Chronic sympathectomy of the caudal artery delays cutaneous heat loss during passive heating

It is unknown whether menstrual cycle or oral contraceptive (OC) use influences nonthermal control of postexercise heat loss responses. We evaluated the effect of menstrual cycle and OC use on the activation of heat loss responses during a passive heating protocol performed pre- and postexercise. Women without OC ( n = 8) underwent pre- and postexercise passive heating during the early follicular phase (FP) and midluteal phase (LP). Women with OC ( n = 8) underwent testing during the active pill consumption (high exogenous hormone phase, HH) and placebo (low exogenous hormone phase, LH) weeks. After a 60-min habituation at 26°C, subjects donned a liquid conditioned suit. Mean skin temperature was clamped at ∼32.5°C for ∼15 min and then gradually increased, and the absolute esophageal temperature at which the onset of forearm vasodilation (Thvd) and upper back sweating (Thsw) were noted. Subjects then cycled for 30 min at 75% V̇o2 peak followed by a 15-min seated recovery. A second passive heating was then performed to establish postexercise values for Thvd and Thsw. Between 2 and 15 min postexercise, mean arterial pressure (MAP) remained significantly below baseline ( P < 0.05) by 10 ± 1 and 11 ± 1 mmHg for the FP/LH and LP/HH, respectively. MAP was not different between cycle phases. During LP/HH, Thvd was 0.16 ± 0.24°C greater than FP/LH preexercise ( P = 0.020) and 0.15 ± 0.23°C greater than FP/LH postexercise ( P = 0.017). During LP/HH, Thsw was 0.17 ± 0.23°C greater than FP/LH preexercise ( P = 0.016) and 0.18 ± 0.16°C greater than FP/LH postexercise ( P = 0.001). Postexercise thresholds were significantly greater ( P ≤ 0.001) than preexercise during both FP/LH (Thvd, 0.22 ± 0.03°C; Thsw, 0.13 ± 0.03°C) and LP/HH (Thvd, 0.21 ± 0.03°C; Thsw, 0.14 ± 0.03°C); however, the effect of exercise was similar between LP/HH and FP/LH. No effect of OC use was observed. We conclude that neither menstrual cycle nor OC use modifies the magnitude of the postexercise elevation in Thvd and Thsw.

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Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647259 ◽

1990 ◽

Vol 64 (01) ◽

pp. 091-096 ◽

Cited By ~ 6

Author(s):

W J Janssens ◽

F J S Cools ◽

L A M Hoskens ◽

J M Van Nueten

Keyword(s):

Smooth Muscle ◽

Blood Vessel ◽

Platelet Activation ◽

Prostaglandin F2α ◽

Thromboxane A2 ◽

Femoral Arteries ◽

Vasoactive Substances ◽

Caudal Artery ◽

Isolated Rat ◽

Rat Platelets

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.

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