous oxide (60%) with oxygen. Both groups of patients were ventilated to normocapnia. Blood pressure, heart rate, central venous pressure and IOP were measured in 5 minute intervals from pre-induction to 30 minutes postinduction. A significantly greater reduction in mean IOP (p less than 0.05) occurred in group 1. A maximum fall in IOP of 61% was obtained, compared to a maximum fall of 45% in group 2. Blood pressure fell in both groups. The fall was greater (23%) in group 2 than in group 1 (18%) and in no case was considered excessive. Total intravenous anaesthesia using etomidate is suggested as a useful technique for open eye surgery.

Adult↗