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Biomedical subjects

N Clavier

Publications and source records attributed to N Clavier.

13 recordsLinked to original sources
PubMed2000

[Analysis of indications fo interhospital transfer].

In France there are no clear guidelines for the transfer of severely head-injured patients, due to the difficulties of combining the requirements of a safe transfer with the necessity of a rapid, adapted and specialized management. These various aspects are discussed in order to facilitate the definition of local strategies for the initial orientation of severely head-injured patients to a centre adapted for severe head trauma management.

Craniocerebral Trauma↗
PubMed1999

[Protective effect of hypothermia in cerebral ischemia].

The use of hypothermia to protect the brain from ischaemic insults is an old concept. During the last decades, studies have mainly shown a modulating effect of hypothermia on biochemical cerebral responses to ischaemia, in addition to the basic effect of energy savings. Thus, the beneficial effects of decreased brain temperature, even when limited during transient ischaemic insults, whether global or focal, complete or incomplete, have been established. The deeper the hypothermia, the longer the ischaemia can be prolonged with acceptable neurological outcome. Conversely, the effects of postischaemic hypothermia remain unclear, while extracerebral deleterious effects cannot be overlooked, and many parameters remain to be evaluated before undertaking a beneficial clinical trial. The only indication for therapeutic postischaemic hypothermia in the near future could be in the control of impending intracranial hypertension occurring after cerebral ischaemia.

Animals↗
PubMed1999

No evidence for cerebral hypoperfusion during cerebral malaria.

OBJECTIVE: Among the mechanisms suggested for altered consciousness during cerebral malaria is the hypothesis of cerebral ischemia, which remains controversial, with little supportive O2 conflicting hemodynamic data. The purpose of this study was to test the hypothesis that cerebral ischemia is a main mechanism for altered consciousness during cerebral malaria. SETTING: University hospital pediatric ward in a region with endemic cerebral malaria. DESIGN: Prospective evaluation of cerebral hemodynamics and cerebral oxygenation during cerebral malaria compared with severe malaria anemia without altered consciousness. PATIENTS: During a 2-wk period, we evaluated all patients who were admitted for cerebral malaria (n = 5). Age-matched patients admitted for severe malaria anemia without altered consciousness (n = 3) and outpatients (n = 3) were investigated for comparison. INTERVENTIONS: All patients received the usual treatment according to their needs, which was determined by the physician in charge. Repeated neurologic evaluations were performed during the early management period in patients with cerebral malaria. METHODS AND MAIN RESULTS: We repeatedly measured cerebral blood flow velocity (transcranial Doppler) and simultaneous systemic determinants of cerebral blood flow (arterial pressure, arterial oxygen saturation, PaCO2, rectal temperature, and hemoglobin concentration). The adequacy of cerebral blood flow to oxygen demands during cerebral malaria was assessed by continuous recording of jugular bulb venous oxygen saturation (using a fiberoptic device). Marked cerebral vasodilation was observed during cerebral malaria (systolic velocity, 1.45 +/- 0.09 m/s; diastolic velocity, 0.75 +/- 0.08 m/s; n = 4) and during severe malaria anemia (systolic velocity, 1.18 +/- 0.14 m/s; diastolic velocity, 0.55 +/- 0.05 m/s; n = 3) compared with control children (systolic velocity, 0.84 +/- 0.13 m/s; diastolic velocity, 0.35 +/- 0.06 m/s; n = 3; p < .05). During cerebral malaria, jugular bulb venous oxygen saturation remained stable, including during neurologic recovery, with initial values of 67.5 +/- 4.3%. CONCLUSIONS: Because jugular bulb venous oxygen saturation remained within the normal range, cerebral hyperemia seems to be an adaptive response to altered systemic determinants, which argues against a hemodynamic mechanism for altered consciousness during cerebral malaria.

Anemia↗
PubMed1998

[Monitoring and maintenance of blood volume in intracranial surgery].

Intraoperative monitoring usually does not assess intravascular blood volume of the patient. The variations of the systolic blood pressure and the right auricular pressure allow to appreciate the intravascular blood volume changes and their consequences on the cerebral perfusion pressure. However, when the autoregulation of the cerebral blood flow is strongly depressed, the evaluation of the cerebral perfusion pressure alone is inadequate. In this case, the optimal monitoring should be metabolic (jugular bulb venous oxygen saturation) to finally assess the cerebral flow-metabolic coupling.

