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Biomedical subjects

L Quintin

Publications and source records attributed to L Quintin.

At least 37 records · Page 2Linked to original sources
PubMed1994

Relationship between oxygen uptake and mixed venous oxygen saturation in the immediate postoperative period.

BACKGROUND: During muscular exercise, a negative correlation has been demonstrated between the value of mixed venous oxygen saturation (SvO2) and the level of muscular work, expressed at each level as the ratio of oxygen uptake (VO2) to each subject's maximal oxygen uptake (VO2max). Because the immediate postoperative period is associated with an increase in whole body oxygen demand, and in this regard resembles the effects of muscular exercise, a similar correlation may exist during this period. METHODS: VO2max was determined in 11 patients 3-5 days before coronary artery bypass surgery. During the first 2 postoperative h, VO2 and SvO2 were monitored. VO2 was measured by indirect calorimetry and SvO2 by a fiberoptic pulmonary arterial catheter. RESULTS: The highest postoperative value of VO2 was most often associated with visible shivering and ranged among patients from 19% to 53% of preoperatively measured VO2max. There was a highly significant negative correlation between SvO2 and the ratio VO2/VO2max. This correlation was observed when data were examined collectively (136 simultaneous determinations of the two variables) and at the individual level (10-18 determinations for each patient). The slopes and the y intercepts of individual lines of correlation were within a narrow range. CONCLUSIONS: During the first 2 postoperative h after coronary artery bypass surgery, VO2 rarely exceeds 50% of preoperative VO2max. Assuming a stable state of myocardial function, SvO2 measurement may provide an indirect means of assessment of the "exercise test" imposed on patients recovering from general anesthesia.

Aged↗
PubMed1994

Systemic acidosis after controlled hypotension activates catechol activity in the vasomotor center.

Activation of the catechol metabolism, assessed with in vivo voltammetry, in the vasopressor area of the vasomotor center was investigated during systemic acidosis occurring after controlled hypotension. Rats anesthetized with halothane were mechanically ventilated. Sodium nitroprusside lowered mean arterial pressure to 55 mmHg for > or = 20 min. Arterial blood gases allowed us to group rats according to whether they showed symptoms of metabolic acidosis (pH < or = 7.34) immediately after controlled hypotension. To assess the effect of systemic acidosis independently of the progressive decline in pressure observed during the recovery period after controlled hypotension, we used phenylephrine infusion to maintain mean arterial pressure at baseline pressure during the recovery period after controlled hypotension in two groups of animals. Systemic acidosis increased the catechol signal in a prolonged manner [nitroprusside with acidosis (n = 7) vs. nitroprusside without acidosis (n = 5); P < 0.0001]. This catechol activation was greater when pressure was restored after hypotension [nitroprusside with acidosis plus phenylephrine (n = 5) vs. nitroprusside with acidosis over the whole interval (from -30 to +150 min); P < 0.05]. When the nitroprusside with acidosis group and nitroprusside with acidosis plus phenylephrine group were compared, hypercapnia had an involvement in the larger increase of the catechol signal observed in the nitroprusside with acidosis plus phenylephrine group [arterial PCO2: nitroprusside with acidosis vs. nitroprusside with acidosis plus phenylephrine over the whole interval (from -30 to +150 min) and at +30 and +60 min; all P < 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1993

Activation of brain noradrenergic neurons during recovery from halothane anesthesia. Persistence of phasic activation after clonidine.

