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Biomedical subjects

G Koski

Publications and source records attributed to G Koski.

31 records · Page 2Linked to original sources
PubMed1990

Fentanyl and sufentanil anesthesia revisited: how much is enough?

This study was undertaken to determine if fentanyl and sufentanil could produce dose-related suppression of hemodynamic and hormonal responses to surgical stimulation. Eighty patients scheduled for elective CABG were studied in two consecutive protocols: protocol I was a randomized double-blind study of 40 patients who received a single dose of fentanyl (50 or 100 micrograms/kg) or sufentanil (10, 20, or 30 micrograms/kg). Hemodynamic measurements and hormonal concentrations (renin, aldosterone, cortisol, and catecholamines) were determined before and after induction and after intubation and sternotomy. Protocol II was an open randomized study of 40 patients who received sufentanil in one of four doses: 30 micrograms/kg as a single dose, 10 micrograms/kg plus infusion 0.05 microgram.kg-1.min-1, 20 micrograms/kg plus infusion 0.1 microgram.kg-1.min-1, or 40 micrograms/kg plus infusion 0.2 microgram.kg-1.min-1. Hemodynamic measurements and plasma sufentanil and catecholamine concentrations were determined before and after induction and after intubation, sternotomy, and aortic cannulation. Both protocols defined a hemodynamic response as a 15% or more increase in systolic blood pressure (SBP) from control and a hormonal response 50% or more increase over control. During protocol I, 18 patients had a hemodynamic response (average increase in SBP 22.6 +/- 2%) and 35 patients had a total of 59 hormonal responses. During protocol II, 24 patients had a hemodynamic response (average increase in SBP - 31 +/- 3%) and there were 15 catecholamine responses. There were no differences between dose groups in either protocol. It was concluded that in these dose ranges, suppression of hemodynamic or hormonal stress responses is not related to opioid dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1989

Acute reduction of extracellular sodium differentially affects receptor-mediated and K+-induced calcium uptake in PC12 pheochromocytoma cells.

Using a rapid-quench method to measure 45Ca2+ uptake into PC12 cells in suspension, we have studied basal, carbachol-stimulated and K+-induced Ca2+ uptake under control conditions [( Na+]o = 130 mM) and in the presence of acutely lowered extracellular sodium concentration [( Na+]o = 65 mM). Acute reduction of [Na+]o stimulates basal and K+-evoked Ca2+ uptake, but reduces net carbachol-stimulated uptake. Since total Ca2+ uptake measured in the presence of carbachol under control and low [Na+]o conditions is unchanged, the reduction in carbachol-stimulated uptake is due to the increase in basal uptake induced by low [Na+]o. These results reconcile apparently conflicting data regarding a specific Na+ requirement for nicotinic acetylcholine receptor-mediated responses in PC12 cells and adrenal chromaffin cells and suggest a mechanism for loss of nicotinic acetylcholine receptor (nAChR) responsiveness to agonists under low Na+ conditions.

Animals↗
PubMed1988

Effect of hypothermic hemodilutional cardiopulmonary bypass on plasma sufentanil and catecholamine concentrations in humans.

The effect of hypothermic hemodilutional cardiopulmonary bypass (CPB) on plasma sufentanil and catecholamine concentrations was studied in four groups of ten patients each, receiving four different doses of sufentanil. Samples for measurement of sufentanil were obtained before CPB, at 15, 30, and 45 minutes of CPB, during rewarming, immediately after and 15, 60, and 240 minutes after CPB. In addition, in groups III and IV, which received the highest dose of sufentanil, blood samples were also obtained for measurement of plasma levels of epinephrine and norepinephrine. Sufentanil concentration decreased in all groups with the start of CPB (group I, 2.92 +/- 0.2 to 2.04 +/- 0.2; group II, 3.30 +/- 0.3 to 1.51 +/- 0.2; group III, 7.08 +/- 0.7 to 3.45 +/- 0.3; group IV, 10.33 +/- 0.5 to 4.59 +/- 0.5 ng/ml). No further decreases occurred during CPB but increases occurred with rewarming. The first measurement after CPB approached the concentration before CPB (group I, 2.82 +/- 0.3; group II, 2.56 +/- 0.5; group III, 4.42 +/- 0.4; group IV, 6.10 +/- 0.4 ng/ml). Norepinephrine concentrations demonstrated a wide variability with no significant changes. Epinephrine levels increased significantly during rewarming in both groups (group III, 141 +/- 23 to 279 +/- 79 pg/ml; P less than 0.05; group IV, 105 +/- 24 to 267 +/- 68 pg/ml, P less than 0.05). The stability of plasma sufentanil concentrations during CPB suggest that no measurable metabolism or excretion occurred. The increase with rewarming and after CPB suggest significant sequestration.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1982

Modulation of sodium-sensitive GTPase by partial opiate agonists. An explanation for the dual requirement for Na+ and GTP in inhibitory regulation of adenylate cyclase.

Opiates and opioid peptides inhibit adenylate cyclase and stimulate specific low Km GTPase activity in membranes from neuroblastoma x glioma NG108-15 hybrid cells. The effects of opiate agonists on both enzymes are mediated by high affinity stereospecific receptors and require Mg2+, GTP, and Na+. In the presence of Mg2+, Na+ inhibits basal GTPase activity; opiates stimulate GTP hydrolysis by antagonizing the Na+-induced inhibition. Activation of GTPase leads, in turn, to inactivation of GTP-stimulated adenylate cyclase activity. The intrinsic activities (or efficacies) of a series of opiates are identical for stimulation of GTPase and inhibition of adenylate cyclase. These results provide a mechanism for the dual requirement for Na+ and GTP in the inhibitory coupling of opiate receptors to the adenylate cyclase system in these cells and may be of general significance to the action of other inhibitory hormones.

