Vecuronium bromide

Objectives: Volatile anesthetics are thought to impair cerebral autoregulation more than i.v. anesthetics. However, few comparative studies have been carried out in humans. The aim of our study was to evaluate the differences in cerebral hemodynamic changes after introduction of isoflurane (a volatile anesthetic) and propofol (an i.v. anesthetic).

Methods: Eighteen consecutive patients submitted to laparoscopic cholecystectomy were selected. After the induction, anesthesia was maintained by isoflurane (one minimum alveolar anesthetic concentration) during the first part of the surgical operation, and then by propofol (5 mg/kg/hour i.v.). Ventilation was adjusted to maintain a constant end-tidal CO2. Middle artery flow velocity was assessed by means of transcranial Doppler ultrasonography. Arterial blood pressure, heart rate (HR), capnometry, pulse oxymetry, inspired fraction of O2, and body temperature, were monitored.

Results: Cerebral artery velocity, HR, and mean arterial pressure all significantly increased from baseline after the introduction of isoflurane (p

Conclusions: Propofol but not isoflurane decreased cerebral blood velocity thus restoring cerebral autoregulation and the coupling between cerebral blood flow and cerebral metabolism. [Neurol Res 2005; 27: 433-435]

Keywords: Cerebral blood flow; isoflurane; intravenous anesthetic; propofol; transcranical Doppler ultrasonography

INTRODUCTION

In physiological conditions, the brain has the capability of regulating cerebral blood flow to maintain a constant perfusion, regardless of blood pressure changes. This mechanism, named cerebral blood flow autoregulation, protects the brain from dangerous oscillations in systemic blood pressure1. Autoregulation is a sensitive mechanism that could be impaired in some pathological conditions, such as head injury, cerebral vascular diseases, and mass occupying lesions1"3.

General anesthesia can affect cerebral blood flow autoregulation as well4. Patients with an abated cerebral blood flow autoregulation, show an increased risk of developing cerebral hyperemia or intracranial hypertension during general anesthesia. Therefore, for these patients, the use of an anesthetic that does not further impair cerebral blood flow autoregulation would be advisable.

Evidence indicates that volatile anesthetics impair autoregulation to a greater extent than i.v. anesthetics5-9. However, so far only a few studies comparing the use of volatile and i.v. anesthetics have been carried out in humans10-13.

The aim of our study was to compare the cerebral blood flow modifications with the introduction first of isoflurane (a volatile anesthetic), then of propofol (an i.v. anesthetic), after the anesthetic induction was obtained by sodium thiopental and fentanyl.

MATERIALS AND METHODS

Eighteen patients (eleven females and seven males, mean age 52, range 38-65) scheduled to undergo Iaparoscopic cholecystecomy, were selected for our study, after they had signed informed consent (Tables 1 and 2). All of them were in good physical condition (ASA 1-11). The exclusion criteria included the presence either of cerebral, pulmonary, cardiac, cerebral vascular diseases, or of vasoactive drug therapy. After premedication with diazepam (8-10 mg per os), anesthetic induction was carried out with sodium thiopental (4 mg/kg) and fentanyl (5 µg/kg), followed by vecuronium bromide (0.1 mg/kg) to facilitate the intubation. During the first part of the surgical procedure, anesthesia was maintained by isoflurane 1 MAC (minimum alveolar anesthetic concentration). Isoflurane was changed to propofol, 30 minutes after intubation. The change to propofol was carried out by interruption of isoflurane, while starting an i.v. 10 mg/kg/hour infusion of propofol, which was kept constant for 15 minutes. The propofol infusion was then gradually reduced to 5 mg/kg/hour during the following 15 minutes, and so maintained until the end of the surgical procedure. Fentanyl (2 µg/kg) and vecuronium bromide (0.02 mg/kg) were added when necessary. Ventilation was adjusted to keep the end-tidal CO2 partial pressure (ETCO^sub 2^) between 28 and 39 mmHg. Standard anesthetic monitoring, including arterial blood pressure, heart rate (HR), capnometry, pulse oxymetry, inspired and expired isoflurane concentration, inspired fraction of O2, body temperature, was performed.