BACKGROUND: alpha 2-Adrenoceptor agonists, known as antihypertensive agents, may be used during general anesthesia for their anesthetic sparing action and to reduce the occurrence of side effects. Previous studies have shown that the brain's noradrenergic nucleus, locus coeruleus, is an important target in mediating the hypnotic action of alpha 2 agonists. The authors studied the effects of recovery from halothane anesthesia on the electrical activity of locus coeruleus neurons to examine cellular substrates underlying the clinical effectiveness of alpha 2 agonists. METHODS: Experiments were performed in locally anesthetized rats, whose circulatory and acid-base stabilities were ensured by mechanical ventilation and volume infusion. Locus coeruleus neurons were recorded continuously while the rats were anesthetized with halothane (1%) and/or after the halothane was discontinued. RESULTS: Under the influence of halothane, locus coeruleus cells exhibited a slow, regular spontaneous discharge (1.95 +/- 0.23 Hz), and contralateral foot or tail pinch elicited a prominent, phasic activation in locus coeruleus neurons. Such phasic activation was blocked by local ejection of kynurenic acid, an excitatory amino acid antagonist, close to recorded neurons, but not by clonidine (up to 64 micrograms.kg-1). Thirty minutes after the halothane was discontinued, the mean firing rate of locus coeruleus neurons was increased by 87 +/- 20%. This excitation resulted from a prominent increase in bursting activity (21 +/- 5% of spikes in bursts vs. 4 +/- 1%) and was reversed by halothane readministration. This activation also was reduced by local ejection of kynurenic acid. Halothane discontinuance revealed the reactivity of locus coeruleus neurons to nonnoxious, sensory stimuli, and considerably reduced the apparent potency of intravenous administration of clonidine to inhibit locus coeruleus activity (effective dose for 50% of maximal effect (ED50), 25.48 +/- 8.26 micrograms.kg-1 vs. 4.81 +/- 0.80 micrograms.kg-1 under halothane). This decrease was caused by the persistence of bursting activity after the administration of clonidine, which was completely suppressed by readministration of halothane or local application of kynurenic acid. CONCLUSION: The data demonstrate: (1) that halothane withdrawal increases locus coeruleus neuronal activity via excitatory amino acid input, and this withdrawal-induced activity is characterized by a prominent burst (phasic) discharge; (2) that sedative doses of clonidine inhibit the tonic component of locus coeruleus activity but not the phasic activation of locus coeruleus neurons; and (3) that readministration of halothane or local ejection of an excitatory amino acid antagonist fully suppresses the bursting activity unaffected by clonidine.

Anesthesia Recovery Period↗
PubMed1993

Spontaneous baroreflex by sequence and power spectral methods in humans.

Beat-by-beat variations in blood pressure and RR-interval are interrelated by the actions of baroreflex and non-baroreflex responses. This study had two purposes: (1) to examine the spontaneous relationships between RR-interval and systolic blood pressure to determine the relative occurrence of baroreflex and non-baroreflex responses in humans, and (2) to compare the beat-sequence method with a cross spectral estimate of the baroreflex response slope. Eight healthy men were studied during 10 h of quiet, seated rest, and six men and three women were studied during rest, rest plus fixed pace breathing, and a cold pressor test. RR-interval and continuous, non-invasive arterial blood pressure were measured with a computerized system. A baroreflex sequence was defined by a series of at least three consecutive heart beats in which systolic pressure and the following RR-interval either both increased or both decreased. A non-baroreflex relationship was defined by sequences of at least three beats by opposite directional changes of RR-interval and systolic pressure of that beat. The results showed that there were approximately 30% as many non-baroreflex compared to baroreflex slopes. Individual subject mean baroreflex and non-baroreflex slopes were highly correlated (r = 0.72, P < 0.001). Absolute slope values were not different, and they were unaffected by time, fixed pace breathing, or cold pressor test. The data showed the relatively simple beat-by-beat sequence method to yield spontaneous baroreflex response slopes that were quantitatively similar to, and highly correlated with (r = 0.85-0.94), baroreflex response slopes calculated by spectral analysis methods.

Adult↗
PubMed1993

Baroreceptor reflex-linked changes in catechol metabolism in the rat rostral ventrolateral medulla.

