MICROVASCULAR OXYGEN DELIVERY AND INTERSTITIAL OXYGENATION DURING SODIUM PENTOBARBITAL-ANESTHESIA

Citation
H. Kerger et al., MICROVASCULAR OXYGEN DELIVERY AND INTERSTITIAL OXYGENATION DURING SODIUM PENTOBARBITAL-ANESTHESIA, Anesthesiology, 86(2), 1997, pp. 372-386
Citations number
45
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
86
Issue
2
Year of publication
1997
Pages
372 - 386
Database
ISI
SICI code
0003-3022(1997)86:2<372:MODAIO>2.0.ZU;2-T
Abstract
Background: Anesthesia may represent a considerable bias in experiment al medicine, particularly in conditions of stress (such as hemorrhage) . Sodium pentobarbital (PB), widely used for cardiovascular investigat ions, may impair oxygen delivery by hemodynamic and respiratory depres sion. The critical issue, however, is whether the microcirculation can still maintain tissue oxygenation during anesthesia. To answer this q uestion, the authors studied the effect of PB anesthesia on subcutaneo us microvascular oxygen delivery and interstitial oxygenation in Syria n golden hamsters. Methods: Sodium pentobarbital anesthesia was induce d by intravenous injection (30 mg/kg body weight) and maintained by a 15-min infusion (2 mg . kg(-1). min(-1)), with animals breathing spont aneously (PB-S) or ventilated with air (PB-V). Systemic parameters eva luated were mean arterial pressure (MAP), heart rate, cardiac index (C I), arterial oxygen tension (Pa-O2), arterial carbon dioxide tension ( Pa-CO), base excess, and pH. Microvascular and interstitial oxygen ten sion (P-O2), vessel diameter, red blood cell velocity (upsilon(RBC)), and blood flow (Q(b)) were measured in a dorsal skinfold preparation. Microcirculatory P-O2 values were determined by phosphorescence decay. Results: Sodium pentobarbital anesthesia significantly decreased CI, MAP, upsilon(RBC), and Q(b). During PB infusion, Pa-O2 values were 56 +/- 12.8 mmHg (PB-S) and 115.9 +/- 14.6 mmHg (PB-V) compared with 69.4 +/- 18.2 mmHg and 61.4 +/- 12.6 mmHg at baseline. However, microvascu lar P-O2 was reduced by 25-55% in both groups, resulting in an interst itial P-O2 decrease from 23.9 +/- 5.6 mmHg (control) to 13.1 +/- 9.1 m mHg (PB-S) and 15.2 +/- 7 mmHg (PB-V). Microcirculatory P-O2 values me re restored 30 min after PB infusion, even though hemodynamic depressi on and a light anesthetic plane mere maintained. Conclusions: Sodium p entobarbital anesthesia caused impairment of microvascular oxygen deli very and interstitial oxygenation, effects that were not prevented by mechanical ventilation. Although these effects were restricted to deep anesthetic planes, prolonged hemodynamic depression suggests that cau tion is warranted when using PB as an anesthetic in cardiovascular inv estigations.