Adenylyl Cyclase Inhibitors↗
PubMed1981

Guanine nucleotides inhibit binding of agonists and antagonists to soluble opiate receptors.

The guanine nucleotides GDP, GTP, and guanosine-5'-(beta, gamma-imido)triphosphate inhibit binding of opiates and opioid peptides to receptors solubilized from membranes of neuroblastoma X glioma NG108-15 hybrid cells. The inhibition reflects decreased affinity of receptors for opioid ligands. Whereas in membranes, only opioid agonist binding is sensitive to guanine nucleotide inhibition, both agonist and antagonist binding is reduced in the case of soluble receptors. Furthermore, soluble receptors are more sensitive to the effects of guanine nucleotides than are membrane-bound receptors. These observations are consistent with the suggestion that solubilized receptors may be complexes of an opiate binding protein and a guanine nucleotide-sensitive regulatory component.

Animals↗
PubMed1981

Opiates inhibit adenylate cyclase by stimulating GTP hydrolysis.

Specific, GTP hydrolysis catalyzed by membranes prepared from neuroblastoma--glioma (NG108-15) hybrid cells can be measured in the presence of adenosine-5'-[beta, gamma-imido] triphosphate (p[NH]ppA), ATP, and a nucleotide triphosphate-regenerating system. Opiates and opioid peptides stimulate low Km GTP hydrolysis when measured in the presence of Na+ and Mg2+. Opiate stimulation is rapid, stereospecific, and reserved by the antagonist naloxone. Potencies of opiates as stimulators of GTP hydrolysis and as inhibitors of adenylate cyclase are closely correlated. Agents that stimulate adenylate cyclase, including prostaglandin E1, 2-Cl-adenosine, secretin, and NaF, have little or no effect upon the rate of GTP hydrolysis. Opiates have no effect upon either adenylate cyclase or GTPase activity in membranes prepared from C6-BU1 glioma cells, which lack opiate receptors. In view of the pivotal role of GTP in the activation of adenylate cyclase, we conclude that receptor-mediated stimulation of GTP hydrolysis is the mechanism by which opiates and other inhibitory hormones lower adenylate cyclase activity in NG108-15 cell membranes.

Adenylyl Cyclase Inhibitors↗
PubMed1980

Solubilization of active opiate receptors.

Receptors that reversibly bind opiates and opioid peptides have been solubilized from brain and neuroblastoma-glioma hybrid cell NG108-15 membranes. Active receptors are specifically solubilized with a new type of detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, which is a zwitterionic derivative of cholic acid. The solubilized receptor complexes behave as large molecules with a Stokes radius of 70 A and contain protein as an essential constituent.

Animals↗
PubMed1975

Extraction of sleep-promoting factor S from cerebrospinal fluid and from brains of sleep-deprived animals.

Sleep-promoting factor (factor S) was extracted, partially purified, and concentrated from cerebrospinal fluid and from acid-acetone extracts of brain stem anc cortex of sleep-deprived goats and sheep. 2. Solutes greater than 500 daltons were largely removed by serial ultrafiltrations through molecular sieves (Amicon membranes UM10 and UM05); solutes less than 350 daltons were largely eliminated by gel filtration through Sephadex G10 columns. Sleep-promoting activity was found in a fraction eluted prior to [14C] sucrose marker. 3. Concentrated fraction were infused intraventricularly in rats (0.1 ml in 30 min just prior to 12-h dark cycle) and in rabbits (0.3 ml in 90 min in morning). Sleep-promoting activity was assayed by decrease in nocturnal locomotor activity of rats and by duration and amplitude of slow-wave cortical EEG in rabbits.

Animals↗
PubMed1971

Factors in cerebrospinal fluid from goats that affect sleep and activity in rats.

1. Intraventricular infusion in the rat of 0.1 ml. cerebrospinal fluid (c.s.f.) from sleep-deprived goats increases the duration of sleep (measured by e.e.g.) and decreases locomotor activity (measured photo-electrically) for at least 6 hr subsequent to the infusion. Subarachnoid infusions are ineffective.2. C.s.f. from control and sleep-deprived goats was fractionated by ultrafiltration through molecular sieves. The sleep-promoting Factor S is found in the low molecular weight fraction (mol. wt. < 500) of c.s.f. from sleep-deprived but not from control goats.3. The concentration of Factor S in c.s.f. increases progressively during the first 48 hr of sleep deprivation.4. The sleep promoting effects of Factor S cannot be duplicated by serotonin, 4-OH-butyrate, butyrolactone, GABA (gamma-amino butyric acid), glutamic acid or 3',5'-cyclic AMP when these substances are added to control fluids in concentrations up to 10 times greater than those found in normal c.s.f.5. Intraventricular or subarchnoid infusion in the rat of 0.1 ml. proteinfree c.s.f. containing molecules in the mol. wt. range of 500-10,000 at 10-30 x normal concentration causes hyperactivity which persists for several days and nights following the infusion. The excitatory material, probably a peptide, is present in c.s.f. from both control and sleep-deprived goats.6. The properties of Factor S suggest that it may play a role in the normal regulation of sleep and wakefulness.

Aminobutyrates↗