Anesthesia, General↗
PubMed1997

[Monitoring head trauma].

Cerebral monitoring after head trauma aims at reducing secondary lesions resulting mainly from additional cerebral ischemia-hypoxia. Such monitoring must include repetitive (preferably continuous) estimation of cerebral blood flow, cerebral oxygenation and their variations. Based on this information the evaluation and modulation of the main determinants of cerebral blood flow (cerebral metabolism, cerebral perfusion pressure, arterial oxygen content and PaCO2 variations) often allows optimization of cerebral blood flow and metabolism balance. This therapeutic strategy may lead to improvement of severe head trauma outcome through reduction of additional cerebral ischemia-hypoxia.

Brain↗
PubMed1997

Continuous jugular bulb venous oxygen saturation validation and variations during intracranial aneurysm surgery.

PURPOSE: During intracranial aneurysm surgery, numerous factors may alter cerebral blood flow and oxygen supply-demand balance. Continuous monitoring of jugular bulb venous oxygen saturation (SvjO2) may help in the anesthetic management of such procedures. MATERIALS AND METHODS: Fiberoptic SvjO2 was continuously monitored in seven patients during intracranial aneurysm surgery. Fiberoptic SvjO2 measurement was compared with IL3 CO-OXIMETER determination from 85 paired samples. The occurrence of large SvjO2 variations (SvjO2 variation reaching 10% or more of stable preceding value) during aneurysm surgery was recorded and classified according to the association or not with systemic clinical or therapeutic changes. RESULTS: Fiberoptic SvjO2 showed a limited accuracy, with limits of agreement with IL3 CO-OXIMETER at -16.8% and +10.7% and a small bias (-3.1%). SvjO2 variations were frequent during aneurysm surgery, ranging from 3 to 22 per patient during procedures lasting 6 hours (range 4.5 to 7). Half of these variations occurred in the absence of any systemic clinical or therapeutic change, most often leading to an increased SvjO2. CONCLUSIONS: Although the accuracy of fiberoptic SvjO2 determination is limited, it allows the detection of cerebral blood flow and oxygen supply-demand imbalance during aneurysm surgery. The frequent occurrence of SvjO2 elevations is suggestive of reactive hyperemia mechanisms.

Adult↗
PubMed1995

Time-dependent inhibition of oxotremorine-induced cerebral hyperemia by N omega-nitro-L-arginine in cats.

BACKGROUND AND PURPOSE: Oxotremorine (OXO) is a cholinergic agonist that increases cerebral blood flow (CBF) when administered intravenously. We tested the hypothesis that OXO causes a dose-related increase in CBF in cats via a muscarinic mechanism that involves stimulation of nitric oxide synthase. METHODS: Halothane-anesthetized male cats were studied under controlled ventilation. In three groups we measured cerebral blood flow (CBF; microspheres) during 30 minutes of intravenous OXO infusion at doses of 0.5 (n = 3), 5 (n = 6), or 50 micrograms.kg-1.min-1 (n = 6). The role of muscarinic receptor activation in the CBF response to OXO (50 micrograms.kg-1.min-1) was assessed by determining the effect of atropine sulfate (2 mg.kg-1, n = 6) pretreatment in a separate group of cats. The role of nitric oxide synthase was assessed by determining the CBF response to OXO (50 micrograms.kg-1.min-1) either 30 (n = 6) or 60 minutes (n = 5) after administration of 50 mg/kg N omega-nitro-L-arginine (LNA). RESULTS: CBF to forebrain (pre-OXO, 144 +/- 12 mL.min-1.100 g-1) was unchanged with OXO 0.5 or 5 micrograms.kg-1.min-1 but increased at 10 (209 +/- 26 mL.min-1 x 100 g-1) and 30 minutes (243 +/- 35 mL.min-1 x 100 g-1) of OXO infusion at 50 micrograms.kg-1.min-1 (P < .05). Atropine sulfate prevented OXO-induced hyperemia at 10 minutes of infusion but not at 30 minutes of infusion (135 +/- 12% of pre-OXO). LNA decreased baseline CBF by approximately 50%. Treatment with LNA 30 minutes before OXO did not affect the extent of OXO-induced hyperemia (CBF, 142 +/- 15% of pre-OXO at 10 minutes and 153 +/- 18% of pre-OXO at 30 minutes of OXO infusion). Treatment with LNA 60 minutes before OXO ablated OXO-induced hyperemia. CONCLUSIONS: In halothane-anesthetized cats, OXO (50 micrograms.kg-1.min-1) increases forebrain CBF by a muscarinic mechanism that involves stimulation of nitric oxide synthase. The ability of nitric oxide synthase inhibitors to block agonist-induced nitric oxide-mediated vasodilation (response to OXO) is time dependent and may not be predicted by ability of the inhibitor to significantly decrease basal CBF.