1. Using in vivo voltammetry, this study relates catecholamine metabolism within the rat rostral ventrolateral medulla to the level of mean arterial pressure (MAP) under halothane anaesthesia. 2. A vasopressor region was circumscribed with electrical stimulations in an area located 1000-1700 microns rostral to the obex. A catechol signal was then ascertained within this area. The recording site was surrounded with phenyl-N-methyl-ethanolamine transferase immuno-positive cell bodies. 3. Three levels of decrease of arterial pressure were induced with nitroprusside infusion: -15, -35 and -55 mmHg (n = 5 in each group) from baseline for 30 min. This led to increases in the catechol signal which were inversely related to the degree of hypotension (P < 10(-4) vs. saline for the 35 and 55 mmHg groups, P < 0.05 for the 35 mmHg group as compared to the 15 and 55 mmHg groups following recovery from hypotension). 4. Following sino-aortic deafferentation, nitroprusside-induced hypotension (-35 mmHg) did not lead to any change in the catechol signal in the rostral ventrolateral medulla (n = 5). Furthermore, controlled hypotension induced in intact rats did not evoke any change in the catechol signal recorded in a dopaminergic area of the midbrain, the ventral tegmental area (A10 area; n = 5). 5. An infusion of phenylephrine increased MAP by 35 mmHg from a baseline pressure of 105 mmHg for 30 min and evoked a non-significant decrease in the catechol signal (n = 5). In another group of rats a lower baseline pressure (80 mmHg) was stabilized (n = 5) with a higher concentration of halothane. An identical increment in pressure was then produced by a phenylephrine infusion and led to a significant reduction in the catechol signal (P < 0.05 vs. saline under similar conditions; n = 5). 6. The new findings of this study are that the level of activity of the metabolism of catecholamine in the rostral ventrolateral medulla (i) is continuously related to the level of arterial pressure, (ii) functions close to its resting level under baseline conditions and is primarily engaged during hypotension and (iii) is baroreflex linked. 7. Given the lack of direct evidence for a link between unit activity and catechol metabolism, these changes in catechol activity, recorded continuously in vivo next to adrenergic cell bodies, may represent the biochemical-specific counterpart of changes in the level of electrical unitary activity of presumed adrenergic cardiovascular medullospinal sympathoexcitatory neurons. Therefore, it provides evidence that adrenaline-synthesizing neurons in the rostral ventrolateral medulla respond to baroreceptor inputs.

Animals↗
PubMed1991

Effect of clonidine on catechol metabolism in the rostral ventrolateral medulla: an in vivo electrochemical study.

The dose-dependent reduction in catechol metabolism induced by an imidazoline with alpha 2-adrenoceptor agonist specificity, clonidine, was assessed (ED50 = 7 micrograms.kg-1 i.v.) with in vivo voltammetry in the rostral ventrolateral medulla of rats kept under halothane anesthesia and strictly controlled circulatory and ventilatory conditions. This reduction in catechol metabolism was observed in intact as well as in barodeafferented rats.

Animals↗
PubMed1991

A method to maintain normal respiratory and metabolic state in artificially respired rats.

Analysis of arterial blood gases (ABG) in awake, paralyzed, locally anesthetized, and artificially respired rats revealed the development with time of severe hypoxemia associated with metabolic acidosis despite adequate ventilation as assessed by normal PaCO2. These respiratory and metabolic disturbances may underlie the progressive deterioration experienced with this preparation frequently used in neuropharmacological experiments. We report here that the intravascular infusion of bicarbonated artificial plasma, associated with continuous positive pressure ventilation, prevents the deterioration of the respiratory and metabolic state in this preparation, which can be maintained within the range of that of the freely moving animal. This stabilized preparation may thus be highly suitable for neuropharmacological experiments extending for several hours.

Anesthesia↗
PubMed1991

Effect of clonidine on the circulation and vasoactive hormones after aortic surgery.

After completion of abdominal aortic graft, 29 patients received an i.v. infusion of placebo (n = 16) or clonidine 7 micrograms kg-1 (n = 13) over 120 min in a double-blind study. Cardiovascular variables were measured and plasma samples obtained up to 5 h after arrival in the recovery room, for assay of noradrenaline, adrenaline, vasopressin and renin concentrations. Noradrenaline, adrenaline and vasopressin concentrations decreased in the clonidine group throughout recovery (P less than 0.001, 0.05 and 0.05, respectively, vs placebo). Heart rate was less in the clonidine group (P less than 0.01). There was no significant difference in mean arterial pressure between groups. Stroke volume was larger (P less than 0.01) and there were fewer episodes of hypertension (P less than 0.05) and tachycardia in the clonidine group. In addition, a reduction in the number of circulatory interventions (P less than 0.05) and episodes of shivering was noted in the clonidine group. Mean (SD) postoperative volume requirements were larger in the clonidine group (total postoperative input: clonidine 1462 (604) ml; placebo 1064 (348) ml (P less than 0.05]. These data are consistent with the observation that clonidine modifies endocrine and circulatory status after major surgery.

