Local O2 Balance in Cerebral Ischemia-Reperfusion Improved during Pentobarbital Compared with Isoflurane Anesthesia.

BACKGROUND: Most anesthetics affect cerebral blood flow and metabolism. We compared microregional O2 balance in cerebral ischemia-reperfusion during pentobarbital and isoflurane anesthesia. METHODS: After 1 hour of middle cerebral artery occlusion and a 2-hour reperfusion under isoflurane (1.4%, n = 14) or pentobarbital (50 mg/kg, n = 14) anesthesia in rats, regional cerebral blood flow using (14)C-iodoantipyrine autoradiography, microregional arterial and venous O2 saturation (20-60 µm in diameter) using cryomicrospectrophotometry, and the size of cortical infarct were determined. RESULTS: Ischemia-reperfusion decreased the average cortical venous O2 saturation in both pentobarbital and isoflurane groups (P < .0001), which was higher (P < .05) with pentobarbital despite a similar average regional cerebral blood flow and O2 consumption. The heterogeneity of venous O2 saturation reported as a coefficient of variation (100 × standard deviation/mean) was smaller (P < .005) with pentobarbital than that with isoflurane (7.5 versus 16.1). The number of veins with low venous O2 saturation (<50%) was smaller (P < .005) with pentobarbital (5 of 80 versus 24 of 80). The percentage of cortical infarct in total cortex was smaller with pentobarbital (5.2 ± 2.5% versus 12.3 ± 2.6%, P < .001). CONCLUSIONS: In the cerebral ischemic-reperfused cortex, the average venous O2 saturation was higher, and its heterogeneity and the number of veins with low O2 saturation were smaller under pentobarbital than isoflurane anesthesia. This improvement in microregional O2 balance with pentobarbital was accompanied by the reduced cortical infarct. Our data suggest that the neurologic outcome could vary during cerebral ischemia-reperfusion depending on the anesthetics used.

Unilateral Rhinorrhea and Sneezing After Upper Gastrointestinal Endoscopy Under Intravenous Propofol Sedation With Supplemental Oxygen Administered via a Nasal Cannula: A Case Report.

We present a rarely described complication of unilateral rhinorrhea and sneezing in a patient who received intravenous sedation with propofol and supplemental oxygen via a nasal cannula during upper gastrointestinal endoscopy. The literature is reviewed and a mechanism is proposed. Mechanical irritation of the nasal mucosa is felt to be the trigger. Suggestions to avoid and to treat are offered.

Explosive Vomiting Associated with Proximal Colonic Distention during a Difficult Propofol-Assisted Colonoscopy.

We present a case of explosive vomiting associated with the extensive manipulation of the proximal colon during a difficult colonoscopy procedure. The cause of vomiting in this case may have been multifactorial; however, proximal colonic distention was the most likely factor because the onset of vomiting coincided with proximal colonic manipulation and happened without any prodromal signs, coughing, and airway obstruction. Propofol, the sedative most commonly administered to the patient during colonoscopy, allows for a deep state of sedation, and consequently extensive colonic distention and scope manipulation. Colonic distention may lead to a higher risk of vomiting. We reviewed the neurocircuitry associated with vomiting and discussed why proximal colonic distention may increase the risk of vomiting. We emphasize vigilance during the manipulation of the proximal colon because vomiting increases the potential for aspiration pneumonitis and pneumonia in patients under deep propofol sedation with attenuated airway responses.

Inhibition of neuronal nitric oxide synthase improves microregional O2 balance in cerebral ischemia-reperfusion.

Objectives Return of regional cerebral blood flow (rCBF) in focal cerebral ischaemia may not ensure proper distribution of blood flow to meet metabolic demand. This study was performed to determine how inhibition of neuronal nitric oxide synthase (NOS) during ischaemia-reperfusion would affect microregional O2 supply/consumption balances and their variation. Methods Twenty minutes before middle cerebral artery (MCA) occlusion, a NOS inhibitor 7-nitroindazole (7-NI) 50 mg/kg ip (7-NI group) or vehicle (control group) was administered. At 1 hour of ischaemia and 2 hours of reperfusion, rCBF, the size of cortical infarct and arteriolar and venular O2 saturations (20-60 µm in diameter) using cryomicrospectrophotometry were determined. Results Ischaemia-reperfusion decreased the average venular O2 saturation and the ratio of O2 supply/consumption. But, 7-NI treatment improved the average O2 supply/consumption ratio and venular O2 saturation (57.6 ± 1.3 vs 52.0 ± 3.8%) in ischaemia-reperfusion. The heterogeneity of venular O2 saturations reported as coefficient of variation (CV = 100 × SD/mean) was much smaller in the 7-NI than the control group (8.8 vs 15.5). The number of veins with low O2 saturation ( < 50%) was also smaller with the 7-NI (4/70) than the control group (18/70). The size of cortical infarct was smaller with 7-NI treatment. Discussion Our data suggest that inhibition of neuronal NOS by 7-NI improved microregional O2 balance in the ischaemic-reperfused cortex (IR-C). The improvement in microregional O2 balance could be one of the contributing factors to the reduced size of cortical infarct.

Restoration of Normal Cerebral Oxygen Consumption with Rapamycin Treatment in a Rat Model of Autism-Tuberous Sclerosis.

Tuberous sclerosis (TSC) is associated with autism spectrum disorders and has been linked to metabolic dysfunction and unrestrained signaling of the mammalian target of rapamycin (mTOR). Inhibition of mTOR by rapamycin can mitigate some of the phenotypic abnormalities associated with TSC and autism, but whether this is due to the mTOR-related function in energy metabolism remains to be elucidated. In young Eker rats, an animal model of TSC and autism, which harbors a germ line heterozygous Tsc2 mutation, we previously reported that cerebral oxygen consumption was pronouncedly elevated. Young (4 weeks) male control Long-Evans and Eker rats were divided into control and rapamycin-treated (20 mg/kg once daily for 2 days) animals. Cerebral regional blood flow ((14)C-iodoantipyrine) and O2 consumption (cryomicrospectrophotometry) were determined in isoflurane-anesthetized rats. We found significantly increased basal O2 consumption in the cortex (8.7 ± 1.5 ml O2/min/100 g Eker vs. 2.7 ± 0.2 control), hippocampus, pons and cerebellum. Regional cerebral blood flow and cerebral O2 extractions were also elevated in all brain regions. Rapamycin had no significant effect on O2 consumption in any brain region of the control rats, but significantly reduced consumption in the cortex (4.1 ± 0.3) and all other examined regions of the Eker rats. Phosphorylation of mTOR and S6K1 was similar in the two groups and equally reduced by rapamycin. Thus, a rapamycin-sensitive, mTOR-dependent but S6K1-independent, signal led to enhanced oxidative metabolism in the Eker brain. We found decreased Akt phosphorylation in Eker but not Long-Evans rat brains, suggesting that this may be related to the increased cerebral O2 consumption in the Eker rat. Our findings suggest that rapamycin targeting of Akt to restore normal cerebral metabolism could have therapeutic potential in tuberous sclerosis and autism.