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A Nistri

Publications and source records attributed to A Nistri.

At least 55 records · Page 3Linked to original sources
PubMed1997

Effects of the neuropeptide thyrotropin-releasing hormone on GABAergic synaptic transmission of CA1 neurons of the rat hippocampal slice during hypoxia.

Because thyrotropin-releasing hormone (TRH) has been suggested to improve recovery of brain neurons from hypoxia, which strongly impairs GABAergic synaptic transmission, the present electrophysiological study used intracellular recording from CA1 neurons of the rat hippocampal slice to examine the cellular mechanisms underlying this phenomenon. Hypoxia induced by superfusion with a medium devoid of oxygen evoked typical membrane hyperpolarization, fall in input resistance, and strong depression of monosynaptic, GABAA receptor-mediated fast inhibitory postsynaptic potentials (IPSPs). The depression of fast IPSPs during hypoxia was found to be due to a combination of factors such as shift in the IPSP reversal potential and membrane hyperpolarization. GABAB receptor-mediated slow IPSPs were comparatively less sensitive to hypoxia. TRH (10 microM), applied 1 min prior to hypoxia, selectively accelerated recovery of membrane potential and delayed return of fast IPSPs to control amplitude without changing the mechanisms responsible for depression of GABAergic transmission. In conclusion, despite a slower recovery of IPSPs, TRH facilitated earlier return of neuronal excitability after the hypoxic period.

Animals↗
PubMed1997

Role of intracellular calcium in fast and slow desensitization of P2-receptors in PC12 cells.

1. Combined whole-cell patch clamp recording and confocal laser scanning microscopy of [Ca2+]i transients were performed on single PC12 cells to study any correlation between membrane currents induced by ATP and elevation in [Ca2+]i. ATP was applied by pressure from micropipettes near the recorded PC12 cells continuously superfused at a fast rate. 2. Brief (20 ms) pulses of ATP elicited monophasic inward currents and [Ca2+]i increases. Long applications (2 s) of ATP (5 mM) evoked peak currents which rapidly faded during the pulse and were followed by a large rebound current, interpreted as due to rapid desensitization and recovery of P2-receptors. The associated [Ca2+]i increase grew monotonically to a peak reached only after the occurrence of the current rebound, indicating that it is unlikely this cation has a role in fast desensitization. 3. Both membrane currents and [Ca2+]i transients were linearly dependent on holding membrane potential, suggesting that Ca2+ influx is the predominant cause of [Ca2+]i elevation. This view was supported by experiments carried out in Ca(2+)-free solution. 4. Brief pulses of ATP applied after a desensitizing pulse (2 s) of the same elicited smaller inward currents and [Ca2+]i rises indicating a role for [Ca2+]i in controlling slow desensitization of P2-receptors. 5. This notion was confirmed in experiments with various [Ca2+]i chelators which differentially affected slow desensitization in relation to their buffering capacity, while sparing fast receptor desensitization. 6. These results suggest a role for [Ca2+]i in slow rather than fast desensitization of P2-receptors, thus proposing this divalent cation as an intracellular factor able to provide an efficient and reversible control over receptor activity induced by ATP.

Adenosine Triphosphate↗
PubMed1997

The effect of the neuropeptide substance P on desensitization of ATP receptors of PC12 cells.

1. Patch clamp recording (whole cell configuration) was employed to investigate the modulatory action of substance P on inward currents elicited by adenosine 5'-triphosphate (ATP, focally applied via a pressure pipette) from phaechromocytoma (PC12) cells usually held at -70 mV. 2. Bath-applied substance P (0.2-20 microM) had no effect on baseline membrane current but reversibly reduced ATP peak currents in a concentration-dependent fashion. The depressant effect was not associated with a change in the ATP current reversal potential. 3. Equiamplitude peak responses induced by 50 microM or 5 mM ATP were differentially affected by substance P which preferentially reduced currents evoked by 5 mM ATP. In the presence of substance P a conditioning pulse of ATP evoked a stronger depression to subsequent test pulses of the same agonist. 4. Combined patch clamping and confocal laser imaging of intracellular Ca2+ ([Ca2+]i) of single PC12 cells showed that substance P (applied by a pressure pipette) per se had no effect on [Ca2+]i or current baseline, although it reduced the inward current and associated [Ca2+]i rise elicited by ATP. 5. These results are interpreted as due to facilitation by substance P of desensitization of ATP-gated P2x2 receptors of PC12 cells. It is proposed that the novel modulation by this peptide of ATP responses may serve as a model for further studies aimed at elucidating the action of substance P on purinergic neurotransmission.

