PHENYLEPHRINE-INDUCED ELEVATIONS IN BLOOD PRESSURE IS ATTENUATED IN HEAT STRESSED HUMANS
Jisheng Cui, Thomas E. Wilson, Craig G. Crandall
Abstract
Jisheng Cui, Thomas E. Wilson, Craig G. Crandall
Abstract
PURPOSE: The objective of this study was to test the hypothesis that phenylephrine-induced elevations in blood pressure is attenuated in heat stressed humans. METHODS: In both normothermic and heat stress conditions, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects. RESULTS: Wholebody heating significantly increased sublingual temperature by 0.5°C, increased muscle sympathetic nerve activity (MSNA) and heart rate (all p < 0.005), but did not change mean arterial blood pressure (MAP; p > 0.05). The elevation in MAP at the highest dose of phenylephrine was significantly attenuated during the heat stress (8.4 ± 1.2 mmHg) when compared to normothermia (15.4 ± 1.4 mmHg, p < 0.001). The sensitivity of baroreflex control of MSNA, expressed as the slope of the relationship between MSNA and diastolic blood pressure, was similar between thermal conditions (normothermia: −1.26 ± 0.31 bursts/min/mmHg; heat stress: −1.77 ± 0.31 bursts/min/mmHg; p > 0.05). Moreover, no significant difference in the slope of the relationship between heart rate and systolic blood pressure was observed between thermal states. CONCLUSION: These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat stressed humans without affecting baroreflex control of MSNA or heart rate. Work funded by NIH:HL61388, HL10488 and NASA:NAG9-1033 grants.
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PURPOSE: The objective of this study was to test the hypothesis that phenylephrine-induced elevations in blood pressure is attenuated in heat stressed humans. METHODS: In both normothermic and heat stress conditions, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects. RESULTS: Wholebody heating significantly increased sublingual temperature by 0.5°C, increased muscle sympathetic nerve activity (MSNA) and heart rate (all p < 0.005), but did not change mean arterial blood pressure (MAP; p > 0.05). The elevation in MAP at the highest dose of phenylephrine was significantly attenuated during the heat stress (8.4 ± 1.2 mmHg) when compared to normothermia (15.4 ± 1.4 mmHg, p < 0.001). The sensitivity of baroreflex control of MSNA, expressed as the slope of the relationship between MSNA and diastolic blood pressure, was similar between thermal conditions (normothermia: −1.26 ± 0.31 bursts/min/mmHg; heat stress: −1.77 ± 0.31 bursts/min/mmHg; p > 0.05). Moreover, no significant difference in the slope of the relationship between heart rate and systolic blood pressure was observed between thermal states. CONCLUSION: These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat stressed humans without affecting baroreflex control of MSNA or heart rate. Work funded by NIH:HL61388, HL10488 and NASA:NAG9-1033 grants.
Key concepts: Phenylephrine, Blood pressure, Baroreflex, Heart rate, Medicine, Anesthesia, Heat stress, Internal medicine