28 resultados para normocapnia


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Réalisé en cotutelle avec l'Université Joseph Fourier École Doctorale Ingénierie pour la Santé,la Cognition et l'Environnement (France)

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Understanding neurovascular coupling is a prerequisite for the interpretation of results obtained from modern neuroimaging techniques. This study investigated the hemodynamic and neural responses in rat somatosensory cortex elicited by 16 seconds electrical whisker stimuli. Hemodynamics were measured by optical imaging spectroscopy and neural activity by multichannel electrophysiology. Previous studies have suggested that the whisker-evoked hemodynamic response contains two mechanisms, a transient ‘backwards’ dilation of the middle cerebral artery, followed by an increase in blood volume localized to the site of neural activity. To distinguish between the mechanisms responsible for these aspects of the response, we presented whisker stimuli during normocapnia (‘control’), and during a high level of hypercapnia. Hypercapnia was used to ‘predilate’ arteries and thus possibly ‘inhibit’ aspects of the response related to the ‘early’ mechanism. Indeed, hemodynamic data suggested that the transient stimulus-evoked response was absent under hypercapnia. However, evoked neural responses were also altered during hypercapnia and convolution of the neural responses from both the normocapnic and hypercapnic conditions with a canonical impulse response function, suggested that neurovascular coupling was similar in both conditions. Although data did not clearly dissociate early and late vascular responses, they suggest that the neurovascular coupling relationship is neurogenic in origin.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The volume-controlled mechanical ventilation and spontaneous ventilation, through haemogasometric, cardiovascular and spirometry variables were evaluated. Twenty-eight rabbits were distributed into two groups: GIVC (isoflurane and volume-controlled ventilation), GIVE (isoflurane and spontaneous ventilation), GSVC (sevoflurane and volume-controlled ventilation) and GSVE (sevoflurane and spontaneous ventilation). Induction was performed by mask with isoflurane (GIVE and GIVC) or sevoflurane (GSVE and GSVC) at 1.5 MAC in 100% oxygen. To maintain anesthesia, MAC was reset to 1. In GIVC and GSVC groups, rocuronium was administered at a dose of 0.6 mg/kg followed by its continuous infusion (0.6 mg/kg/h). In GSVE and GIVE, 0.9% NaCl was administered instead of rocuronium. Controlled ventilation was started by adjusting the capnometry in order to obtain values between 35 and 45 mmHg. Parameters were measured 60 minutes after induction of anesthesia (M0), 15 minutes after the bolus of rocuronium or 0.9% NaCl (M15) and every fifteen minutes (M30, M45 and M60). Hypercapnia and acidosis was evident in GIVC, GSVC and GSVE. We concluded that the volume-controlled mechanical ventilation was not able to maintain normocapnia in rabbits, producing acidosis in them, especially when using sevoflurane. The use of isoflurane showed greater stability than the sevoflurane anesthetic in the species studied.

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The periaqueductal gray (PAG) is a midbrain structure directly involved in the modulation of defensive behaviors. It has direct projections to several central nuclei that are involved in cardiorespiratory control. Although PAG stimulation is known to elicit respiratory responses, the role of the PAG in the CO2-drive to breathe is still unknown. The present study assessed the effect of chemical lesion of the dorsolateral and dorsomedial and ventrolateral/lateral PAG (dlPAG, dmPAG, and vPAG, respectively) on cardiorespiratory and thermal responses to hypercapnia. Ibotenic acid (IBO) or vehicle (PBS, Sham group) was injected into the dlPAG, dmPAG, or vPAG of male Wistar rats. Rats with lesions outside the dlPAG, dmPAG, or vPAG were considered as negative controls (NC). Pulmonary ventilation (Ve), mean arterial pressure (MAP), heart rate (HR), and body temperature (Tb) were measured in unanesthetized rats during normocapnia and hypercapnic exposure (5, 15, 30 min, 7 % CO2). IBO lesioning of the dlPAG/dmPAG caused 31 % and 26.5 % reductions of the respiratory response to CO2 (1,094.3 +/- 115 mL/kg/min) compared with Sham (1,589.5 +/- 88.1 mL/kg/min) and NC groups (1,488.2 +/- 47.7 mL/kg/min), respectively. IBO lesioning of the vPAG caused 26.6 % and 21 % reductions of CO2 hyperpnea (1,215.3 +/- 108.6 mL/kg/min) compared with Sham (1,657.3 +/- 173.9 mL/kg/min) and NC groups (1,537.6 +/- 59.3). Basal Ve, MAP, HR, and Tb were not affected by dlPAG, dmPAG, or vPAG lesioning. The results suggest that dlPAG, dmPAG, and vPAG modulate hypercapnic ventilatory responses in rats but do not affect MAP, HR, or Tb regulation in resting conditions or during hypercapnia.