Adenosine Triphosphate↗
PubMed1997

Imaging of intracellular calcium during desensitization of nicotinic acetylcholine receptors of rat chromaffin cells.

1. The possible role of intracellular Ca2+ levels ([Ca2+]i) in desensitization of nicotinic acetylcholine receptors (AChRs) was investigated in rat cultured chromaffin cells by use of combined whole-cell patch clamping and confocal laser scanning microscopy with the fluorescent dye fluo-3. 2. On cells held at -70 mV, pressure-application of nicotine elicited inward currents with associated [Ca2+]i rises mainly due to influx through nicotinic AChRs. These responses were blocked by (+)-tubocurarine (10 microM) but were insensitive to alpha-bungarotoxin (1 microM) or Cd2+ (0.1 mM). 3. Pressure applications of 1 mM nicotine for 2 s (conditioning pulse) evoked inward currents which faded biexponentially to a steady state level due to receptor desensitization and were accompanied by a sustained increase in [Ca2+]i. Inward currents evoked by subsequent application of brief test pulses of nicotine were depressed but recovered with a time course reciprocal to the decay of the [Ca2+]i transient induced by the conditioning pulse. 4. Omission of intracellular Ca2+ chelators or use of high extracellular Ca2+ solution (10 mM) lengthened recovery of nicotinic AChRs from desensitization while adding BAPTA or EGTA intracellularly had the opposite effect. When the patch pipette contained fluo-3 or no chelators, after establishing whole cell conditions the rate of recovery became progressively longer presumably due to dialysis of endogenous Ca2+ buffers. None of these manipulations of external or internal Ca2+ had any effect on onset or steady state level of desensitization. 5. High spatial resolution imaging of [Ca2+]i in intact cells (in the presence of 0.1 mM Cd2+) showed that its level in the immediate submembrane area decayed at the same rate as in the rest of the cell, indicating that Ca2+ was in a strategic location to modulate (directly or indirectly) AChR desensitization. 6. The present data suggest that desensitized nicotinic AChRs are stabilized in their conformation by raised [Ca2+]i and that this phenomenon retards their recovery to full activity.

Animals↗
PubMed1997

Pharmacological block of the electrogenic sodium pump disrupts rhythmic bursting induced by strychnine and bicuculline in the neonatal rat spinal cord.

The cellular mechanisms underlying rhythmic bursts induced in the isolated neonatal rat spinal cord by bath application of strychnine and bicuculline (which block glycine- and gamma-aminobutyric acid-A-receptor-mediated inhibition, respectively) were probed with pharmacological tools. Such spontaneous bursts were recorded either intracellularly from lumbar motoneurons or extracellularly from ventral roots. As previously described, these network-driven events consisted of large-amplitude depolarizations arising abruptly from baseline with a highly regular period (on average 28 s). Burst episodes (lasting on average 7 s) comprised several oscillations and appeared synchronously on flexor and extensor motoneuron pools of both sides of the spinal cord. Their diffuse location made convenient to use bath-applied substances in the attempt to selectively block distinct membrane processes operating through the network. Application of apamin (0.4 microM) shortened both cycle period and burst duration without changing their regular rhythmicity. Similar results were obtained with carbachol (10 microM). Cs+ (4 mM) reversibly hyperpolarized the motoneuron membrane potential and largely increased burst duration, which was characterized by a long series of repetitive oscillatory waves. Cycle period and rhythmicity remained unaltered. Ouabain (10 microM), strophanthidin (4 microM), or K(+)-free solutions disrupted rhythmic bursting, which was fragmented into irregularly occurring paroxysmal activity mixed with short depolarizing events, still developing simultaneously on both sides of the spinal cord. Bursting activity eventually ceased after approximately 30-40 min of application of ouabain or strophanthidin. Prolonged washout of strophanthidin or K(+)-free solutions reestablished regular bursting patterns, whereas no recovery from ouabain was observed. At the time of strong depression of bursting, it was still possible to evoke bursts by single electrical pulses applied to the segmental dorsal root. Antidromic spikes of motoneurons could still be evoked by ventral root stimulation. These results demonstrate that, in a spinal bursting network mainly made up by excitatory processes, blockers of slow Ca(2+)-dependent K+ currents, such as apamin or carbachol, or of the slow inward rectifier, such as Cs+, did not suppress rhythmicity, suggesting that these conductances simply contributed to control cycle period and/or burst duration. Conversely, pharmacological blockers of the electrogenic Na+ pump such as ouabain, strophanthidin, or K(+)-free solutions severely disrupted all characteristics of rhythmic bursting. It is proposed that the operation of the electrogenic Na+ pump of premotoneurons was a crucial element for rhythmic bursting.