Animals↗
PubMed1995

Cerebral blood flow during inhibition of brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats.

BACKGROUND AND PURPOSE: Because tonic production of nitric oxide (NO) is important in regulating cerebrovascular tone and NO may be important in the mechanism of brain injury from focal ischemia, we speculated that stroke predisposition in spontaneously hypertensive stroke-prone rats (SHR-SP) may be related to impaired tonic production of NO. This study was designed to test the hypothesis that the cerebral blood flow (CBF) response to inhibition of NO synthase in SHR-SP would be different than that observed in normal Wistar-Kyoto (WKY) rats and non-stroke-prone spontaneously hypertensive rats (SHR). METHODS: Pentobarbital-anesthetized, mechanically ventilated rats were tested for CBF response to saline, 5 or 20 mg/kg IV of NG-monomethyl-L-arginine (L-NMMA), or 20 mg/kg IV of N omega-nitro-L-arginine (L-NA). In addition, specificity for an NO-dependent mechanism was assessed by determining the ability to reverse any alteration in CBF with L-arginine. Hemorrhage was used to minimize any increase in mean arterial blood pressure (MABP) from NO synthase inhibition. In a separate cohort of rats, differential sensitivity of NO synthase for inhibition by nitro-arginine analogues was determined. RESULTS: Baseline MABP was greater in SHR-SP (185 +/- 3, n = 38) and SHR (169 +/- 3, n = 38) compared with WKY rats (101 +/- 2 mm Hg, n = 38, P < .05). Baseline CBF was similar between strains; however, cerebrovascular resistance was higher in SHR-SP (2.16 +/- 0.09, n = 27) and SHR (1.94 +/- 0.07, n = 27) compared with WKY rats (1.23 +/- 0.06 mm Hg/mL per minute per 100 g, n = 27, P < .05). CBF was unchanged with 5 mg/kg L-NMMA or with L-arginine in the absence of L-NMMA in each strain. CBF decreased similarly in SHR and SHR-SP (n = 9 each) in response to 20 mg/kg L-NMMA (SHR, 85 +/- 6 to 67 +/- 6; SHR-SP, 87 +/- 7 to 69 +/- 5 mL/min per 100 g) and was completely reversed by L-arginine. CBF did not decrease with 20 mg/kg L-NMMA in WKY rats. Administration of L-NA (n = 5 each) produced similar reduction of CBF (WKY rats, 67 +/- 6%; SHR, 49 +/- 9%; SHR-SP, 61 +/- 6% of baseline) and inhibition of NO synthase in each strain (approximately 80% inhibition). CONCLUSIONS: There was no difference in the cerebrovascular response to NO synthase inhibition in SHR-SP and non-stroke-prone SHR. Therefore, it is unlikely that an altered sensitivity of NO synthase to inhibition can explain predisposition to stroke in SHR-SP.

Amino Acid Oxidoreductases↗
PubMed1994

Cerebral blood flow is reduced by N omega-nitro-L-arginine methyl ester during delayed hypoperfusion in cats.

