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Copyright of Canadian Journal of Anaesthesia / Journal Canadien d'Anesthésie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The turtle shell, an evolutionarily novel structure, contains a bony exoskeleton that includes a dorsal carapace and a ventral plastron. The development of the carapace is dependent on the carapacial ridge (CR), a bulge in the dorsal flank that contains an ectodermal structure analogous to the apical ectodermal ridge (AER) of the developing limb (Burke. 1989a. J Morphol 199:363-378; Burke. 1989b. Fortschr Zool 35:206-209). Although the CR is thought to mediate the initiation and outgrowth of the carapace, the mechanisms of shell development have not been studied on the molecular level. Here, we present data suggesting that carapace formation is initiated by co-opting genes that had other functions in the ancestral embryo, specifically those of limb outgrowth. However, there is divergence in the signaling repertoire from that involved in limb initiation and outgrowth. In situ hybridizations with antisense riboprobes derived from Trionyx spiniferous fibroblast growth factor-10 (tfgf10) and Trachemys scripta (T. scripta) fibroblast-growth factor 8 (tfgf8) cDNAs were performed on sections of early T. scripta embryos (< 30 days). Expression of tfgf10 was localized to the mesenchyme subjacent to the ectoderm of the CR. In the chick limb bud, FGF10 is known to be expressed in the early limb-forming mesenchyme and is capable of inducing FGF8 in the AER to initiate the outgrowth of the limb bud. Although the expression of tfgf8 was found in the AER of the developing turtle limb, it was not seen in the CR. Thus, the initiation of the carapace is in agreement with FGF10 expression in the CR, but FGF8 does not appear to have a role in mediating early carapace outgrowth., (Copyright 2001 Wiley-Liss, Inc.)

The authors studied the effect of changes in arterial carbon dioxide tension on plasma lidocaine concentrations during a constant lidocaine infusion in eight healthy volunteers. With a PaCO2 of 41.4 +/- 0.9 mmHg (mean +/- SE), total plasma lidocaine concentrations were 3.97 +/- 0.20 microgram X ml-1. There was no significant change associated with hypercarbia (PaCO2 = 55.7 +/- 1.5 mmHg, lidocaine = 3.93 +/- 0.18 microgram X ml-1) or hypocarbia (PaCO2 = 19.5 +/- 1.4 mmHg, lidocaine = 4.29 +/- 0.25 microgram X ml-1), despite the known effects of changes in CO2 tension on hepatic blood flow and lidocaine protein binding. During hypercarbia, plasma lidocaine binding decreases while total plasma lidocaine remains essentially constant; therefore, increased CO2 tensions could cause toxicity if total lidocaine concentrations were in the high therapeutic range (5 micrograms X ml-1). Four subjects experienced transient symptoms of mild lidocaine toxicity during acute increases in carbon dioxide tension.

The authors determined the accuracy of the Ohmeda 3700 (version J) pulse oximeter in healthy volunteers rendered hypoxic (SaO2 from 60-98%) by breathing mixtures of O2 in N2. When equipped with an ear probe, the pulse oximeter reading (y) reliably predicted arterial saturation (x) under steady-state conditions (y = 1.05x - 4.66, r = 0.98) as well as when oxygen saturation was rapidly decreasing (y = 1.05x - 6.38, r = 0.96). Conversely, when equipped with a finger probe, the oximeter tended to significantly underestimate steady-state arterial saturation (y = 1.21x - 19.1, r = 0.98, P less than 0.001). In response to this information, the manufacturer modified the oximeter's software (version XJ1), resulting in improved agreement between oximeter readings and arterial values (y = 0.96x + 4.59, r = 0.99). Despite the close correlation between steady-state oximeter readings and arterial saturation, the 99% prediction limits for both the ear and finger probes (version XJ1) were +/- 8%. Finger probe readings did not reliably reflect radial arterial oxygenation during rapid desaturation (y = 0.55x + 45.2, r = 0.78). This may be related to the time required to "arterialize" the blood in the finger; during acute resaturation, we found that the ear- to finger-probe delay was 24.0 +/- 2.3 s (means +/- SE, P less than 0.001).