Animals↗
PubMed1997

Afferent inputs modulate the activity of a rhythmic burst generator in the rat disinhibited spinal cord in vitro.

Application of strychnine and bicuculline to the isolated spinal cord of the neonatal rat induces spontaneous bursting of regular rhythmicity (cycle period approximately 30 s). This phenomenon is important because it shows that a spinal network, made up by excitatory connections only, generates a very reliable rhythmic pattern. To find out how signals from the periphery or higher centres might influence the operation of the rhythmogenic network, the present experiments examined whether synaptic inputs from dorsal root (DR) or ventrolateral (VL) afferent fibers could modulate this spontaneous rhythmicity. This issue was addressed with intracellular recording from motoneurons or extracellular recording from ventral roots after eliciting bursting with strychnine plus bicuculline. Single electrical shocks (0.1 ms; intensity 1-4 times threshold) applied to one DR reset spontaneous bursting without altering its period or duration. Repetitive stimulations at periods ranging from 20 to 2 s entrained bursts on a 1:1 basis. Burst duration was shorter at lower stimulation periods whereas burst amplitude was unchanged. The lowest stimulation period compatible with burst entrainment depended on stimulus strength. At stimulation periods <2-s entrainment was always lost and spontaneous bursts unexpectedly returned even if electrical pulses still elicited ventral root reflexes. Such spontaneous bursts had similar properties as those recorded in the absence of electrical pulses. Analogous results were obtained with VL stimulations. It is concluded that the spinal rhythmogenic network was highly susceptible to external synaptic inputs, which paced burst generation whereas burst duration was adapted to interstimulus interval. A scheme is provided to explain the modulatory role of synaptic inputs as well as the escape of bursting from fast stimulus entrainment in terms of a rhythmogenic network functionally separated from reflex pathways activated by DR or VL tracts.

Afferent Pathways↗
PubMed1996

NMDA receptor-independent mechanisms responsible for the rate of rise of cumulative depolarization evoked by trains of dorsal root stimuli on rat spinal motoneurones.

The mechanisms responsible for the rate of rise (RR) of cumulative depolarization induced by dorsal root stimulus trains were investigated with intracellular recordings from motoneurones of the rat isolated spinal cord. The NMDA receptor antagonists CPP or APV depressed the cumulative depolarization but not its RR which could still be fast enough to elicit action potential wind-up. RR size was correlated with a slow synaptic potential (detected in CPP or APV solution) with which it shared similar voltage dependence. The NK1 antagonist SR 140333 depressed cumulative depolarization, RR and slow synaptic potentials. It appears that the RR (and the ability to express wind-up) was determined by summation of slow synaptic potentials partly mediated via activation of NK1 receptors.

2-Amino-5-phosphonovalerate↗
PubMed1996

Localization of rhythmogenic networks responsible for spontaneous bursts induced by strychnine and bicuculline in the rat isolated spinal cord.

Spontaneous rhythmic bursting induced by coapplication of strychnine (1 microM) and bicuculline (20 microM) was observed with electrophysiological recording from pairs of lumbar ventral roots (usually L5) in an isolated preparation of the neonatal rat spinal cord. Bursting was insensitive to exogenously applied GABA or glycine, confirming that it was attributable to block of glycine and GABAA receptor-mediated inhibition. NMDA accelerated bursting in a dose-dependent manner. Complete coronal spinal transection at L3 or L6 level did not block bursting recorded from L5 or L2 roots, respectively. Gradual cutting of the cord along the midline through a sagittal plane preserved bursting activity in both disconnected sides but led to loss of synchronicity. Once the spinal cord was fully separated into left and right halves, regular bursting persisted on each side with no phase-coupling between the two preparations. Section along a frontal plane to remove dorsal horns and much of the central canal area did not affect burst frequency or left-to-right synchronicity, whereas it reduced burst duration. A quadrant preparation containing mainly a single ventral horn displayed enhanced burst frequency while bursts became very short events. Bath application of 5-hydroxytryptamine (30 microM) or NMDA (5 microM) increased burst frequency and decreased burst duration in all types of preparation except the isolated quadrants, in which brief bursts were accelerated but not shortened by these chemical agents. These results suggest that bursting induced by strychnine and bicuculline apparently relied on distinct mechanisms for burst triggering and intraburst structure. The first required a relatively smaller neuronal network that was confined to a ventral quadrant. Intraburst structure was dependent on a larger circuitry comprising either both ventral horns or one side of the spinal cord including more than two segments.