We tested the hypothesis that decreased tonic release of nitric oxide (NO) or a NO-containing compound, during postischemic delayed hypoperfusion, would result in an impaired response of cerebral blood flow (CBF) to NO synthase inhibition. We measured CBF (microspheres), cerebral oxygen consumption, and physiological variables in 30 halothane-anesthetized cats. In 12 animals, complete cerebral ischemia (verified by midischemic CBF measurement) was produced for 12 min by brachiocephalic and left subclavian artery occlusion with hemorrhagic hypotension (mean arterial blood pressure = 40 mmHg). Steady-state hypoperfusion was present by 120 min of reperfusion (30 +/- 4% of baseline). Nonischemic animals (n = 12) were submitted to the same surgical procedures and anesthetic duration. N omega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv) or saline was administered 160 min after baseline measurements, equivalent to 140 min of reperfusion for animals treated with ischemia (n = 6 in each group). Blood pressure was controlled (aortic ligature) so that there was no change following L-NAME administration both in the ischemic and nonischemic groups. L-NAME reduced CBF during reperfusion in ischemic animals (from 37 +/- 2 to 24 +/- 2 ml.min-1 x 100 g-1) and in nonischemic animals (from 122 +/- 15 to 68 +/- 8 ml.min-1 x 100 g-1) with no change in cerebral oxygen consumption. In six additional cats, administration of L-arginine (250 mg/kg iv) reversed the effect of L-NAME. We conclude that tonic NO-mediated cerebral vasodilation occurs following transient global ischemia despite delayed hypoperfusion.

Animals↗
PubMed1994

Effect of postischemic hypoperfusion on vasodilatory mechanisms in cats.

We addressed the mechanism for reduced pial vascular reactivity to muscarinic stimulation by evaluating pial vessel responses to receptor-dependent [10(-5) M acetylcholine (ACh)] and independent (10(-5) M A-23187) agonists and the endothelium-independent nitric oxide (NO) donor [10(-5) M nitroprusside (NP)]. Cerebral blood flow (CBF, microspheres) and pial arteriolar diameters (intravital microscopy) were measured in halothane-anesthetized cats. Cats (n = 13) were treated with 12 min of near-complete global cerebral ischemia, whereas control animals (n = 9) were identically instrumented but were not submitted to ischemia. Postischemic hypoperfusion was evident in most animals at 60 min of reperfusion, accompanied by attenuated pial arterial dilation to topical ACh (baseline dilation 23 +/- 4% vs. postischemia 11 +/- 3%) and A-23187 (16 +/- 4 vs. 0 +/- 3% dilation). Dilation to NP was unaffected. CBF response to intravenous administration of the muscarinic receptor agonist oxotremorine was also decreased throughout the forebrain (162 +/- 12 vs. 116 +/- 6% increase in flow) in these cats. These data suggest that endothelium-dependent vasodilation with topical muscarinic agonists is impaired during hypoperfusion, but vascular smooth muscle responsivity to NO remains intact. We conclude that the defect in the signal transduction pathway is not limited to the receptor and may involve an abnormality with NO synthesis or its destruction within endothelium.

Acetylcholine↗
PubMed1994

Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats.

BACKGROUND AND PURPOSE: Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats. METHODS: A colony of spontaneously hypertensive stroke-prone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n = 6) and in spontaneously hypertensive (n = 6) and genetically related Wistar-Kyoto rats (n = 6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present. RESULTS: Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: cerebral cortex, 10.6 +/- 0.9; cerebellum, 50.1 +/- 12.0; brain stem, 14.7 +/- 10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: spontaneously hypertensive stroke-prone, 10.6 +/- 0.9; spontaneously hypertensive, 10.8 +/- 0.5; Wistar-Kyoto, 10.9 +/- 0.7 pmol/mg protein per minute) or at any calcium concentration tested. CONCLUSIONS: A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.

Amino Acid Oxidoreductases↗
PubMedDate not supplied

[The importance of software for the planning and adjusting of dosage. Application with aminoglycosides].

We are presenting a Mac Intosh--Apple computer program (Excel*) for the aminoglycosides (AG) drug monitoring useful in the following situations: --initiation of an AG's dosing regimen depending on the desired peak and through concentration (AG's pharmacokinetic parameters have been calculated according to the AG's literature values). --an adequate dosing regimen after revision of the patient's parameters (calculated with the observed concentrations). The technique has been validated comparing desired (des. C) and measured concentrations (mes. C). --either at the beginning of the treatment, --or after revision of the individual parameters. In the first case, the correlation coefficient obtained between 14 des C and 14 mes. C is equal to 0.91 and is improved when individual parameters are calculated (0.94).

Adolescent↗