Response to: Comment on “Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema”

Received Dec 15, 2017; Accepted Mar 28, 2018

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We would like to thank G. Sikri and S. Bhattachar for their insightful comment [1] on our article suggesting a role of low-grade cellular-based inflammation as indicated by elevated soluble urokinase-type plasminogen activator receptor (suPAR) plasma concentrationon in the pathogenesis of high altitude pulmonary edema (HAPE) [2].

The adaptation of the cardiovascular system to hypobaric hypoxia is an important entity in all high altitude studies. Recent data from a study using pharmacological blockade of the sympathetic and parasympathetic nervous system [3] suggest that even though sympathetic nervous system activity increases as compared to normoxic state, parasympathetic withdrawal rather than sympathetic activation seems to be the cause of the increase in heart rate observed in healthy humans subjected to hyperbaric hypoxia. Even though the effect of dexamethasone on the autonomic nervous system is not fully understood, dexamethasone administration has previously been shown to decrease heart rate during hypoxic exposure [4]. It is thus in concordance with current literature that dexamethasone intake is the likely cause of the different course of HR during hypoxic exposure seen in our study population (ΔHR +16/min versus −7/min, $p<0.01$, in the no prophylaxis ($n=31$) versus the dexamethasone prophylaxis ($n=10$) group).

As G. Sikri and S. Bhattachar point...