Biomedical subjects

S Jamali

Publications and source records attributed to S Jamali.

8 recordsLinked to original sources

PubMed1998

Increase in the chronically monitored cerebrospinal fluid pressure after experimental brain injury in rats.

The early effects of experimental brain injury with diffuse axonal lesions on intracranial pressure (i.c.p.), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) in rats have been already studied. The aim of this experiment was to examine the effects of brain injury on ICP, MAP and CPP during the first few days post-injury. In order to do that, an accurate technique of ICP measurement had to be developed. In a series of eight rats, a translumbar intrathecal catheter (TIC) was surgically introduced allowing repeated measurements of cerebrospinal fluid pressure (CSFP). Under anaesthesia, a second series of nine rats were equipped simultaneously with TIC and an intracranial fiberoptic device to measure ICP. Simultaneous measurements of CSFP and ICP were recorded for baseline values, than during and after jugular compression which was intended to induce an acute and significant increase in ICP. A third series of 53 rats having TIC received an experimental severe brain injury. MAP was measured non-invasively and CPP was calculated as CPP-MAP. CSFP, MAP and CPP were intermittently measured during 5-6 post-traumatic days and compared to the values obtained during ten control rats (SHAM). A clinical score was used to compare clinical condition. The results showed that the translumbar CSFP accurately measured ICP in rats having normal or acutely increased ICP. The experimental brain injury induced increased CSFP lasting up to 5-6 days, with increased MAP during the first 6 hours. CPP values were compromised at 24-48 hours. The clinical performance was reduced in the brain-injured rats. The translumbar technique of CSFP measurement reflected exact ICP in normal and acutely increased ICP in rats. Experimental brain injury with diffuse axonal lesions can increase lumbar CSFP in rats for many days.

Analysis of Variance↗

PubMed1998

Respiratory effects of desflurane anesthesia on spontaneous ventilation in infants and children.

UNLABELLED: Volatile anesthetics depress spontaneous ventilation in a dose-dependent manner with variations in effects among different drugs. The goal of this prospective study was to assess respiratory changes during spontaneous ventilation using desflurane/O2/N2O anesthesia in two groups of children. Both groups were undergoing minor surgery and consisted of children < 2 yr old (Group I) and children > 2 yr old (Group II). They were examined at 0.5, 1, and 1.5 minimum alveolar anesthetic concentration desflurane anesthesia. Induction of anesthesia was performed via a face mask and a mixture of O2/N2O (40:60) with halothane. At lease 20 min after stopping halothane, the respiratory variables were recorded on desflurane anesthesia. Tidal volume and minute ventilation decreased significantly (P <0.05) as desflurane increased from 0.5 to 1.5 MAC in both groups. At 1.5 MAC, the respiratory rate was greater in Group II than in Group I (P <0.05). In both groups, the increase in end-tidal CO2 was significant at 1.5 MAC versus 1 and 0.5 MAC (P <0.05). Apnea, i.e., no respiratory movement for 20 s, occurred at 1.5 MAC in one patient in each group. The respiratory duty cycle did not change in any of the groups. Both indices of paradoxical respiration--amplitude index and delay index--did not change. IMPLICATIONS: Desflurane induces respiratory depression at concentrations higher than 1 minimum alveolar anesthetic concentration mainly due to a decrease in tidal volume. Therefore, desflurane at high concentrations should be used cautiously in infants and children with spontaneous ventilation.

Anesthesia, Inhalation↗

PubMed1997

Strong expression of GFAP mRNA in rat hippocampus after a closed-head injury.

We investigated the spatiotemporal GFAP mRNA expression over a period of 11 days following brain injury in rats caused by impact acceleration, which is known to produce diffuse axonal injury (DAI). We observed widespread GFAP mRNA expression throughout the brain, which was more rapid and intense in the hippocampus. This expression was obvious in most animals 2 days after injury and appeared maximal at day 6. Although it decreased by day 11, the level of expression remained high compared with control levels. We noted slight differences in time of onset and the magnitude of the response between hippocampus and white matter structures or cortical areas. The different mechanisms able to trigger this response are discussed in regard to histopathological changes observed in DAI models.

Analysis of Variance↗

PubMed1997

The effect of skull-pin insertion on cerebrospinal fluid pressure and cerebral perfusion pressure: influence of sufentanil and fentanyl.

