Vasopressin decreases pulmonary-to-systemic vascular resistance ratio in a porcine model of severe hemorrhagic shock.

Vasopressors are gaining renewed interest as treatment adjuncts in hemorrhagic shock. The ideal vasoconstrictor will increase systemic blood pressure without increasing pulmonary vascular resistance (PVR), which hinders pulmonary perfusion and exacerbates hypoxemia. However, the selectivity of pressors for pulmonary versus systemic vasoconstriction during hemorrhage has not been characterized. The purpose of this study was to test the hypothesis that vasopressin (VP) has distinct effects on pulmonary versus systemic hemodynamics, unlike the catecholamine vasopressors norepinephrine (NE) and phenylephrine (PE). Anesthetized and ventilated pigs were assigned to resuscitation with saline only (n = 7) or saline with VP (n = 6), NE (n = 6), or PE (n = 6). Animals were hemorrhaged to a target volume of 30 mL/kg and a mean arterial pressure of 35 mmHg. One hour after the start of hemorrhage, animals were resuscitated with saline up to one shed blood volume, followed by either additional saline or a vasopressor. Hemodynamics and oxygenation were measured hourly for 4 h after the start of hemorrhage. Vasopressin increased systemic vascular resistance (SVR) while sparing the pulmonary vasculature, leading to a 45% decrease in the PVR/SVR ratio compared with treatment with PE. Conversely, NE induced pulmonary hypertension and led to an increased PVR/SVR ratio associated with decreased oxygen saturation. Phenylephrine and crystalloid had no significant effect on the PVR/SVR ratio. Sparing of pulmonary vasoconstriction occurs only with VP, not with administration of crystalloid or catecholamine pressors. The ability of VP to maintain blood oxygenation indicates that VP may prevent hypoxemia in the management of hemorrhagic shock.

Percutaneous temporary aortic valve: a proof-of-concept animal model.

BACKGROUND AND AIM OF THE STUDY: An early prototype of a temporary aortic valve (TAV) catheter system was evaluated for its potential to serve as an integrated device for aortic valve intervention and replacement. The prototype consisted of two essential components: a central catheter for the delivery of aortic valve interventional tools (valve debulking, resection, replacement); and a balloon-inflatable temporary valve for hemodynamic support when the native aortic valve is removed. After valve replacement, the TAV catheter system is designed to be readily withdrawn from the subject. METHODS: Individual aspects of both components of the prototype were examined in experiments with four pigs. The central catheter was used to deliver a self-expanding stent for native aortic valve ablation to create acute severe aortic insufficiency (AI). The balloon-TAV was deployed in the proximal aorta to control the induced AI. Electrocardiographic (ECG), cardiac output (CO), pulmonary wedge pressure (PWP), left ventricular (LV) pressure, and aortic pressure proximal and distal from the TAV were recorded. RESULTS: The central catheter was successful in delivering and deploying the valve ablation stent at the annulus to create massive AI; the LV diastolic pressure was increased from 12.6 +/- 1.1 to 32.4 +/- 2.0 mmHg (p < 0.001) with valve ablation. The deployed TAV in the proximal aorta led to a re-narrowing of the distal pulse pressure with a drop in the LV diastolic pressure to 21.5 +/- 1.5 mmHg (p < 0.001). During TAV support, some PWP lowering and a CO rise occurred, but these did not achieve statistical significance; no significant acute ECG changes were noted. CONCLUSION: In this early prototype, the TAV catheter system demonstrated the potential to serve as an integrated device for both aortic valve modification and replacement.