scholarly journals Effects of local heating of the testis on testicular blood flow and testosterone secretion in the rat

1988 ◽  
Vol 11 (1) ◽  
pp. 73-85 ◽  
Author(s):  
K. A. A. GALIL ◽  
B. P. SETCHELL
1975 ◽  
Vol 64 (1) ◽  
pp. 17-26 ◽  
Author(s):  
P. H. ROWE ◽  
P. A. RACEY ◽  
G. A. LINCOLN ◽  
M. ELLWOOD ◽  
J. LEHANE ◽  
...  

SUMMARY It has been suggested recently that testosterone secretion by the human testis may be controlled by factors other than luteinizing hormone (LH). In order to re-examine this hypothesis, plasma LH and testosterone concentrations were determined throughout the day in eight studies. A new method of data analysis revealed that the levels of the two hormones were closely related, but that the testicular response to LH was sluggish. These results explain some inconsistencies in the literature. It was demonstrated that average values for LH varied throughout the day, with a morning maximum and an evening minimum. It was also shown that injections of LH releasing hormone in man resulted in an increase in plasma testosterone above control levels. These results are consistent with the concept that LH controls the major changes in testosterone secretion in men. They do not exclude, however, the possible existence of other factors which might affect the peripheral concentration of testosterone, such as changes in testicular blood flow.


Choonpa Igaku ◽  
2014 ◽  
Vol 41 (6) ◽  
pp. 801-810
Author(s):  
Kimihiko MORIYA

2006 ◽  
Vol 100 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah J. Williams ◽  
Christopher T. Minson

The precise mechanism(s) underlying the thermal hyperemic response to local heating of human skin are not fully understood. The purpose of this study was to investigate a potential role for H1 and H2 histamine-receptor activation in this response. Two groups of six subjects participated in two separate protocols and were instrumented with three microdialysis fibers on the ventral forearm. In both protocols, sites were randomly assigned to receive one of three treatments. In protocol 1, sites received 1) 500 μM pyrilamine maleate (H1-receptor antagonist), 2) 10 mM l-NAME to inhibit nitric oxide synthase, and 3) 500 μM pyrilamine with 10 mM NG-nitro-l-arginine methyl ester (l-NAME). In protocol 2, sites received 1) 2 mM cimetidine (H2 antagonist), 2) 10 mM l-NAME, and 3) 2 mM cimetidine with 10 mM l-NAME. A fourth site served as a control site (no microdialysis fiber). Skin sites were locally heated from a baseline of 33 to 42°C at a rate of 0.5°C/5 s, and skin blood flow was monitored using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/mean arterial pressure. To normalize skin blood flow to maximal vasodilation, microdialysis sites were perfused with 28 mM sodium nitroprusside, and control sites were heated to 43°C. In both H1 and H2 antagonist studies, no differences in initial peak or secondary plateau phase were observed between control and histamine-receptor antagonist only sites or between l-NAME and l-NAME with histamine receptor antagonist. There were no differences in nadir response between l-NAME and l-NAME with histamine-receptor antagonist. However, the nadir response in H1 antagonist sites was significantly reduced compared with control sites, but there was no effect of H2 antagonist on the nadir response. These data suggest only a modest role for H1-receptor activation in the cutaneous response to local heating as evidenced by a diminished nadir response and no role for H2-receptor activation.


2002 ◽  
Vol 93 (6) ◽  
pp. 1918-1924 ◽  
Author(s):  
Robert Carter ◽  
Thad E. Wilson ◽  
Donald E. Watenpaugh ◽  
Michael L. Smith ◽  
Craig G. Crandall

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 ± 3, forearm: 48 ± 3%max) compared with during inactive recovery (chest: 21 ± 2, forearm: 25 ± 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 ± 0.10, forearm: 0.46 ± 0.10 mg · cm−2 · min−1) compared with during inactive recovery (chest: 0.28 ± 0.10, forearm: 0.14 ± 0.20 mg · cm−2 · min−1); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.


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