This randomized prospective study measured the effects of an intravenous opioid bolus on cerebrospinal fluid pressure (CSFP), mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) during skull-pin insertion. Twenty-two adult patients scheduled for elective craniotomy for supratentorial lesions were studied. Outcome variables were MAP, heart rate (HR), and lumbar CSFP. The standardized anesthetic regimen included fentanyl (2 microg/kg), thiopental (5-7 mg/kg), lidocaine (1.5 mg/kg), isoflurane (0.3-0.7 minimum alveolar anesthetic concentration), and vecuronium (0.1 mg/kg). During stable anesthesia, sufentanil (0.8 microg/kg) or fentanyl (4.5 microg/kg) was given as a bolus before skull-pin insertion. The hemodynamic effects of the opioid injection were modified with phenylephrine and/or atropine when indicated. CSFP remained unchanged in both treatment groups. MAP and CPP increased approximately 10 mm Hg after skull-pin insertion (P<0.001). In the sufentanil group, HR decreased approximately 10 bpm after opioid injection and remained decreased throughout the study. In fentanyl-treated patients, HR decreased 8 bpm after opioid injection but returned to preopioid rates after skull-pin insertion. In conclusion, in anesthetized patients, an intravenous bolus of fentanyl or sufentanil prior to skull-pin insertion results in stable values of CSFP, CPP, BP, and HR when the hemodynamic effects of the opioid are modified with phenylephrine and atropine.

Adjuvants, Anesthesia↗

PubMed1996

[Effects of different loading solutions on plasma osmolality].

OBJECTIVE: As hydratation of the normal brain is much more dictated by osmotic gradients than by hydrostatic or oncotic pressures, this study aimed to compare the effect of the infusion of currently used volume loading solutions on plasma osmolality. STUDY DESIGN: Randomized, comparative trial. PATIENTS: Thirty ASA 1-2 patients, scheduled for lumbar intervertebral disc surgery were randomly allocated to three groups receiving either 2,000 mL of lactated Ringer's solution (RL, n = 10), 750 mL of hydroxyethylstarch 6% (HEA, n = 10) or 2,000 mL of normal saline (NaCl, n = 10). METHODS: Baseline osmolality, natraemia, glycaemia and protidaemia were measured before induction of anaesthesia (T1), after the infusion of 375 mL of hydroxyethylstarch or 1,000 mL of crystalloids (T2) and at the end of the infusion (T3). RESULTS: The three groups were identical for age, weight, initial plasma osmolality and natraemia. However, osmolality in the RL group was decreased at T2 and T3 compared to T1 (respectively: 299 +/- 5 mOsm.kg-1, 295 +/- 4 mOsm.kg-1 and 292 +/- 5 mOsm.kg-1. Osmolality at T2 and T3 was also lower in the RL group compared to the HEA and NaCl groups (respectively: 301 +/- 6 mOsm.kg-1 and 304 +/- 13 mOsm.kg-1 for T2 and T3 in the HEA group, and 299 +/- 5 mOsm.kg-1 and 298 +/- 5 mOsm.kg-1 in the NaCl group). In the HEA and NaCl groups, osmolality was unchanged at T2 and T3 compared to T1. CONCLUSION: Both normal saline and hydroxyethylstarch 6% maintain plasma osmolality, whereas Ringer lactate tends to decrease it. For that reason normal saline and hetastarch 6% but not lactated Ringer's solution, may be administered in patients experiencing blood-brain barrier damage.

Blood Glucose↗

PubMed1996

Maternal and fetal effects of adrenaline with bupivacaine (0.25%) for epidural analgesia during labour.

The use of adrenaline added to bupivacaine during epidural analgesia for labour is controversial. The effects of epidural analgesia with bupivacaine containing adrenaline on maternal blood pressure and heart rate, uterine activity, progress of labour, fetal heart rate and Apgar scores, were assessed using visual analogue pain scores, upper level of sensory block and motor blockade in 60 parturients who were allocated randomly to receive: 10 mL of bupivacaine 0.25% plain (group I) or with adrenaline 5 micrograms mL-1 (group II) or with adrenaline 1.66 micrograms mL-1 (group III). The first stage of labour was significantly longer in group II than in group I [414 +/- 49 vs. 296 +/- 24 min (+/- SD)]. There were no other significant differences. It is concluded that adrenaline at 5 micrograms mL-1 significantly prolongs the first stage of labour. Neither adrenaline 5 micrograms mL-1 nor 1.66 micrograms mL-1 has any beneficial effect.

