Introduction: Pronounced vasodilatation during vasovagal syncope indicate the role of endothelium in its patomechanis. The endothelial release of nitric oxide is seems to be an important factor in the vasovagal syncope. The aim of study was evaluation of Nitric Oxide (NO) serum changes during head-up tilt-test in patients with vasovagal syncope (VVS). Study population: 25pts (11 men, 14 women) aged 18-42 years (median of age: 21yrs) with VVS referred to HUTT. Cardio- and neurological causes of syncope were previously excluded in all studied pts.
Methods: In all pts HUTT according Westminetr protocol was done with sublingual nitroglycerine (NTG) provocation, in the case of negative result of passive tilting. During HUTT continuous, noninvasive beat-to-beat monitoring of heart rate and blood pressure were performed using NEXFIN (Bmeye) monitor. Before the test, after completion of both – passive and active phases (after NTG provocation) and 15 minutes after finishing the test (syncope induction or protocol completion) the blood samples were taken, to evaluation of serum concentration of NO2- and NO3-. Serum concentration of NO was evaluated as the difference before concentration of NO2- and NO3-. Changes of NO serum concentrations during HUTT were analysed in relation to the type of vasovagal response during the test.
Results: HUTT was positive in 21 pts (84%) – in 5 pts there were cardioinhibitory response, in 14 pts. – mixed and in 2 - vasodepressive. Serum NO concentration before the test in pts with negative HUTT was significantly lower in relation to pts with positive HUTT (12,2 vs 22,6 uM). After completion of passive phase of HUTT significant decline of NO concentration was noticed in HUTT-negative pts (9,7 vs 12,1 uM), whereas pts with positive HUTT revealed non-significant trend to decrease. (20,7 vs 22,6 uM). After sublingual NTG administration, increase of NO concentration was observed in both, HUTT negative and HUTT positive pts. (HUTT- : 14,2 vs 9,7 p < 0,01; HUTT + : 25,3 vs 20,7 uM p < 0,05). After the test, NO concentration decreased below the value observed prior to HUTT. There were no relation between serum NO concentration and type of vasovagal response to the orthostatic stress.
Conclusions:1. Serum nitric oxide concentration decreased during the passive phase of HUTT, next significantly increased after NTG provocation and finally decreased below initial values. This changes were much more pronounced in patients with negative result of the HUTT 2. Syncope induction during HUTT was related to significantly higher values of serum nitric oxide concentration in relation to the HUTT-negative patients. 3. Changes of nitric oxide concentrations seems to important role in the pathomechanism of vasovagal response to orthostatic stress in patients with vasovagal syncope.