Animals↗
PubMed1996

ALS IgGs suppress [Ca2+]i rise through P/Q-type calcium channels in central neurones in culture.

Confocal laser scanning microscopy (with the fluorescent calcium dye fluo-3) was used to test the effect of IgG obtained from patients with amyotrophic lateral sclerosis (ALS) on the KCl-induced [Ca2+] rise in rat hippocampal neurones in culture. In the presence of tetrodotoxin and ionotropic glutamate receptor antagonists, ALS IgGs depressed (by 30-40%) Ca2+ transients evoked by influx of Ca2+ through voltage-activated channels; such an effect did not occur with IgG obtained from healthy donors. The depressant action of ALS IgG was selectively prevented by the inhibitor of P/Q-type Ca2+ channels, omega-agatoxin IVA (which alone reduced Ca2+ transients by 40%). The reduced Ca2+ transients might impair Ca(2+)-dependent glutamate receptor desensitization and thus facilitate excitotoxic damage.

Amyotrophic Lateral Sclerosis↗
PubMed1996

Changes in intracellular calcium induced by NMDA in cultured rat hippocampal neurons require exogenous glycine.

Confocal laser scanning microscopy was used to study changes in intracellular free calcium concentration ([Ca2+]i) at the level of the soma of cultured hippocampal neurones following pressure application of glutamate or N-methyl-D-aspartate (NMDA). [Ca2+]i was imaged in the presence of tetrodotoxin after loading cells with the fluorescent dye indicator fluo-3/AM. Responses to glutamate were potently antagonized by 6-cyano-7 nitroquinoxaline-2,3-dione (CNQX: 20 microM). They were also strongly and reversibly depressed by 3-((+/-)-2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP; 20 microM), leaving a small CNQX-sensitive component. Responses to NMDA were also blocked by CNQX. In the presence of saturating concentrations of glycine (100 microM), the depression of glutamate or NMDA responses by CNQX was greatly reduced. Exogenously applied glycine also potentiated the NMDA response. These data indicate that the glycine binding site of the NMDA receptor channel is not saturated in cultured hippocampal neurones and thus is susceptible to the action of agonists or antagonists.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1996

Voltage-activated fast currents of frog optic tectum neurones are blocked by ouabain or K(+)-free solution.

Frog optic tectum neurones in vitro (under whole cell patch clamp with a Cs(+)-filled electrode) generated, in response to voltage steps negative to -80 mV from -60 mV holding potential, transient inward currents dependent on extracellular Na+ and blocked by tetrodotoxin (TTX). Depolarizing steps from the same holding potential induced conventional, fast Na+ currents followed by a transient outward cationic current (Icat). Voltage-activated Na+ currents (induced by negative or positive steps) and Icat were blocked by ouabain or K(+)-free solution with comparable timecourse. It is suggested that transient inward and outward currents of frog tectal neurones were at least partly dependent on the rapid operation of a membrane cation transporter.

Animals↗
PubMed1996

A transient outward cationic current activated by Na+ influx into frog visual neurones in vitro.

Whole cell patch clamp recording from neurones of a slice preparation of the frog optic tectum showed that depolarizing step commands from -70 mV holding potential generated a fast inward current always followed by a fast outward current. The fast outward current was blocked by tetrodotoxin (TTX) or 4-aminopyridine (4-AP), or by replacing external Na+ with Li+. When the patch pipette contained Cs+ instead of K+ the outward current was fully preserved, suggesting that the membrane channels responsible for this response were relatively non-selective in their permeability properties. This current (termed Icat) is a novel example of a non-specific cationic current dependent on influx of Na+ and presumably important to control the firing characteristics of these cells.

