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ABSTRACT: Previous studies to determine whether desflurane increases cerebrospinal fluid (CSF) pressure are inconclusive because none have included all of the following: multiple doses of desflurane, administration for at least several hours, examination at normo- and hypocapnia, a concurrent comparison group, direct measurement of both intra- and extracranial CSF pressures, and measurement of venous pressures that influence CSF pressure. The present study was designed to determine whether CSF pressure increases during 4.0 h desflurane anesthesia using a study design that included the above elements. Catheters were placed in the lateral cerebral ventricle, cisterna magna, sagittal sinus, and jugular vein of 12 dogs anesthetized with thiopental 12 mg.kg-1.h-1 and halothane 0.5 to 0.8%. Catheter pressures were measured, and the CSF-sagittal sinus pressure gradient and slope of the gradient to CSF pressure relationship were determined during control conditions. Then, 6 dogs were anesthetized with desflurane and 6 dogs were anesthetized with isoflurane, and the same values were determined for 1.0 h at each of four experimental conditions: 0.5 and 1.0 minimum alveolar concentration (MAC) during normocapnia (PaCO2 35-39 mm Hg) and 0.5 and 1.0 MAC during hypocapnia (PaCO2 20-24 mm Hg). CSF and sagittal sinus pressures, but not jugular venous pressure, increased with both desflurane and isoflurane. The greater increase of CSF pressure with 4.0 h desflurane (to 40.2 +/- 12.7 cm H2O) than with 4.0 h isoflurane (to 26.2 +/- 11.5 cm H2O) was attributable to an increase of CSF pressure that was greater during 2.0 h desflurane and normocapnia than during 2.0 h isoflurane and normocapnia, and to an increase of CSF pressure during 2.0 h desflurane and hypocapnia that was similar to that during 2.0 h isoflurane and hypocapnia. The greater increase of CSF pressure during desflurane may have resulted, in part, from increased CSF volume as indicated by a positive CSF-sagittal sinus pressure gradient (in contrast, there was little or no CSF-sagittal sinus pressure gradient during isoflurane) and a steeper slope of the gradient to CSF pressure relationship.
Journal of Neurosurgical Anesthesiology 11/1994; 6(4):239-48. · 2.23 Impact Factor
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ABSTRACT: Mannitol is used widely to decrease intracranial pressure (ICP); however, the mechanism by which this effect occurs is unclear. This study was designed to examine the effects of mannitol on cerebrospinal fluid (CSF) formation rate (Vf), resistance to reabsorption of CSF (Ra), and brain tissue water content (BTWC). Eighteen New Zealand White rabbits were allocated into one of three groups and studied at baseline and at two sequential doses of 20% mannitol: 0.75 g/kg followed by 4.4 mg.kg-1.min-1, and 2.0 g/kg (1.25 g/kg added to the initial dose of 0.75 g/kg) followed by 8.6 mg.kg-1.min-1. In Group 1, closed ventriculocisternal perfusion (VCP) was performed to determine changes in ICP due to mannitol. In Group 2, the increase in CSF osmolality due to mannitol was determined. In Group 3, mock CSF was used for open VCP to determine Vf and Ra. At the conclusion of each study, brain tissue samples were taken for determination of BTWC. Mannitol increased CSF and plasma osmolality. Ra was increased by 104% with the low dose of mannitol and not significantly changed by the high dose. Mannitol decreased BTWC, Vf (by 49% with the high dose), ICP, and hematocrit. The authors conclude that two of the mechanisms contributing to decreased ICP with mannitol are: 1) decreased CSF volume as indicated by decreased Vf, and 2) decreased brain tissue volume as indicated by decreased BTWC.
Anesthesia & Analgesia 02/1994; 78(1):58-66. · 3.29 Impact Factor
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ABSTRACT: Hypoxic pulmonary vasoconstriction (HPV) may be manifest in one of two ways: either an increase in the pulmonary artery pressure, or flow diversion away from the portion of the pulmonary bed with reduced conductance. We tested the hypothesis that the magnitude of the HPV response differs under conditions of constant flow perfusion, where pulmonary artery pressure (Ppa) rises during hypoxia, vs conditions of constant pressure perfusion, where Ppa remains constant and flow (Q) is diverted away from the lungs during hypoxia. In isolated, perfused rabbit lungs, the HPV response to four levels of hypoxia (12, 6, 3 and 0% oxygen) was of greater magnitude and more sustained under conditions of constant pressure perfusion as compared to constant flow perfusion. The possible significance of these findings as they relate to interpretation of studies in both the perinatal and mature pulmonary circulation is discussed.
Respiration Physiology 11/1993; 94(1):75-90.
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ABSTRACT: The effects of amrinone on pulmonary vascular resistance (PVR) were studied in an isolated, perfused rabbit lung model where all the major determinants of PVR were controlled. In this preparation, the alveolar oxygen and carbon dioxide tensions, vascular pH and vascular oxygen and carbon dioxide tensions, and zonal conditions of the lung and phasic variations of pulmonary artery pressures could be precisely measured and controlled. Measurements of PVR were made by a complete determination of the pulmonary pressure-flow curve and determination of the PVR under identical flow conditions for all studies. This approach allowed a more precise determination of the primary effects of amrinone on normal and elevated PVR than has been previously possible. We found that amrinone in final concentrations of either 4 or 8 micrograms/ml had no effect on basal PVR and no effect on lung water weight to dry ratios. When PVR was elevated by the addition of the thromboxane A2 mimetic U46619, amrinone reduced the PVR by 27% at a final concentration of 4 micrograms/ml and by 74% at a final concentration of 8 micrograms/ml. We conclude that in the doses tested, amrinone has no effects on basal PVR but is able to reduce elevated PVR in a dose-dependent manner. These results are the first to demonstrate clearly that amrinone has the ability to reduce elevated pulmonary vascular tone through a direct mechanism and not through secondary effects on other determinants of PVR such as left atrial pressure (Pla), increased cardiac output with resultant vascular recruitment, or increases in mixed venous oxygen tension. The possible implications for the clinical use of amrinone in situations of elevated PVR are discussed.
Journal of Cardiovascular Pharmacology 08/1991; 18(1):85-94. · 2.29 Impact Factor
