Photothermal ablation of human lung cancer by low-power near-infrared laser and topical injection of indocyanine green.

The present study was designed to evaluate the efficacy of photothermal ablation therapy for lung cancer by low-power near-infrared laser and topical injection of indocyanine green (ICG). In vitro study 1: an 808 nm laser with 250 mW was irradiated for 10 minutes using different dilutions of ICG and the temporal thermal effect was monitored. ICG (1 mL of 0.5 g/L) was heated to a temperature of >30°C from the base temperature by laser irradiation. In vitro study 2: the cytotoxic effect of hyperthermia on human lung cancer cells was examined in different temperature and time settings. Cell viability was quantified by both an MTS assay and reculturing. Fatal conditions evaluated by reculturing were as follows: thermal treatment at 55°C for 5 minutes, 53°C for 10 minutes, and 51°C for 15 minutes. The MTS assay study suggested that thermal treatment at 59°C for 5 minutes and 57°C for 20 minutes showed a severe cytotoxic effect. In vivo study: nude mouse subcutaneous NCI-H460 human lung cancer xenograft models were used for the study. Saline or 0.5 g/L of ICG was injected topically into the tumor (n=3/group). Tumors were irradiated with a laser at 500 mW for 10 minutes. Although the tumor diameter reached 1 cm within 24 days after treatment in all 3 mice using saline/laser, tumor sizes were gradually reduced in all 3 mice using the ICG/laser. In 2 of the 3 mice using ICG/laser, tumors had disappeared macroscopically. The efficacy of the photothermal ablation therapy by low-power near-infrared laser and a topical injection of ICG was clarified using a mouse subcutaneous a lung cancer xenograft model.

Low-dose edaravone injection into the clamped aorta prevents ischemic spinal cord injury.

Previous studies have indicated that high-dose intravenous edaravone (3-10mg/kg) protects against ischemic spinal cord injury. This study examined whether direct injection of low-dose edaravone into the clamped segment of the aorta prevents ischemic spinal cord injury. Spinal cord ischemia was induced in rabbits by aortic clamping below the renal artery and above the aortic bifurcation for 15min at normothermia. In groups A and B, 3 and 1mg/kg of edaravone, respectively, was injected into the clamped segment of the aorta immediately following aortic clamping. In group C, saline was injected. Neurological function was assessed at 8, 24, and 48hr and 7 days after reperfusion with Tarlov criteria. The spinal cord was histologically examined at 7 days with hematoxylin-eosin staining and in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. The Tarlov score remained grade 4 throughout the period in groups A and B, whereas it dropped to grade 0 or 1 at 7 days in group C, significantly higher in the former two groups. The number of intact motor neurons was significantly greater in groups A and B with less necrotic motor neurons than in group C. There was no significant difference in terms of spinal cord protection between groups A and B. There was no TUNEL-positive neuron in any group, indicating the absence of apoptosis. Low-dose intra-aortic edaravone injection prevents immediate neuronal injury by reducing neuronal cell damage in the early stage as well as delayed neuronal injury at 7 days.

Transcranial motor-evoked potentials following intra-aortic cold blood infusion facilitates detection of critical supplying artery of spinal cord.

OBJECTIVE: In order to determine whether critical intercostal artery is present in the aneurysm during descending thoracic or thoracoabdominal aortic surgery, changes of transcranial motor-evoked potentials (Tc-MEPs) were monitored following infusion of cold blood into the aorta as an adjunct 'on-site assessment'. Accuracy of this method was evaluated. METHODS: Fourteen patients were examined for Tc-MEPs changes following infusion of cold blood (4 degrees C, 300-450 ml) into the aneurysm. The intercostal arteries in the aneurysm were reconstructed when the Tc-MEPs amplitude decreased to below 50% of the baseline within 3 min after cold blood infusion. When the amplitude did not decrease, every intercostal artery in the aneurysm was ligated. RESULTS: The Tc-MEPs amplitude did not decrease in eight cases (57%), while it decreased in six cases (43%). In the former, no case presented with paraplegia despite every intercostal artery being ligated. In the latter, the amplitude recovered after reconstruction in four patients, who had no paraplegia postoperatively. In the remaining two cases, however, the amplitude did not recover: one died of multiple organ failure with postoperative assessment unfeasible; the other developed paraplegia following surgery. Except one case with operative death, both sensitivity and specificity of our criteria with cold blood infusion was 100% in this series. CONCLUSIONS: Cold blood infusion into the clamped segment of aorta accelerates Tc-MEPs changes and can possibly reduce ischemic insults of spinal cord during diagnostic process, while it accurately detects presence of critical intercostal artery in the segment. This method appears to be promising adjunct on-site assessment.

Intra-aortic injection of propofol prevents spinal cord injury during aortic surgery.

OBJECTIVE: We investigated whether propofol, a widely used anesthetic, injected into clamped aortic segments quickly attenuated transcranial spinal motor-evoked potential (MEP) amplitudes and protected against spinal cord injury during thoracoabdominal aortic surgery. METHODS: Eighteen beagle dogs were divided into three groups (n=6, each group): group 1 (20 ml of saline, intra-aortic injection), group 2 (1.5 mg/kg of propofol, intravenous injection), and group 3 (1.5 mg/kg of propofol, intra-aortic injection). Aortic cross-clamping was performed for 30 min. In each group, MEP amplitudes were recorded before, during, and after aortic cross-clamping. Tarlov score and histopathological examination were used to evaluate the protective effects of intra-aortic propofol injections. RESULTS: MEP amplitudes in group 3 attenuated to a value that was 60% of the control in just a minute after aortic cross-clamping, but maintained 40% of the control value during aortic cross-clamping. However, MEP amplitudes in groups 1 and 2 gradually attenuated and almost disappeared. Groups 1 and 2 amplitudes were lower than those in group 3, 30 min after aortic cross-clamping (p<0.001). Twenty-four hours after ischemia, the Tarlov score in group 3 was 3.5+/-0.5 and was higher than scores from groups 1 and 2, which were 0.5+/-0.5 and 1.3+/-1.2 (mean+/-SD, p<0.001, and p<0.001), respectively. Histopathologically, normal spinal cord motor neurons in group 3 were preserved to a significantly greater extent than in groups 1 and 2 (p=0.0031, and p=0.0282, respectively). There was a strong correlation between Tarlov scores at 24h and the number of normal motor neurons in the anterior horns of spinal cords (r=0.897; p<0.001). CONCLUSIONS: Intra-aortic propofol injections produce the quick suppression of MEP amplitudes and protect spinal cords from ischemia during aortic cross-clamping.