Animals↗
PubMed1996

The neuropeptide thyrotropin-releasing hormone modulates GABAergic synaptic transmission on pyramidal neurones of the rat hippocampal slice.

The modulatory action of thyrotropin-releasing hormone (TRH), an endogenously occurring neuropeptide, on synaptic potentials mediated by activation of GABAA or GABAB receptors was studied using intracellular recordings from CA1 pyramidal neurones of the rat hippocampal brain slice preparation. Bath-applied TRH (10 microM) produced a reversible depression of fast IPSPs (mediated by GABAA receptors) induced by electrical stimulation of the stratum lacunosum moleculare (LM) or stratum pyramidale (SP). This phenomenon was not associated with changes in the IPSP reversal potential, resting potential, or input resistance. GABAB receptor-mediated slow IPSPs elicited by SP stimulation were found insensitive to TRH whereas those induced by LM stimulation were attenuated by the peptide. AMPA receptor-mediated EPSPs and postsynaptic responses to isoguvacine or baclofen were unchanged by TRH. These data suggest that the action of TRH on GABAergic transmission was probably exerted at presynaptic level within the local circuitry comprising CA1 neurones. Such an effect of TRH represents an interesting example of transient downregulation of inhibitory processes by a physiological neuropeptide and is expected to augment excitability of pyramidal cells.

Animals↗
PubMed1996

Effects of thyrotropin-releasing hormone on GABAergic synaptic transmission of the rat hippocampus.

The effect of thyrotropin-releasing hormone (TRH), a neuropeptide physiologically present in the mammalian hippocampus, on spontaneous, miniature and evoked GABAergic postsynaptic currents was investigated using whole-cell patch-clamp recording from pyramidal cells and interneurons of the rat hippocampal thin slice preparation. Bath application of 10 microM TRH induced an increase in the frequency of spontaneous postsynaptic currents from 1.07 +/- 0.68 to 3.16 +/- 0.73 Hz in pyramidal neurons and interneurons of the stratum lacunosum-moleculare (SL-M). In tetrodotoxin solution TRH did not change miniature postsynaptic currents. Application of TRH to minislices containing only the CA1 region still produced an increase in the spontaneous postsynaptic current frequency, indicative of an action by TRH upon a GABAergic circuitry. Paired recordings from one pyramidal cell and one stratum lacunosum moleculare interneuron displayed synchronous events whose frequency rose after TRH application, suggestive of a common, TRH-sensitive input. In a small subset of cells TRH induced the appearance of highly rhythmic large postsynaptic currents at a frequency of approximately 2 Hz, as confirmed by autocorrelation analysis. Postsynaptic currents electrically evoked by focal stimulation of stratum lacunosum-moleculare were depressed from 90 +/- 27 to 44 +/- 15 pA after application of TRH. This phenomenon was solely due to an increase in the number of synaptic failures. It is proposed that the effect of TRH on the GABAergic system was primarily exerted on a subset of interneurons controlling the activity of pyramidal cells as well as stratum lacunosum-moleuclare interneurons.

Animals↗
PubMed1996

Fading and rebound of currents induced by ATP in PC12 cells.

1. Patch clamp recording (whole cell configuration) was used to study the action of ATP on rat phaeochromocytoma (PC12) cells usually held at -70 mV and rapidly superfused with buffered saline. ATP (0.5, 1 or 5 mM), applied from micropipettes by pressure application with brief (< or = 50 ms) pulses, induced inward currents with rapid onset and decay. ADP and alpha, beta-methylene ATP were ineffective. 2. ATP (5 mM) applied with pulses > 200 ms long elicited a complex current response characterized by a rapid peak which faded and was followed by a strong current rebound (lasting several s) as soon as the application was terminated. This type of response was readily replicated as long as ATP applications were spaced at 2-3 min intervals. The amplitude of peak and rebound currents was dependent on the length of pressure pulse and was similarly depressed by bath application of a threshold dose (25 microM) of ATP. Rapid fading and rebound of ATP-induced membrane currents were also observed when the Y-tube method was used for applying this agonist. 3. The reversal potential for peak and rebound currents was the same while the time constant values for peak fading and rebound onset were insensitive to changes in membrane potential between -70 and -40 mV. When ATP was applied to a cell clamped at depolarized potential, no current was observed but rapid return of the membrane potential to -70 mV immediately at the end of ATP application was associated with a large rebound current. 4. Brief (20 ms) application of ATP during the onset of the rebound current strongly and transiently suppressed it. The same application performed during the gradual decay of the rebound wave elicited a transient inward current which was much smaller and shorter than the one observed when the cell was in its resting state. Application of 2 s ATP pulses at 20 s intervals equally reduced the initial peak and rebound currents which recovered at the same rate. 5. The present data are interpreted according to a scheme which suggests two types of ATP receptor desensitization. The first one (D1) would be characterized by fast kinetics and low agonist affinity; rapid recovery from D1 would then be manifested as current rebound presumably due to receptor reactivation. The second desensitized state (D2) has slow kinetics and high affinity for the agonist: it is therefore typically seen with sustained application of a low dose of ATP. It is proposed that desensitization and its recovery can influence the time course of membrane responses mediated by purinoceptors.