Aorta, Abdominal↗
PubMed1991

Oxygen uptake after major abdominal surgery: effect of clonidine.

To examine the effect of an alpha-2 agonist, clonidine, on oxygen uptake and on the incidence of postoperative shivering, 28 patients presenting for major abdominal surgery were randomly assigned in a double-blind manner to one of two groups. Intraoperatively, 14 patients received 5 micrograms.kg-1 clonidine infused over 3 h (clonidine group), and 14 patients received placebo (placebo group). Oxygen uptake was measured continuously over the first 3 postoperative hours with a mass spectrometer system. Circulatory variables, esophageal temperature, and skin temperature were measured over the first 6 postoperative hours. Heart rate, mean arterial pressure, rate pressure product, and norepinephrine concentration were decreased in the clonidine group (P less than 2 x 10(-4)). There were no differences among groups in the incidence of shivering and in the rate of increase of esophageal temperature. By contrast, oxygen uptake was lower in the clonidine group (P = 4 x 10(-4)). This contrasting pattern may be secondary to a reduction in the intensity of mean muscular tremor in the clonidine group.

Adjuvants, Anesthesia↗
PubMed1990

Changes in catecholamine metabolism in the rostral ventrolateral medulla following halothane and nitroprusside-induced hypotension: an in vivo electrochemical study.

The objective was to observe changes in rostral ventrolateral medulla (RVLM) catecholamine metabolism using in vivo voltammetry following induced hypotension with halothane or nitroprusside (SNP). Rats anesthetized (halothane, metocurine) and ventilated were stereotaxically implanted with carbon microelectrodes in the RVLM. The catechol oxidation current (CA.OC, % baseline) was used as an index of RVLM catecholaminergic metabolism. Groups of rats (n = 5) were given (A) halothane 0.75% for 60 min; (B) halothane 2.75% plus phenylephrine infusion to maintain mean arterial pressure (MAP) for 30 min, then halothane 0.75% for 30 min; (C) halothane (2.5-3.0%) for 30 min (MAP 60 +/- 5 mmHg) then halothane 0.75% for 30 min; (D) halothane 0.75% and sodium nitroprusside (SNP) for 30 min (MAP 60 +/- 5 mmHg), then halothane 0.75% for 30 min. Halothane 0.75% produced no significant change in CA.OC or MAP (A), while halothane 2.5-3.0% produced a significant decrease in MAP and a symmetrical significant increase in CA.OC (ANOVA, P less than 0.5). This increase peaked at 30 min (180 +/- 28%) and reached 110 +/- 9% baseline at 60 min. The halothane and phenylephrine combination produced no significant change in CA.OC or MAP during the 30 min exposure (B). SNP (D) produced a significant increase in CA.OC (peak 48 min, 224 +/- 35%) which remained elevated at 60 min (198 +/- 32%). Thus, the induced hypotension produced activation of RVLM catecholaminergic neurons. SNP induced a prolonged significant increase in RVLM catecholamine metabolism which may relate to rebound hypertension following use of this drug.

Animals↗
PubMed1990

Pharmacological and functional evidence for extracellular 3,4-dihydroxyphenylacetic acid as an index of metabolic activity of the adrenergic neurons: an in vivo voltammetry study in the rat rostral ventrolateral medulla.

Catecholamine metabolism was studied in vivo in the C1 adrenergic area of the rostral ventrolateral medulla oblongata in rats, using differential normal pulse voltammetry coupled with an activated carbon fiber microelectrode. Pharmacological evidence indicates that 3,4-dihydroxyphenylacetic acid, the major dopamine metabolite, is responsible for the electrochemical signal appearance in the C1 group, and that it reflects the catecholamine synthesis rate, as previously reported in the locus coeruleus. Indeed, 3,4-dihydroxyphenylacetic acid was estimated to be formed from 77% of the intracellular dopamine, since its synthesis was increased by only 23%, after blockade of the dopamine-beta-hydroxylase activity. Neuronal activation by retrograde electrical stimulation increased the electrochemical signal, as well as hemorrhage and hypotension, suggesting that the level of extracellular 3,4-dihydroxyphenylacetic acid is a good biochemical index of the C1 adrenergic cellular activity in baseline conditions and during cellular activation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Aortic surgery: effect of clonidine on intraoperative catecholaminergic and circulatory stability.

