# Effect of Controlled Expiratory Pressures on Cerebrovascular Changes During Valsalva Maneuver
## 4 Discussion
Repeated VM stimulation, particularly with a high-pressure VM of 40 mmHg, can increase the RI. Since RI tends to increase as vascular stiffness increases, repeated VMs could lead to an increase in PWV. RI and HR showed significant differences between PRE and POST VM only at 40 mmHg VM, likely due to the baroreceptor reflex response. In POST1, HR decreased in response to an overshoot in BP. The increase in peripheral vascular resistance due to sympathetic activation in phase II could increase RI until phase IV. In other words, the response to hypertensive stimuli appeared more clearly at 40 mmHg than at 30 mmHg VM. In particular, an increase in RI indicates a limitation of the end-diastolic velocity, which suggests a circulation problem in small vessels [35]. Thus, 40 mmHg VM may be useful for testing sympathetic responses, but it seems less suitable as a stimulus to relieve vascular stiffness. Brain hemodynamic function showed different changes following VM at the two pressures. A decrease in the right HbO after VM was observed only at 30 mmHg VM, while no significant change was observed at 40 mmHg VM. A decrease in HbO level implies an increase in cerebral oxygen consumption during the VM [36]. Previous studies have shown that VM causes changes in autonomic regulation mechanisms and cardiovascular function and contributes to increased brain activity in the brainstem and cerebellum [37]. At 40 mmHg VM, the right rSO2 significantly increased after VM (\(p\) = 0.035). In particular, an increase occurred during the VM, while a significant increase was observed in POST1. This shows that VM influences an increase in rSO2. According to the cerebral autoregulation system, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) affect cerebral blood flow. Generally, when BP increases at VM onset, ICP also rises, which does not significantly alter CPP, leading to only a slight increase in cerebral blood velocity (Phase I). Moreover, in Phase IIa, there is a significant decrease in CPP due to suppressed venous return, reduced BP, and increased ICP, which has been reported to lead to a substantial reduction in cerebral flow. However, in phase IV, increased BP and cerebral blood velocity were observed [11]. This phenomenon may explain the notable increase in rSO2 during POST1 compared to the VM phase in this study. Indeed, one previous study reported that as blood pressure increases, cerebral saturation also increases [38], and it was also reported that there is a positive correlation with HbO [39]. In other words, the blood flow rate and blood pressure increased by the VM have a strong relationship with increased rSO2, and increased arterial oxygen saturation can act as a stimulus for vasoconstriction, which appears to be the mechanism for increasing RI [40]. Based on the results, the 30 mmHg VM can improve vascular function with fewer changes in hemodynamics compared to the 40 mmHg VM. This suggests that the VM can be used not only as a conventional method for assessing autonomic nervous system function but also for stimulating vascular elasticity.