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Biomedical subjects

S Strebel

Publications and source records attributed to S Strebel.

27 records · Page 2Linked to original sources

Cerebral vasomotor responsiveness to carbon dioxide is preserved during propofol and midazolam anesthesia in humans.

Carbon dioxide reactivity, as measured by transcranial Doppler ultrasonography, was determined during total intravenous anesthesia with propofol or midazolam in comparison with an awake control group. Thirty ASA physical status I neurosurgical patients undergoing lumbar laminectomy participated in the study. In randomized order they were subjected to a CO2 reactivity challenge, either under an intravenous anesthesia technique or in the awake state. CO2 reactivity was calculated in each study group as a relative change in middle cerebral artery (MCA) flow velocity per mm Hg change in end-tidal CO2 (PETCO2) (%/mm Hg). The cerebrovascular response to changes in CO2 was preserved during intravenous anesthesia. There was a significant difference (P < 0.05) in the reactivity slopes between the awake and the anesthetized patients with a small but not significant difference between the propofol and the midazolam group. We conclude that hypocarbia is effective in reducing cerebral blood flow velocity (CBFV) during intravenous anesthesia, either with propofol or midazolam.

Adult↗

Effect of neuroprotective N-methyl-D-aspartate antagonists on increased intracranial pressure: studies in the rat acute subdural hematoma model.

Glutamate antagonists are the most powerful neuroprotective drugs in laboratory studies of focal cerebral ischemia. Because the majority of clinical conditions in which focal brain ischemia occurs are associated with high intracranial pressure (ICP), we have used the rat acute subdural hematoma model to evaluate the effects of three glutamate N-methyl-D-aspartate antagonists, MK-801, CGS 19755 (SELFOTEL), D-CPP-ene, and mannitol, upon ICP and also upon the volume of ischemic brain damage. Only mannitol produced a significant reduction in ICP and improved cerebral perfusion pressure. The three glutamate antagonists did not significantly affect ICP or cerebral perfusion pressure, but they were associated with a significantly smaller zone of focal brain damage, when compared to the mannitol and saline groups. N-methyl-D-aspartate antagonists do not increase ICP or jeopardize cerebral perfusion pressure when administered under anesthesia with a controlled PaCO2 level. Further studies in humans are indicated.

Acute Disease↗

Cerebrovascular carbon dioxide reactivity during exposure to equipotent isoflurane and isoflurane in nitrous oxide anaesthesia.

We have studied the effects of hypocapnia on cerebrovascular changes in two MAC-equivalent anaesthetic regimens, using the transcranial Doppler technique as an index of cerebral blood flow (CBF) in 24 healthy ASA I patients undergoing spinal surgery. Eight of the patients were subjected to carbon dioxide reactivity challenges in the awake state. Before surgery, the other 16 patients received, in random order, either 1.15% isoflurane in oxygen or 0.5% isoflurane with 70% nitrous oxide. Carbon dioxide reactivity was calculated for each group as the increase in flow velocity per kPa change in PE'CO2 (cm s-1 kPa-1). It was significantly greater for the isoflurane group (14.09 (SD 2.44) cm s-1 kPa-1) and significantly less for the isoflurane-nitrous oxide group (7.95 (1.32) cm s-1 kPa-1) compared with the awake group (11.24 (0.95) cm s-1 kPa-1). We conclude that cerebrovascular responsiveness to changes in arterial carbon dioxide concentration is influenced markedly by the anaesthetic procedure. Hyperventilation is more likely to affect CBF during isoflurane anaesthesia than during an MAC-equivalent isoflurane-nitrous oxide anaesthesia.

Adult↗

Neuroprotective doses of N-methyl-D-aspartate receptor antagonists profoundly reduce the minimum alveolar anesthetic concentration (MAC) for isoflurane in rats.

N-methyl-D-aspartate (NMDA) receptor antagonists, which block one of the glutamate receptors, have provided evidence of cerebral protection in animal models of focal cerebral ischemia. We examined the effect of neuroprotective doses of one noncompetitive (dizocilpine) and two competitive (D-CPP-ene, CGS 19755) NMDA antagonists on the minimum alveolar anesthetic concentration (MAC) of isoflurane in rats. A single bolus injection of any of the three NMDA antagonists produced a significant (P < 0.01) and sustained (> 3 h) decrease in the MAC of isoflurane. Dizocilpine decreased MAC by 33%-38% at a dose of 0.15 mg/kg and 48%-54% at a dose of 0.5 mg/kg. D-CPP-ene decreased MAC by 32%-37% at a dose of 1.5 mg/kg and 39%-45% at a dose of 4.5 mg/kg. CGS 19755 decreased MAC by 19%-24% at a dose of 3 mg/kg and 49%-58% at a dose of 10 mg/kg. Dizocilpine, but not the competitive antagonists, produced a small transient decrease in mean arterial blood pressure. The sustained anesthetic potency of neuroprotective doses of NMDA antagonists supports the idea that glutaminergic receptor activity is involved in determining the anesthetic state.

Anesthesia, Inhalation↗

Central nervous system symptoms after intravenous lignocaine: dose-response during pregnancy.

There is continuing controversy over what dose of what drug should be used to identify an accidental intravascular or subarachnoid catheter placement in obstetric epidural anaesthesia. The purpose of this randomized, double-blind study was to evaluate the dose-effect relationship for the production of central nervous system (CNS) symptoms by intravenous lignocaine. Sixty first-trimester, pregnant patients divided into groups of 10 received saline or one of five doses of lignocaine (0.39, 0.5, 0.63, 0.79, and 1.0 mg kg-1) i.v. An ED95 of 1.12 mg kg-1 was calculated to produce reliable CNS symptoms when injected intravascularly. Lignocaine is an effective and reliable marker for intravenous injection in pregnant women.

Abortion, Therapeutic↗

[Non-respiratory therapy of adult respiratory distress syndrome].

Several approaches to non-respiratory management of adult respiratory distress syndrome (ARDS) are discussed. (1) Diagnosis and therapy of the underlying disease is a primary goal in order to avoid the ongoing process of lung injury. (2) Specific pharmacologic therapy for primary lung injury is not available even after 25 years of immunologic research, because no specific mediator has yet been identified as a primary pathogenic factor in ARDS, which is a heterogenous clinical syndrome. (3) Supportive therapy (i.e. improving right ventricular dysfunction and treating pulmonary arterial hypertension) should be emphasized. (4) The most important approach is to optimize prophylactic management to avoid nosocomial infection by eliminating unnecessary invasive techniques, changing the patients' positioning and conserving organ function. So far the latter approach seems to be the only way to improve survival in respiratory failure.

Anti-Inflammatory Agents↗

Propofol-fentanyl anesthesia for pheochromocytoma resection.

Numerous anesthetic techniques and agents have been used for anesthetizing pheochromocytoma patients. However, a comparison based on literature reports is difficult, since most describe only isolated cases. We discuss current anesthetic techniques and a case report of a patient who successfully received a combined propofol-fentanyl anesthesia for pheochromocytoma resection.

Adrenal Gland Neoplasms↗

[Outcome prognosis in severe craniocerebral trauma: important predictors in the early phase].

An early prognosis may influence the management of severely head-injured patients. Clinical aspects (age, Glasgow Coma Score, pupil reaction) and neuroradiological findings (basal cysternes, midline shift) are the most important facts for prognosis; evoked potentials, stress parameters and the quality of resuscitation also correlate with definitive outcome. Despite a clear correlation between these single factors and outcome, prognosis during the first 48 hours remains too uncertain to justify an influence on initial management.

Aged↗