The effects of norepinephrine on hemodynamics, vascular elasticity, cardiac pump function, and inflammatory factors in patients with septic shock remained unknown. In this study, we included 124 cases of severe septic shock patients in our hospital. The patients were randomly divided into control group (treated with dopamine) and experimental group (treated with dopamine plus norepinephrine), while the hemodynamic index (heart rate (HR)), blood vessel elasticity index, heart pump function, and inflammatory factor index were recorded. After 12 h of treatment, both groups showed decreased HR, increased levels of cardiac index (CI), mean arterial pressure (MAP), central venous pressure (CVP), peripheral vascular resistance index (PVRI), and vascular elasticity (P < 0.05). To date, lower HR, higher levels of CI, MAP, CVP, and PVRI were observed in the experimental group (P < 0.05). Furthermore, the vascular elastic coefficient, stiffness index, arterial compliance, and the precursors of plasma amino-terminal brain natriuretic peptide were also significantly higher in the experimental group than those in the control group (P < 0.05). However, inflammatory cell tumor necrosis factor alpha factor test group (TNF alpha), interleukin-1 (IL-1), and interleukin-6 (IL-6) concentrations were significantly lower than the control group (P < 0.05), compared to experimental group (P < 0.05). This research indicates that phenylephrine could significantly improve hemodynamics in patients with severe septic shock, by maintaining blood vessel elasticity, improving heart pump function, and reducing the inflammatory factors' activities, and this method could be used as a line of vascular tension of the medications used in patients with septic shock.

To investigate the molecular mechanism of dihydrocapsaicin (DHC)-induced mild hypothermia in rats, and to compare its protective effect on the central nervous system with that of a conventional method of inducing hypothermia, 24 healthy male Sprague Dawley rats were randomly divided into four groups based on the following conditions: control group, cardiopulmonary resuscitation (CPR) group, body surface cooling group, and DHC group. Tracheal clipping was used to mimic asphyxia arrest. Rats were assessed for their neurological deficit scores. After sacrifice, immunohistochemical staining was used to examine caspase-3 expression in the cerebral cortex and TRPV1 (transient receptor potential vanilloid subfamily, member 1) expression in the hypothalamus. Terminal TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining was used to evaluate cell apoptosis in the cerebral cortex. Furthermore, intracellular Ca concentration in the hypothalamus and arginine vasopressin (AVP) concentration in ventral septal tissues were also detected in these four groups. Results of our study showed that neurological deficit scores in the DHC group were significantly higher than those in the CPR and body surface cooling groups (p < 0.05). Caspase-3 expression in the cerebral cortex of control group rats was significantly lower than that in other three groups (p < 0.05). Hypothalamic TRPV1 expression, hypothalamic intracellular Ca concentration, and AVP concentration in the ventral septum in the DHC group were significantly higher than that in the other three groups (p < 0.05). Within these three groups, there were significantly fewer apoptotic cells in the DHC and body surface cooling group rats than in the CPR group rats (p < 0.05). DHC has the neuroprotective effect. DHC induced mild hypothermia and reduces apoptosis through a mechanism whereby DHC activates TRPV1 on hypothalamic cells to cause a large Ca influx, which alters corresponding physiological functions and causes the release of AVP to induce hypothermia.