Acute Beneficial Effects of Sodium Nitroprusside in a Rabbit Model of Massive Pulmonary Embolism Associated with Circulatory Shock

Abstract

We established a rabbit model of acute massive pulmonary embolism (PE) with associated circulatory shock using autologous blood clots. Rabbits were randomly assigned to a sham operation group (S group), model group (M group; equal volume of saline intravenously after shock), and sodium nitroprusside group (SNP group; sodium nitroprusside intravenously after shock). SNP treatment significantly decreased mean pulmonary arterial pressure and increased mean arterial pressure and arterial partial pressure of oxygen and resulted in a partial reversal of the acute circulatory failure. The shock-reversal rate was 0% in the M group and 80% in the SNP group. Moreover, pulmonary artery angiography and echocardiography examinations evidenced alleviated PE-induced changes after SNP therapy. 5-Hydroxytryptamine was significantly reduced in both PE and non-PE tissues, thromboxane A level was significantly reduced in PE and tended to be lower in non-PE tissues, neutrophil accumulation was significantly reduced in both PE and non-PE tissues after SNP therapy. Our study demonstrated that pulmonary vasospasm in the nonembolic region might be a major pathologic factor leading to reduced left ventricular filling and circulatory shock after massive PE. Reduction of pulmonary vasospasm in the nonembolic area after SNP might serve as a major therapeutic mechanism involved in the observed beneficial effects of SNP in this model.

Association Between Inflammatory Mediators and Pulmonary Blood Flow in a Rabbit Model of Acute Pulmonary Embolism Combined With Shock

“…Pulmonary artery spasm and blood flow attenuation could jointly result in the reduction of blood filling to the left ventricle. Our previous studies have shown that pulmonary artery spasm in both PE and non-PE tissues contributed to acute pulmonary failure in this MPE model ( Yu et al, 2018 ; Wang et al, 2019 ). The present study further highlighted the potential role of increased inflammatory responses in both PE and non-PE tissues on enhancing the vicious progression of pulmonary hypertension in the disease course of MPE.…”

“…The 5F sheath tube (Radiofocus TERUMO) was inserted into the femoral artery. Second, the MPE model was established as previously described ( Yu et al, 2018 ; Wang et al, 2019 ). The autologous blood clots [3 mm (± 0.5) × 10 mm] were prepared and placed at the tail end of the 4F catheter and then slowly injected into the main pulmonary artery of the rabbit with 5 mL saline.…”

“…At the end of the experiment, the rabbits were sacrificed under deep anesthesia ( Yu et al, 2018 ). Based on a previous report ( Dias-Junior et al, 2006 ), 120 min post MPE was chosen for measurement of inflammation.…”

“…Several studies have explored means to reduce the high mortality in the acute phase of massive PE (MPE) and improve its long-term prognosis, however, the achieved benefits were limited ( Kinoshita et al, 2000 ; Neto-Neves et al, 2011 ; Chun et al, 2012 ). Our previous studies ( Yu et al, 2018 ; Wang et al, 2019 ) found that reduced pulmonary artery blood flow in case of APE was jointly induced by pulmonary artery spasm in PE tissues and pulmonary vasculature spasm in non-PE regions. Nonetheless, the detailed mechanism regarding pulmonary vasospasm of PE and non-PE tissues in MPE is not fully understood.…”

A novel echocardiographic parameter for assessment of right ventricular function in acute pulmonary embolism: an experimental study

“…The acute PE model was established in this study by intravenous infusion of autologous blood clot [ 8]. Rabbits were anaesthetized using intravenous injection of pentobarbital sodium (Sigma-Aldrich) at a dosage of 30 mg/kg via ear marginal venous.…”