Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

Jian Cui, Thad E. Wilson, Craig G. Crandall

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ∼0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [AMAP 8.4 ± 1.2 mmHg; ATPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (ΔMAP 15.4 ± 1.4 mmHg, ΔTPR 7.13 ± 1.18 PRU; all P< 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume283
Issue number5 52-5
StatePublished - Nov 1 2002

Fingerprint

Phenylephrine
Vascular Resistance
Arterial Pressure
Hot Temperature
Heart Rate
Blood Pressure
Muscles
Baroreflex
Cardiac Output
Heating
Healthy Volunteers
Temperature

Keywords

  • Baroreflex sensitivity
  • Heart rate
  • Muscle sympathetic nerve activity
  • Vasoconstrictor agents
  • Whole body heating

ASJC Scopus subject areas

  • Physiology

Cite this

@article{e9e5c75afb19417f9494ed04099324a2,
title = "Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans",
abstract = "To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ∼0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [AMAP 8.4 ± 1.2 mmHg; ATPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (ΔMAP 15.4 ± 1.4 mmHg, ΔTPR 7.13 ± 1.18 PRU; all P< 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.",
keywords = "Baroreflex sensitivity, Heart rate, Muscle sympathetic nerve activity, Vasoconstrictor agents, Whole body heating",
author = "Jian Cui and Wilson, {Thad E.} and Crandall, {Craig G.}",
year = "2002",
month = "11",
day = "1",
language = "English (US)",
volume = "283",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "5 52-5",

}

TY - JOUR

T1 - Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

AU - Cui, Jian

AU - Wilson, Thad E.

AU - Crandall, Craig G.

PY - 2002/11/1

Y1 - 2002/11/1

N2 - To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ∼0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [AMAP 8.4 ± 1.2 mmHg; ATPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (ΔMAP 15.4 ± 1.4 mmHg, ΔTPR 7.13 ± 1.18 PRU; all P< 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.

AB - To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ∼0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [AMAP 8.4 ± 1.2 mmHg; ATPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (ΔMAP 15.4 ± 1.4 mmHg, ΔTPR 7.13 ± 1.18 PRU; all P< 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.

KW - Baroreflex sensitivity

KW - Heart rate

KW - Muscle sympathetic nerve activity

KW - Vasoconstrictor agents

KW - Whole body heating

UR - http://www.scopus.com/inward/record.url?scp=0036838480&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036838480&partnerID=8YFLogxK

M3 - Article

VL - 283

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 5 52-5

ER -