A theoretical model for testis thermoregulation.
Studies going back as far as the early 1920's show that there is a clear relationship between testis temperature and semen quality. The most intriguing question is whether there is a mechanism of thermoregulation which, in the human, maintains testis temperature within certain limits that permit euspermia. Thermoregulation is defined as maintaining some specified (optimum?) temperature plus or minus an error over internal and ambient loss factors. A computer Model has been evolved which contains no regulation or feedback. It appears to predict human testis temperature data gathered in earlier studies. The Model accounts for countercurrent heat exchange in the pampiniform plexus and predicts, with an open loop analysis, that there is no feedback or regulation. As far as thermoregulation is concerned, there appear to be no first-order effects taking place in the human testis. This suggests that ambient temperature changes cause corresponding changes in testis temperature. Also any internal changes in thermal properties such as core temperature variations or variability of the countercurrent heat exchanger will also cause temperature change. Testis temperature as predicted by this Model is the result of the heat energy entering the testis from arterial inflow minus the venous outflow and heat loss from the scrotum. The Model predicts that the heat exchanger will function to provide precooling of arterial blood as external temperatures drop but will fail to precool effectively as temperature rises. This is predicated on the fact that the countercurrent heat exchanger becomes less effective as the temperature gradient across the exchanger becomes smaller and less heat energy is able to be transferred from arterial flow to venous flow. The Model also predicts that any diminution of the heat exchanger mechanism either from reduced venous flow or restricted scrotal heat loss will result in higher testis temperature. Lastly, the Model correctly predicted that febrile patients would experience elevated testis temperature during periods of elevated core temperature. Since more heat energy is available in the arterial blood, more heat energy is delivered to the testis under these conditions. In the human it appears that any internal or external factor causing a temperature change will not trigger or activate a feedback mechanism to control the resulting testis temperature. A major factor in subfertile semen may be the inability to check excessive temperature of the testis which impairs the ability to produce and mature fertile spermatozoa.