Water-induced pressor response appears mediated through the activation of transient receptor potential channel TRPV4 on hepatic portal circulation in animals. We sought to elucidate the mechanism of portal vein signaling in this response. Forty-five rats were divided into four groups: control rats without water ingestion (WI), control rats with WI, portal vein denervation rats with WI (PVDWI), and TRPV4 antagonist-treated rats with WI (anti-TRPV4WI). Cardiovascular responses were monitored throughout the experiments. Data analysis was performed using descriptive methods and spectral and cross-spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV). Key results showed that at baseline (PreCS) before cold stress trial (CS), WI elicited robust pressor and tachycardia responses accompanied by spectral power changes, in particular, increases of low-frequency BPV (LFBPV) and very-LFBPV (VLFBPV), but decrease of very-low-frequency HRV. PVDWI, likewise, elicited pressor and tachycardia responses accompanied by increases of high-frequency BPV, high-frequency HRV, LFBPV, low-frequency HRV, and VLFBPV. When compared with WI at PreCS, WI at CS elicited pressor and tachycardia responses accompanied by increases of high-frequency BPV, LFBPV, and VLFBPV, whereas in WI, the CS-evoked pressor response and the accompanied LFBPV and VLFBPV increases were all tended augmented by PVDWI. When compared with WI and PVDWI at both PreCS and CS, however, anti-TRPV4WI attenuated their pressor responses and attenuated their increased LFBPV, VLFBPV, and very-low-frequency HRV. The results indicate that the portal vein innervation is critical for a buffering mechanism in splanchnic sympathetic activation and water-induced pressor response.

Previous studies have indicated that patients with migraine have a higher prevalence of risk factors known to be associated with cardiovascular diseases. There are also shared epidemiology and molecular mechanisms between migraine and abdominal aortic aneurysm (AAA). We hypothesized that patients with migraine could have an increased risk of AAA. To test this hypothesis, we used the National Health Insurance Research Database (NHIRD) to evaluate whether associations exist between migraine and AAA. The data for this nationwide population-based retrospective cohort study were obtained from the NHIRD in Taiwan. The assessed study outcome was the cumulative incidence of AAA in patients with migraine during a 15-year follow-up period. Among the 1,936,512 patients from the NHIRD, 53,668 (2.77%) patients were identified as having been diagnosed with migraine. The patients with migraine had a significantly higher cumulative risk of 3.558 of developing an AAA 5 years after the index date compared with the patients without migraine. At the end of the 15-year follow-up period, a significantly higher incidence of AAA (0.98%) was observed in the patients with migraine than in those without migraine (0.24%). We revealed an association between the development of migraine and AAA.

No abstract

Spasticity measured using clinical scales, such as the modified Ashworth scale (MAS), may not sufficiently evaluate the effectiveness of therapeutic interventions and predict prognosis. This study aimed to compare changes in H-reflex excitability in the spastic and unimpaired upper and lower limbs of patients with acute and chronic stroke. We also investigated the relationship between the degree of spasticity as assessed by the MAS and motor neuron pool excitability with by analyzing H-reflex excitability. Sixty adult patients with a first-ever stroke were recruited for this study. MAS scores were recorded in the post-stroke upper and lower limb muscles. H-reflexes and M-responses of the bilateral flexor carpi radialis and soleus were tested by stimulating the median and tibial nerves. The results showed that both the ratio of the maximal size of the H-reflex (Hmax) to the maximal size of the M-response (Mmax) and the ratio of the developmental slope of H-reflex (Hslp) to that of the M-responses (Mslp) were significantly higher on the spastic side than on the unimpaired side for the upper and lower limbs. In contrast, the ratio of the threshold of the H-reflex (Hth) to the threshold of the M-response (Mth) only showed significant differences between the two sides in the upper limbs. The Hslp/Mslp paretic/non-paretic ratio was increased in patients with MAS scores of 2 or 3 compared to MAS scores of 1 for both the upper and lower limbs, whereas the Hmax/Mmax paretic/non-paretic ratio showed significant differences between MAS scores of 2 or 3 and 1 only in the upper limbs. Moreover, in either the spastic or unimpaired sides, there were no significant differences in any of the three motoneuron pool excitability parameters, Hmax/Mmax, Hslp/Mslp, and Hth/Mth, between the shorter chronicity (time post-stroke ≤6 months) and longer chronicity groups (time post-stroke >6 months) for both the upper and lower limbs. These results suggest that Hslp/Mslp could be a potential neurophysiological indicator for evaluating the degree of spasticity in both the upper and lower limbs of patients with hemiplegia. The MAS and Hslp/Mslp characterize clinical and neurophysiologic spasticity, respectively, and could be used as an integrated approach to evaluate and follow up post-stroke spasticity.