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Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress.
Am J Physiol Regul Integr Comp Physiol. 2005 Aug; 289(2):R432-R440.AJ

Abstract

The aim of this study was to elucidate the interactive effect of central hypovolemia and plasma hyperosmolality on regulation of peripheral vascular response and AVP secretion during heat stress. Seven male subjects were infused with either isotonic (0.9%; NOSM) or hypertonic (3.0%; HOSM) NaCl solution and then heated by perfusing 42 degrees C (heat stress; HT) or 34.5 degrees C water (normothermia; NT) through water perfusion suits. Sixty minutes later, subjects were exposed to progressive lower body negative pressure (LBNP) to -40 mmHg. Plasma osmolality (P(osmol)) increased by approximately 11 mosmol/kgH(2)O in HOSM conditions. The increase in esophageal temperature before LBNP was much larger in HT-HOSM (0.90 +/- 0.09 degrees C) than in HT-NOSM (0.30 +/- 0.07 degrees C) (P < 0.01) because of osmotic inhibition of thermoregulation. During LBNP, mean arterial pressure was well maintained, and changes in thoracic impedance and stroke volume were similar in all conditions. Forearm vascular conductance (FVC) before application of LBNP was higher in HT than in NT conditions (P < 0.001) and was not influenced by P(osmol) within the thermal conditions. The reduction in FVC at -40 mmHg in HT-HOSM (-9.99 +/- 0.96 units; 58.8 +/- 4.1%) was significantly larger than in HT-NOSM (-6.02 +/- 1.23 units; 44.7 +/- 8.1%) (P < 0.05), whereas the FVC response was not different between NT-NOSM and NT-HOSM. Plasma AVP response to LBNP did not interact with P(osmol) in either NT or HT conditions. These data indicate that there apparently exists an interactive effect of P(osmol) and central hypovolemia on the peripheral vascular response during heat stress, or peripheral vasodilated conditions, but not in normothermia.

Authors+Show Affiliations

Department of Physiology, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15845884

Citation

Ito, Tomoyuki, et al. "Plasma Hyperosmolality Augments Peripheral Vascular Response to Baroreceptor Unloading During Heat Stress." American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 289, no. 2, 2005, pp. R432-R440.
Ito T, Itoh T, Hayano T, et al. Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress. Am J Physiol Regul Integr Comp Physiol. 2005;289(2):R432-R440.
Ito, T., Itoh, T., Hayano, T., Yamauchi, K., & Takamata, A. (2005). Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 289(2), R432-R440.
Ito T, et al. Plasma Hyperosmolality Augments Peripheral Vascular Response to Baroreceptor Unloading During Heat Stress. Am J Physiol Regul Integr Comp Physiol. 2005;289(2):R432-R440. PubMed PMID: 15845884.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress. AU - Ito,Tomoyuki, AU - Itoh,Toshiyuki, AU - Hayano,Takashi, AU - Yamauchi,Katsuya, AU - Takamata,Akira, Y1 - 2005/04/21/ PY - 2005/4/23/pubmed PY - 2005/9/2/medline PY - 2005/4/23/entrez SP - R432 EP - R440 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 289 IS - 2 N2 - The aim of this study was to elucidate the interactive effect of central hypovolemia and plasma hyperosmolality on regulation of peripheral vascular response and AVP secretion during heat stress. Seven male subjects were infused with either isotonic (0.9%; NOSM) or hypertonic (3.0%; HOSM) NaCl solution and then heated by perfusing 42 degrees C (heat stress; HT) or 34.5 degrees C water (normothermia; NT) through water perfusion suits. Sixty minutes later, subjects were exposed to progressive lower body negative pressure (LBNP) to -40 mmHg. Plasma osmolality (P(osmol)) increased by approximately 11 mosmol/kgH(2)O in HOSM conditions. The increase in esophageal temperature before LBNP was much larger in HT-HOSM (0.90 +/- 0.09 degrees C) than in HT-NOSM (0.30 +/- 0.07 degrees C) (P < 0.01) because of osmotic inhibition of thermoregulation. During LBNP, mean arterial pressure was well maintained, and changes in thoracic impedance and stroke volume were similar in all conditions. Forearm vascular conductance (FVC) before application of LBNP was higher in HT than in NT conditions (P < 0.001) and was not influenced by P(osmol) within the thermal conditions. The reduction in FVC at -40 mmHg in HT-HOSM (-9.99 +/- 0.96 units; 58.8 +/- 4.1%) was significantly larger than in HT-NOSM (-6.02 +/- 1.23 units; 44.7 +/- 8.1%) (P < 0.05), whereas the FVC response was not different between NT-NOSM and NT-HOSM. Plasma AVP response to LBNP did not interact with P(osmol) in either NT or HT conditions. These data indicate that there apparently exists an interactive effect of P(osmol) and central hypovolemia on the peripheral vascular response during heat stress, or peripheral vasodilated conditions, but not in normothermia. SN - 0363-6119 UR - https://www.unboundmedicine.com/medline/citation/15845884/Plasma_hyperosmolality_augments_peripheral_vascular_response_to_baroreceptor_unloading_during_heat_stress_ L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00027.2004?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -