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C K Pac-Soo

Publications and source records attributed to C K Pac-Soo.

5 recordsLinked to original sources

Comparison of the effects of inhalational anaesthetic agents on sympathetic activity in rabbits.

The effects of inhalational anaesthetic agents on renal sympathetic nerve activity (RSNA) were compared in anaesthetized rabbits. Concentrations of 6% desflurane, 1.2% isoflurane, and 2.4% enflurane increased mean RSNA up to 32, 36 and 44% while higher concentrations, of 12, 2.4 and 3.2% depressed it by 42, 83 and 5%, respectively. For halothane RSNA was unchanged up to 0.8% and decreased by 36% at 1.6% concentration. Nitrous oxide increased RSNA up to 28% at 50% concentration. Maximum reductions in mean arterial pressure (MAP) were 60% for both 2.4% isoflurane and 3.2% enflurane, 50% for 12% desflurane and 1.6% halothane, while 70% nitrous oxide increased MAP by 22%. In conclusion, unlike the entirely depressive effects of halothane, the effects of desflurane, isoflurane and enflurane were biphasic involving excitation at lower concentrations and depression of RSNA and a reduction in MAP at higher concentrations. Nitrous oxide caused increases in both RSNA and MAP.

Anesthetics, Inhalation↗

Vagally mediated sympathoexcitation and central depression by desflurane in rabbits.

The effects of desflurane on renal sympathetic nerve activity (RSNA) were studied in intact or vagotomized anaesthetized rabbits with initial concentrations of 4.5-18%, subsequently equilibrated to end-tidal concentrations from 3%, 6%, 9% and 12% each for 20 min allowing sympathetic activity to stabilize. In intact animals, immediate transient increases in mean sympathetic activity from 27% to 63% were closely related to initial concentrations from 4.5% to 18%. During subsequent equilibration this remained elevated by 25-30% up to 6%, returned to control at 9% and fell by 33% at 12%. Bilateral vagotomy abolished sympathoexcitation apart from small increases in sympathetic activity, for example 14% at 4.5% (P < 0.05). We conclude that increases in inspired desflurane concentrations evoked rapid transient vagally mediated reflex sympathoexcitation with a small extra-vagal contribution. Central depression of sympathetic activity started at 6% and was 33% below baseline at 12%.

Anesthetics, Inhalation↗

Specific actions of halothane, isoflurane, and desflurane on sympathetic activity and A delta and C somatosympathetic reflexes recorded in renal nerves in dogs.

BACKGROUND: This was a study of the relative effects on directly recorded sympathetic activity of desflurane, isoflurane, and halothane. METHODS: Renal sympathetic nerve activity (RSNA) was recorded with bipolar electrodes in renal nerves exposed retroperitoneally in anesthetized (alpha-chloralose), paralyzed (succinylcholine), and artificially ventilated dogs. Somatosympathetic responses were evoked by supramaximal electrical stimulation of radial nerves (0.33 Hz, 30 V, 0.5 ms). Spontaneous and evoked activity were rectified, averaged, and integrated to allow quantitative comparison of the effects of 3-12% desflurane, 0.6-2.4% isoflurane, and 0.4-1.6% halothane. RESULTS: Increasing concentrations of isoflurane progressively depressed mean RSNA, Adelta, and C reflexes by 40% (P < 0.01), 50% (P < 0.01) and 70% (P < 0.001) respectively at 2.4% concentration. Halothane depressed both reflexes equally by approximately 60% (P < 0.01) at 1.6% concentration, without significant depression of spontaneous RSNA. Desflurane increased and subsequently decreased RSNA by 37% (P < 0.02) and 65% (P < 0.001) at concentrations of 6% and 12% respectively, and although somatosympathetic reflexes remained unchanged up to 9%, both were depressed equally by 70% (P < 0.01) at 12% concentration. CONCLUSION: After equilibration, lower concentrations of desflurane remained excitatory, but, like isoflurane, higher concentrations depressed RSNA. The effect of halothane on RSNA was insignificant. Isoflurane depressed C more than Adelta somatosympathetic reflexes, which is uncorrelated with lipid solubility because desflurane and halothane, which have the highest and lowest minimum alveolar concentration, respectively, depressed both equally.

Anesthetics, Inhalation↗

Dissociation between the effect of nitrous oxide on spontaneous and reflexly evoked sympathetic activity in dogs.

We have examined the effect of nitrous oxide on spontaneous sympathetic activity and A delta- and C-fibre mediated somatosympathetic reflexes in renal nerves, evoked by supramaximal electrical stimulation of radial nerves in anaesthetized, paralysed dogs undergoing mechanical ventilation. In six preparations, nitrous oxide was administered at end-tidal concentrations of 10%, 30%, 50% and 70%, each for 20 min. Spontaneous renal sympathetic activity increased significantly to 147.8% and 151.2% of control values with 50% and 70% nitrous oxide, respectively (P < 0.05), but there were no significant changes in A delta and C reflexes. We conclude that the large increase in spontaneous sympathetic activity was dissociated from somatosympathetic reflexes which remained unchanged at these concentrations of nitrous oxide.

Anesthetics, Inhalation↗

Patient-controlled sedation for cataract surgery using peribulbar block.

Patients undergoing cataract surgery using peribulbar block were allocated randomly to self-administer doses of either midazolam 0.1 mg or propofol 3.3 mg without a lock-out facility; in the control group the syringe was charged with saline, not as a placebo, but to "blind" the surgeon and the nurse observer. For midazolam and propofol, median doses were 2.54 (0.1-6.0) mg and 87.4 (0-145) mg, respectively. Patient-controlled sedation significantly reduced the level of anxiety, with median visual analogue anxiety scores in the midazolam, propofol and saline groups of 5 (0-38) mm, 5 (0-25) mm and 15 (0-92) mm, respectively (P < 0.05). Some patients did not administer the sedative when available while others in the saline group would have benefited from anxiolytic drugs. While both drugs prevented an increase in heart rate, only midazolam prevented an increase in arterial pressure during surgery.

Adult↗