Ultrasonographic appearance of intraneural injections in the porcine model.

BACKGROUND: Ultrasonographic (US) images of apparent intraneural injection of local anesthetic solutions have been reported. We aimed to define US signs of intraneural (ie, subepineural) injection using a histologic standard in an animal model and compare these signs with other potential markers of intraneural injection, including low nerve stimulation current thresholds and high injection pressures. METHODS: In 6 anesthetized adult swine, bilateral brachial plexus and femoral nerves were contacted by needles and penetrated. India ink was injected intraneurally under US monitoring. The minimum current that elicited a motor response was recorded. Injection pressures were measured using a digital manometer. Nerves were then excised, processed, and subjected to histologic analysis. RESULTS: Nerve expansion during injection was visualized under ultrasonography in all procedures. Electrical current intensity to elicit motor response to nerve stimulation varied between 0.2 and 3.3 mA with the needle tip positioned intraneurally. The mean injection pressure was 7.40 +/- 8.07 psi (range, 0.07-31.5 psi), with 80% of injections between 0.61 and 15.0 psi. None of 24 intraneural injections resulted in histologic evidence of intrafascicular injection (95% confidence interval, 0.0%-16.3%). CONCLUSIONS: Ultrasonographic images compatible with nerve swelling during an injection are consistent with true intraneural injections as demonstrated by histologic analysis. Under the conditions studied, intensity of the stimulating current required to elicit motor response was not associated with intraneural needle placement. In the absence of fascicular injury, intraneural injections were associated with low injection pressure, although false-positive results can occur.

Hyperoxia impairs postnatal alveolar epithelial development via NADPH oxidase in newborn mice.

Hyperoxia disrupts postnatal lung development in part through inducing inflammation. To determine the contribution of leukocyte-derived reactive oxygen species, we exposed newborn wild-type and NADPH oxidase p47(phox) subunit null (p47(phox-/-)) mice to air or acute hyperoxia (95% O(2)) for up to 11 days. Hyperoxia-induced pulmonary neutrophil influx was similar in wild-type and p47(-/-) mice at postnatal days (P) 7 and 11. Macrophages were decreased in wild-type hyperoxia-exposed mice compared with p47(phox-/-) mice at P11. Hyperoxia impaired type II alveolar epithelial cell and bronchiolar epithelial cell proliferation, but depression of type II cell proliferation was significantly less in p47(-/-) mice at P3 and P7, when inflammation was minimal. We found reciprocal results for the expression of the cell cycle inhibitor p21(cip/waf) in type II cells, which was induced in 95% O(2)-exposed wild-type mice, but significantly less in p47(phox-/-) littermates at P7. Despite partial preservation of type II cell proliferation, deletion of p47(phox) did not prevent the major adverse effects of hyperoxia on alveolar development estimated by morphometry at P11, but hyperoxia impairment of elastin deposition at alveolar septal crests was significantly worse in wild-type vs. p47(phox-/-) mice at P11. Since we found that p47(phox) is expressed in a subset of alveolar epithelial cells, its deletion may protect postnatal type II alveolar epithelial proliferation from hyperoxia through effects on epithelial as well as phagocyte-generated superoxide.

Inclusion of a nitric oxide congener in the insufflation gas repletes S-nitrosohemoglobin and stabilizes physiologic status during prolonged carbon dioxide pneumoperitoneum.

A method to maintain organ blood flow during laparoscopic surgery has not been developed. Here we determined if ethyl nitrite, an S-nitrosylating agent that would maintain nitric oxide bioactivity (the major regulator of tissue perfusion), might be an effective intervention to preserve physiologic status during prolonged pneumoperitoneum. The study was conducted on appropriately anesthetized adult swine; the period of pneumoperitoneum was 240 minutes. Cohorts consisted of an anesthesia control group and groups insufflated with CO2 alone or CO2 containing fixed amounts of ethyl nitrite (1-300 ppm). Insufflation with CO2 alone produced declines in splanchnic organ blood flows and it reduced circulating levels of S-nitrosohemoglobin (i.e., nitric oxide bioactivity); these reductions were obviated by ethyl nitrite. In a specific example, preservation of kidney blood flow with ethyl nitrite kept serum creatinine and blood urea nitrogen concentrations constant whereas in the CO2 alone group both increased as kidney blood flow declined. The data indicate ethyl nitrite can effectively attenuate insufflation-induced decreases in organ blood flow and nitric oxide bioactivity leading to reductions in markers of acute tissue injury. This simple intervention provides a method for controlling a major source of laparoscopic-related morbidity and mortality: tissue ischemia and altered postoperative organ function.

Inhaled ethyl nitrite prevents hyperoxia-impaired postnatal alveolar development in newborn rats.

RATIONALE: Inhaled nitric oxide (NO) has been used to prevent bronchopulmonary dysplasia, but with variable results. Ethyl nitrite (ENO) forms S-nitrosothiols more readily than does NO, and resists higher-order nitrogen oxide formation. Because S-nitrosylation is a key pathway mediating many NO biological effects, treatment with inhaled ENO may better protect postnatal lung development from oxidative stress than NO. OBJECTIVES: To compare inhaled NO and ENO on hyperoxia-impaired postnatal lung development. METHODS: We treated newborn rats beginning at birth to air or 95% O(2) +/- 0.2-20.0 ppm ENO for 8 days, or to 10 ppm NO for 8 days. Pups treated with the optimum ENO dose, 10 ppm, and pups treated with 10 ppm NO were recovered in room air for 6 more days. MEASUREMENTS AND MAIN RESULTS: ENO and NO partly prevented 95% O(2)-induced airway neutrophil influx in lavage, but ENO had a greater effect than did NO in prevention of lung myeloperoxidase accumulation, and in expression of cytokine-induced neutrophil chemoattractant-1. Treatment with 10 ppm ENO, but not NO, for 8 days followed by recovery in air for 6 days prevented 95% O(2)-induced impairments of body weight, lung compliance, and alveolar development. CONCLUSIONS: Inhaled ENO conferred protection superior to inhaled NO against hyperoxia-induced inflammation. ENO prevented hyperoxia impairments of lung compliance and postnatal alveolar development in newborn rats.