Adenosine Triphosphate↗
PubMed1996

Spontaneous rhythmic bursts induced by pharmacological block of inhibition in lumbar motoneurons of the neonatal rat spinal cord.

1. The effects of blocking gamma-aminobutyric acid- and glycine-mediated synaptic transmission by bicuculline and strychnine on the neonatal rat isolated spinal cord were investigated by intracellular recording from motoneurons with the use of current-clamp and voltage-clamp techniques and by extracellular recording from homologous ventral roots of the L5 segment. 2. Bicuculline per se evoked irregular bursts of motoneuron membrane potential, often comprising individual events fused together. Strychnine alone did not elicit spontaneous bursting in the large majority of preparations. Simultaneous application of bicuculline and strychnine consistently induced regular rhythmic bursts (frequency approximately 2 per min, duration approximately 7 s), comprising a rapid depolarization followed by large-amplitude oscillations. 3. Burst frequency, duration, and intraburst oscillation time course were independent of motoneuron membrane potential. Burst and oscillation amplitude decreased with membrane depolarization and, under voltage-clamp conditions, inverted polarity near 0 mV. 4. The regular bursts produced by bicuculline and strychnine were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione, tetrodotoxin, or Cd2+. 5. N-methyl-D-aspartate antagonists [R-5-aminophosphonovalerate or 3-((RS)-2-carboxypiperazine-4-yl)-propyl-1-phosphonate (CPP)] reversibly blocked or slowed down bursting induced by bicuculline and strychnine. Addition of cyclothiazide to the bicuculline and strychnine solution increased bursting frequency while preserving the regular burst structure; under these conditions bursts became insensitive to CPP. 6. In the presence of bicuculline and strychnine, 5-hydroxytryptamine (5-HT) increased burst frequency and decreased burst duration in a dose-dependent fashion. 7. In the presence of bicuculline and strychnine, L5 ventral roots developed synchronous rhythmic activity with a time course similar to that recorded from individual motoneurons. The rhythmic activity was accelerated by 5-HT on both roots, in accordance with observations on single motoneurons. 8. Rhythmic bursts thus appear to result from large, synchronous synaptic events generated by a network modulated by 5-HT and highly sensitive to variations in efficacy of glutamatergic synaptic transmission. These results show that in the rat spinal cord highly patterned motor output can occur despite block of inhibition.

Animals↗
PubMed1996

Effect of taurohyodeoxycholic acid on biliary lipid secretion in man: preliminary report.

Taurohyodeoxycholic acid and tauroursodeoxycholic acid were infused intraduodenally at a rate of 0.8 g/h for three hours in 3 cholecystectomized T-tube patients. Biliary lipid secretion and bile acid composition were evaluated before and after replacement of the endogenous bile acid pool with the two bile acids. As compared to basal values (2.78 +/- 1.67 mM/l), taurohyodeoxycholic acid induced a greater increase in the biliary concentration of phospholipids (4.12 +/- 1.23 mM/l) as compared to tauroursodeoxycholic acid (3.14 +/- 0.98 mM/l). Biliary cholesterol concentration after taurohyodeoxycholic acid (1.89 +/- 0.63 mM/l) was unchanged as compared to the pretreatment period (1.98 +/- 0.58 mM/l), while it decreased significantly after tauroursodeoxycholic acid (0.85 +/- 0.08 mM/I). Biliary cholesterol secreted per unit of bile acid was greater during taurohyodeoxycholic acid than during tauroursodeoxycholic acid, while the opposite was observed for the secretion of phospholipids.

Bile↗