Analgesia, Epidural↗

PubMed1996

The effects of bolus administration of opioids on cerebrospinal fluid pressure in patients with supratentorial lesions.

In many studies reporting an increase in cerebrospinal fluid pressure (CSFP) after opioid administration, concomitant decreases in mean arterial pressure (MAP) have been observed. Autoregulatory cerebral vasodilation may therefore have been a factor in the CSFP increases. We tested the hypothesis that increases in CSFP after bolus injection of opioids could be minimized by modifying concomitant decreases in MAP with phenylephrine. Thirty-three patients with supratentorial mass lesions were studied in a randomized, prospective, double-blind, saline-controlled comparative trial. The principal outcome measures were lumbar CSFP, MAP, and heart rate (HR). Study drugs, sufentanil 0.8 micrograms/kg (n = 12), fentanyl 4.5 micrograms/kg (n = 11), or normal saline (n = 10), were injected intravenously (IV) during stable general anesthesia with 0.3-0.7 minimum alveolar anesthetic concentration (MAC) of isoflurane in oxygen and controlled ventilation (end-tidal carbon dioxide 32-35 mm Hg). Phenylephrine 50-100 micrograms was injected IV when MAP decreased by more than 15% of initial values, and atropine 0.5 mg IV when HR decreased to less than 45 bpm. Opioid administration was associated with significant decreases in MAP, 21 +/- 9 mm Hg (mean +/- SD) in the sufentanil group and 16 +/- 7 mm Hg in the fentanyl group; P < 0.001. These decreases in MAP were of short duration (i.e., corrected with 1-2 min). Patients in the sufentanil group needed more phenylephrine than patients in the fentanyl group (170 +/- 89 micrograms vs 100 +/- 47 micrograms; P < 0.05). No significant change in the CSFP was seen in either the sufentanil (1 +/- 6 mm Hg) or fentanyl-treated patients (O +/- 2 mm Hg). No significant changes in MAP or CSFP were observed in the saline-treated patients. HR decreased after injection of either study drug (P < 0.01) but remained unchanged in the saline group. In summary, during stable anesthesia with isoflurane in oxygen, bolus injections of fentanyl or sufentanil, despite producing rapidly corrected mean decreases in MAP of 18% and 25%, respectively, were not associated with any change in CSFP.

Adult↗

PubMed1994

Clonidine in pediatric caudal anesthesia.

Extradural clonidine produces analgesia in adults. To assess its efficacy in children, we randomized 45 pediatric patients aged 1-7 yr presenting for a subumbilical surgery into three groups of 15 each. After halothane and N2O/O2 induction, and with a double-blind protocol, caudal anesthesia was performed with 1 mL/kg of 0.25% bupivacaine. Epinephrine 1/200,000 was added in one group (EG), 1 microgram/kg of clonidine in another group (CG), and no additional medication in the last group (BG). Postoperative analgesia was evaluated using the Broadman "objective pain/discomfort scale" (OPS) at 1-h intervals until the first analgesic administration. There were no differences among the groups in age, weight, duration of surgery, baseline systolic arterial pressure, and heart rate. The mean (+/- SD) duration of analgesia was longer in the CG (987 +/- 573 min) than in the EG (377 +/- 341 min) and BG (460 +/- 439 min); P < 0.01. The maximal OPS scores were lower in the CG than in the EG and BG (2.3 +/- 1.6 vs 3.4 +/- 1.4 and 3.4 +/- 1.8, respectively; P < 0.05). More patients in the CG (n = 7) than in the EG (n = 1) and BG (n = 2) required no postoperative analgesia; P < 0.05. No differences were found among the groups for the minimal respiratory rate and minimal Spo2 values in the postoperative phase, and there were no differences among the groups for heart rate and systolic arterial pressure during the 3 h after caudal anesthesia. We conclude that the duration of postoperative analgesia with caudal bupivacaine was significantly increased by the addition of 1 microgram/kg of clonidine.

Anesthesia, Caudal↗