Letter to the Editor - Methylene Blue as Treatment for Contrast Medium-induced Anaphylaxis

Nitric oxide seems to play an important pathophysiological role in modulating the systemic changes associated with anaphylaxis.1 Considering nitric oxide to be the final mediator of vasoplegia, we have used methylene blue to treat anaphylactic shock secondary to radio-contrast material and penicillin2 in three patients, with a good immediate response. We have also used the drug to treat vasoplegia in cardiac surgery.3,4,5,

Sildenafil selectively inhibits acute pulmonary embolism-induced pulmonary hypertension

Selective pulmonary vasodilators attenuate acute pulmonary embolism (APE)-induced pulmonary hypertension. We examined the effects of intravenous sildenafil on the hemodynamic and respiratory changes caused by APE in anesthetized dogs. Sham operated animals (n = 3) received only saline infusions. APE was induced by intravenous injections of microspheres in amounts adjusted to increase mean pulmonary artery pressures (MPAP) by 20 mmHg. Hemodynamic evaluation was performed and arterial blood samples were drawn for blood.-as analysis at baseline, 15 and 30 min after APE was induced, and then 15, 30, and 45 min after the sildenafil infusion (1 mg kg(-1) infused intravenously in 15 min followed by 0.3 mg kg(-1)h(-1) for 30 min) started in the Sildenafil group (n = 7), or saline infusion started in the control group (n = 8). APE induced sustained pulmonary hypertension and 325% increase in pulmonary vascular resistance index (PVRI) without significant changes in the other hemodynamic parameters. While the animals in the control group showed no further changes in MPAP and PVRI, a significant decrease in MPAP and PVRI (-25 and -45%, respectively; P < 0.05 both) was observed with sildenafil. No significant changes in the other hemodymamic parameters were observed in both groups. APE decreased PaO2, whereas sildenafil attenuated the decrease in PaO2 (P < 0.05). We conclude that intravenous sildenafil can selectively attenuate the increases in MPAP and PVRI after APE. (C) 2005 Elsevier Ltd. All rights reserved.18318118

Hemodynamic effects of combined sildenafil and L-arginine during acute pulmonary embolism-induced pulmonary hypertension

Sildenafil attenuates acute pulmonary embolism-induced pulmonary hypertension. However, the hemodynamic effects of sildenafil in combination with other vasodilators during acute pulmonary embolism have not been examined yet. In the present study, we examined the hemodynamic effects of combined sildenafil (0.25 mg/kg, i.v.) and L-arginine (100, 200, 500, and 1000 mg/kg/h, i.v.) in an anesthetized dog model of acute pulmonary embolism. Plasma nitrite/nitrate (NOx) and cGMP concentrations were determined using an ozone-based chemiluminescence assay and a commercial enzyme immunoassay, respectively. We found that L-arginine alone did not attenuate acute pulmonary embolism-induced pulmonary hypertension. However, significant decreases in mean pulmonary artery pressure were observed 30, 45, 60, and 75 min after the administration of sildenafil alone or after the combined administration of sildenafil and L-arginine (all P<0.05). No significant differences among groups were observed in the respiratory parameters. While L-arginine significantly increased NOx concentrations, cGMP concentrations increased only when sildenafil was administered (all P<0.05). These results suggest that while sildenafil attenuates acute pulmonary embolism-induced pulmonary hypertension, L-arginine does not enhance the beneficial hemodynamic effects of sildenafil. In addition, these findings suggest that stimulation of NO synthesis with L-arginine during acute pulmonary embolism does not produce beneficial effects. (c) 2005 Elsevier B.V. All rights reserved.5244169912613