Measurement of mean arterial blood velocity (MFV) was obtained by isonating the right middle cerebral artery (MCA) using a 2-mHz pulsed wave probe (Multiplan Dop T, DWL GmnH, Germany), according to the method described by Aaslid14. Briefly, the MCA was isonated through the temporal bone above the zygomatic arch. The Doppler signals were measured at a depth of 50-60 mm, to provide the highest mean flow velocity. The probe was secured to the patient's head by means of special headgear in a position allowing for continuous monitoring of MFV.

The values of ETCO^sub 2^, mean arterial pressure (MAP), HR, and MFV were recorded four times during our study: at baseline (before anesthesia induction), after intubation, during isoflurane anesthesia (1 MAC), and finally during propofol anesthesia (5 mg/kg/hour).

A f-test for paired samples was used to analyze the data. A p value of

RESULTS

The data are summarized in TaWe 2. The mean duration of surgery was 134 minutes, ranging from 75 to 165 minutes. No significant variations in ETCO^sub 2^ were observed during our study. MAP and HR significantly increased from baseline values after isoflurane and propofol introduction (p

DISCUSSION

All of the patients enrolled in our study were scheduled to undergo laparoscopic surgery because in a precedent study we showed that PCO^sub 2^ intra-peritoneal insufflation did not cause CBF variations15.

Transcranial Doppler is a non-invasive and reliable method to assess blood flow velocity in the basal cerebral artery16. MFV in the MCA and CBF poorly correlate, but changes in MFV are proportional to changes in CBF17'18.

In our study MFV, but not MAP and HR, was significantly higher during isoflurane anesthesia than during propofol anesthesia. ETCO^sub 2^ was kept to baseline values during the whole surgical procedure and therefore the difference in MFV could not be ascribed to arterial blood CO2 pressure variations. Instead, isoflurane could have increased CBF by means of an induction of the cerebral resistance vessels vasodilatation, thus impairing cerebral blood flow autoregulation. Isoflurane has indeed a direct cerebrovasodilatatory effect on cerebral blood vessels and produces vasodilatation regardless of the cerebral metabolism reduction19'20. Moreover, vasodilatation produces an important narrowing of the cerebral autoregulation range1. In contrast, propofol preserves the coupling between CBF and cerebral metabolism, decreasing metabolism and indirectly producing vasoconstriction21. The increase in MFV, observed after the introduction of isoflurane, was presumably due to both the MAP increase and the cerebral autoregulation impairment. The propofol introduction instead preserved the cerebral autoregulation and re-established the coupling between CBF and cerebral metabolism, thus reducing MFV.

CONCLUSIONS

MFV is significantly higher during isoflurane anesthesia than during propofol anesthesia. This difference is probably due to the cerebral autoregulation impairment produced by isoflurane. The risk of inducing cerebral hyperemia or intracranial hypertension is reasonably low for healthy patients but could be particularly high for those patients who have a reduced cerebral autoregulation like those suffering from a cerebrovascular disease or a head injury. In such patients, use of the i.v. anesthetic propofol would be more advisable then the use of the volatile anesthetic (isoflurane).

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G. De Cosmo*, I. Cancell[dagger], A. Adduci*, G. Merlino[dagger], P. Aceto* and M. Valente[dagger]

[dagger] Neurological Clinic, DPMSC University of Udine, Italy Piazzale Rodolone 2, 33100 Cemona Del Friuli (UD), Italy

* lnstitute of Anesthesiology and Reanimation, Catholic University of Rome, Italy Largo A. Cemelli, 00168 Roma, Italy

Correspondence and reprint requests to: Mariarosaria Valente, Piazzale Rodolone 2, 33013 Gemona Del Friuli (UD), Italy, [mariarosaria. valente@uniud.it] Accepted for publication October 2004

Copyright Maney Publishing Jun 2005
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