Purpose Hemodynamic instability during tracheal intubation in elderly patients poses significant perioperative risks. This study aimed to determine the effective doses (ED50/ED95) of remifentanil combined with remimazolam to suppress intubation-induced stress responses while minimizing hypotension in patients aged ≥60. Patients and Methods In this prospective, double-blind trial, 29 elderly patients received remimazolam (0.3 mg/kg) followed by rocuronium and remifentanil (initial dose: 1 µg/kg, adjusted via Dixon’s up-down method). Hemodynamic parameters (blood pressure, heart rate, systemic vascular resistance, cardiac output) and bispectral index (BIS) were recorded. Probit regression analyzed dose–response relationships. A positive hemodynamic response was defined as an increase in systolic blood pressure or heart rate exceeding 20% of the baseline value within 5 minutes after endotracheal intubation. Dixon’s up-and-down method and probit regression analysis to determine the ED50 and ED95 of remifentanil combined with remimazolam to suppress intubation-induced stress responses in elderly patients. Results The ED50 and ED95 of remifentanil were 0.85 µg/kg (95% CI: 0.80–0.90) and 0.97 µg/kg (95% CI: 0.91–1.21), respectively. Positive responders showed elevated blood pressure at 30s–1 min post-intubation (P<0.05), while cardiac output and systemic vascular resistance remained comparable between groups. Hypotension incidence was low (14.3–20%), with transient BIS elevations (60–70) in 51.7% of patients but no intraoperative awareness. Conclusion In this exploratory dose-finding study, the estimated ED50 and ED95 of remifentanil for suppressing intubation-related hemodynamic responses during remimazolam-based induction were 0.85 and 0.97 μg/kg, respectively.
Yue Ma, Jianting Huang, Haipeng Zhou et al.· Clinical Interventions in Ag...· 0 citations
Neuroinflammation is recognized as a pivotal pathological process underlying a spectrum of neurological disorders. The exploration of natural flavonoids as therapeutic agents has substantially advanced our understanding of strategies to mitigate neuroinflammatory injury. Accumulating evidence indicates that kaempferol—a dietary flavonoid abundantly present in various fruits and vegetables—exerts potent neuroprotective effects in multiple neurological conditions. Its beneficial actions are mediated through multi-target mechanisms, primarily involving the suppression of microglial activation, modulation of immune cell reactivity, and enhancement of endogenous antioxidant defenses. These mechanisms collectively contribute to reduced production of inflammatory mediators, alleviation of oxidative stress, and inhibition of neuronal apoptosis, thereby counteracting the pathogenesis of various neuroinflammatory diseases. This review summarizes current knowledge on the protective role of kaempferol in the pathogenesis and progression of central nervous system disorders. We further elucidate the underlying molecular and cellular mechanisms, as well as autophagy and oxidative stress. Additionally, potential challenges in clinical translation, such as bioavailability and blood-brain barrier permeability, are discussed to guide future research in this promising field. Elucidating the pleiotropic actions of kaempferol will not only deepen our understanding of its pharmacodynamics but may also open new avenues for the prevention and treatment of neuroinflammatory-related neurological diseases.
Yanan Zou, Jianting Huang, Junbo Yin et al.· Frontiers in Immunology· 0 citations