Twenty-eight patients presenting for aortic surgery were randomly assigned in a double-blind, placebo-controlled protocol to receive placebo (n = 14) or clonidine (4.7 +/- 1.2 micrograms.kg-1 po; n = 14), in addition to flunitrazepam 120 min before induction of anesthesia. Plasma catecholamines (CA) and hemodynamic variables were determined at 7 stages during surgery. In the placebo group, plasma epinephrine (E) and norepinephrine (NE) had risen twofold at skin closure compared to baseline (E: from 109 +/- 51 pg.ml-1 to 294 +/- 161 pg.ml-1; NE: from 658 +/- 226 to 1150 +/- 494 pg.ml-1). Plasma CA were significantly lower in the clonidine group (P less than 0.001 and 0.01 vs placebo for NE and E respectively). In both groups, similar directional changes were observed for the circulatory variables, upon aortic clamping and declamping. In the clonidine group, however, mean arterial pressure was lower at most stages (P less than 0.05 vs placebo); moreover, stroke volume index was greater in the clonidine group (P less than 0.05) upon declamping. This improved stability in the clonidine group was achieved with a halving in the number of anesthetic/circulatory interventions (P less than 0.05 vs placebo). Provided intravascular volume is adequate, clonidine suppresses the increase in plasma catecholamines induced by aortic surgery and improves circulatory stability, with a reduced number of anesthetic, circulatory adjustments.

Adult↗
PubMed1990

Head injury: clonidine decreases plasma catecholamines.

Seven patients who had suffered head injury 3 to 5 days before the study was undertaken received clonidine (2.5 micrograms/kg iv over 10 min). This resulted in a reduction of plasma norepinephrine (p less than .05) and in normalization of plasma epinephrine (p less than .05). Neither common carotid blood flow nor diastolic blood flow as index of global cerebral perfusion as measured by pulsed Doppler changed. The reduction of sympathetic overactivity, probably due to the specific action of clonidine on alpha 2-adrenoceptors within the rostral ventrolateral medulla, may be of interest in the management of head injury because of the maintenance of cephalic hemodynamics.

Acute Disease↗
PubMed1989

Fentanyl increases catecholamine oxidation current measured by in vivo voltammetry in the rat striatum.

A proposed mechanism for fentanyl-induced muscular rigidity is the effect of opioids on dopaminergic transmission in the striatum. The objective of this study was to observe the effect of fentanyl on the rat striatal catechol oxidation current (CA.OC) which reflects extracellular DOPAC (3-4,dihydroxyphenylacetic acid) concentration (a major metabolite of dopamine), as measured by in vivo voltammetry. Male Sprague-Dawley rats, anaesthetized with halothane, were stereotaxically implanted with carbon fibre electrodes in the striatum and after an initial stabilization period of an hour were given a control saline IV injection followed 30 min later by fentanyl 10 micrograms.kg-1 IV over 10 min and at 70 min by the monoamine oxidase inhibitor pargyline 70 mg.kg-1 IP. Fentanyl produced a significant (P less than 0.05 Anova) increase in CA.OC in all animals. This reached a plateau 15 min following the administration of fentanyl and was at a maximum of 148 +/- 10.2 per cent of control 35 min after the administration of fentanyl. Pargyline produced a rapid decline in CA.OC peak height which went from 143 +/- 11.6 to 39 +/- 6.8 per cent of control over 30 min. There were no significant differences between the pH, PaO2 and PaCO2 during the saline and fentanyl injection periods and there was no significant variation of blood pressure throughout the experiment. This study shows that under stable physiological conditions, fentanyl produces a significant increase in CA.OC in the rat striatum.

Animals↗