A simple and effective technique for identification of intersegmental planes by infrared thoracoscopy after transbronchial injection of indocyanine green.

OBJECTIVE: Pulmonary segmentectomy has been recognized as an operative option for complete resection of early-stage lung cancer in patients with poor pulmonary function. However, identification of anatomic pulmonary segments is sometimes difficult in patients with emphysema. We developed an intraoperative method for identifying intersegmental planes of the lung with high-sensitivity infrared fluorescence imaging after transbronchial injection of indocyanine green. METHODS: The study included 10 patients with early-stage lung cancer who underwent thoracoscopic segmentectomy. Under general anesthesia, indocyanine green was injected into the bronchus of target pulmonary segments. The target segments of the lung were identified using the indocyanine green fluorescence endoscope (Hamamatsu Photonics, Hamamatsu, Japan). The intersegmental lines and planes were identified and allowed removal of the segments. To evaluate operative outcomes, we compared the indocyanine green injection group with a retrospective control group with 10 matched-pair patients who underwent traditional thoracoscopic segmentectomy. RESULTS: Accurate, real-time intraoperative detection of indocyanine green with an infrared thoracoscope was confirmed. Sparing of intersegments was safely performed using both staples and electric cautery. Furthermore, infrared thoracoscopy allowed visualization of any residual portion of resected segments after segmentectomy. There was no difference between the experimental indocyanine green and control groups in terms of operative time, duration of postoperative chest drainage, or postoperative complications. Length of stay was shorter in the indocyanine green group than in the control group (P = .055). CONCLUSIONS: Transbronchial indocyanine green injection into the relevant bronchus with the use of an infrared thoracoscope allows identification of intersegmental lines and planes during thoracoscopic segmentectomy.

[The influence of intraoperative oxygen inhalation on patients with idiopathic pulmonary fibrosis].

Idiopathic pulmonary fibrosis (IPF) is a high risk factor for acute exacerbation of interstitial pneumonia (IP) after pulmonary resection. Other risk factors for inducing IP exacerbation are thought to be intraoperative inhalation of high concentration of oxygen, high pressure mechanical ventilation, major thoracic surgery, massive blood transfusion and preoperative chemotherapy and irradiation. The prophylactic strategy for this phenomenon has not been established, although mechanical ventilation by low pressure and low oxygen concentration, minimum invasive surgery and prophylactic administration of steroid, ulinastatin and sivelestat sodium hydride are performed. Acute exacerbation of IP is the same concept with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). This pulmonary injury is closely associated with reactive oxygen species (ROS). In particular, high concentration of oxygen induces excessive production of ROS. ROS stimulates alveolar macrophages and neutrophils to release inflammatory cytokines, such as TNF-alpha, IL-8, IFN-gamma, IL-6 and IL-1beta. These cytokines injure pulmonary endothelium and alveolus, and atelectasis, pulmonary hemorrhage, lung edema, hyalinization and alveolar thickness occur, and this is a manifestation of ALL Therefore, although there is no evidence, high pressure ventilation and inhalation of high oxygen concentration during anesthesia should be avoided.

Dehydroepiandrosterone sulfate induces acute vasodilation of porcine coronary arteries in vitro and in vivo.

Although an inverse relationship between dehydroepiandrosterone sulfate (DHEAS) and coronary artery disease has been demonstrated in men, the vascular effects of DHEAS are not well defined. The vasoactive effects of intracoronary DHEAS and testosterone (0.1 nM to 1 microM) were examined in vivo in 24 pigs. Epicardial cross-sectional area was measured by intravascular ultrasound, and coronary flow velocity by intravascular Doppler velocimetry. We also examined the effects of antagonism of the androgen receptor, nitric oxide synthase, and potassium channels on DHEAS-induced vasodilation in vitro in coronary rings from male and female pig hearts. DHEAS and testosterone induced increases in cross-sectional area, average peak velocity, and coronary blood flow. The maximal increase in coronary blood flow in response to testosterone was 1.26-fold (P=0.02), and in average peak velocity 1.43-fold (P=0.05), greater than that to DHEAS, whereas increases in cross-sectional area were similar. Vasodilation to both hormones was rapid, with maximal responses occurring <10 minutes after administration. In vitro, DHEAS and testosterone induced vasodilation in coronary rings, greater with testosterone. At doses of 0.1 and 1 microM, the vasodilator effects of DHEAS and testosterone were inhibited by the androgen receptor antagonist flutamide but not the estrogen receptor antagonist ICI 182,780. At 10 microM, neither DHEAS- nor testosterone-induced vasorelaxation was inhibited by flutamide, ICI 182,780, L-NAME, or deendothelialization, but both were attenuated by pretreatment with glibenclamide. No gender differences were observed in any of the responses examined. In conclusion, DHEAS is an acute coronary artery vasodilator, but less potent than testosterone. Its effect might be mediated via androgen receptors and may involve ATP-sensitive potassium channels.