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Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats.
Am J Physiol. 1998 11; 275(5):R1703-11.AJ

Abstract

To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (DeltaPV) = -20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (DeltaPosm) = 23 mosmol/kgH2O, DeltaPV = -16%], and hypovolemic and more hyperosmotic (HL2, DeltaPosm = 52 mosmol/kgH2O, DeltaPV = -17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35 degreesC air temperature, approximately 20% relative humidity) for 1-2 h until rectal temperatures (Tre) reached 40.0 degreesC. Mean arterial pressure in L decreased with rise in Tre (P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to approximately 30% of that in C (P < 0. 001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Tre threshold for TVD was highly correlated with Posm (r = 0.94, P < 0. 001). Heart rate in the HL groups increased with rise in Tre (P < 0. 001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.

Authors+Show Affiliations

Departments of Anesthesiology and Physiology, Kyoto Prefectural University of Medicine, Kyoto 602-0841, Japan.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

9791093

Citation

Nakajima, Y, et al. "Plasma Hyperosmolality and Arterial Pressure Regulation During Heating in Dehydrated and Awake Rats." The American Journal of Physiology, vol. 275, no. 5, 1998, pp. R1703-11.
Nakajima Y, Nose H, Takamata A. Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats. Am J Physiol. 1998;275(5):R1703-11.
Nakajima, Y., Nose, H., & Takamata, A. (1998). Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats. The American Journal of Physiology, 275(5), R1703-11. https://doi.org/10.1152/ajpregu.1998.275.5.R1703
Nakajima Y, Nose H, Takamata A. Plasma Hyperosmolality and Arterial Pressure Regulation During Heating in Dehydrated and Awake Rats. Am J Physiol. 1998;275(5):R1703-11. PubMed PMID: 9791093.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats. AU - Nakajima,Y, AU - Nose,H, AU - Takamata,A, PY - 1998/10/29/pubmed PY - 1998/10/29/medline PY - 1998/10/29/entrez SP - R1703 EP - 11 JF - The American journal of physiology JO - Am. J. Physiol. VL - 275 IS - 5 N2 - To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (DeltaPV) = -20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (DeltaPosm) = 23 mosmol/kgH2O, DeltaPV = -16%], and hypovolemic and more hyperosmotic (HL2, DeltaPosm = 52 mosmol/kgH2O, DeltaPV = -17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35 degreesC air temperature, approximately 20% relative humidity) for 1-2 h until rectal temperatures (Tre) reached 40.0 degreesC. Mean arterial pressure in L decreased with rise in Tre (P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to approximately 30% of that in C (P < 0. 001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Tre threshold for TVD was highly correlated with Posm (r = 0.94, P < 0. 001). Heart rate in the HL groups increased with rise in Tre (P < 0. 001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress. SN - 0002-9513 UR - https://www.unboundmedicine.com/medline/citation/9791093/Plasma_hyperosmolality_and_arterial_pressure_regulation_during_heating_in_dehydrated_and_awake_rats_ L2 - http://journals.physiology.org/doi/full/10.1152/ajpregu.1998.275.5.R1703?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -