Bovine Reproduction. Группа авторов

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(scrotal surface); 33.3, 33.0, and 32.9 °C (scrotal subcutaneous); and 34.3, 34.3, and 34.5 °C (intratesticular), respectively [12]. Therefore, top‐to‐bottom differences (gradients) in temperature were 1.6, 0.4, and –0.2 °C for scrotal surface, scrotal subcutaneous, and intratesticular temperatures, respectively. Moving dorsal to ventral, the scrotum gets cooler, whereas the testis (independent of the scrotum) gets warmer. These temperature gradients are consistent with their vasculature, as the scrotum is vascularized from top to bottom, whereas the testis is essentially vascularized from bottom to top. In that regard, the testicular artery exits the bottom of the testicular vascular cone, courses the length of the testis (under the corpus epididymis), and at the bottom of the testis ramifies into multiple branches that spread dorsally and laterally across the surface of the testis before entering the testicular parenchyma [13]. Blood within the testicular artery was a similar temperature at the top of the testis compared to the bottom of the testis, but was significantly cooler at the point of entry into the testicular parenchyma (intra‐arterial temperatures at these locations were 34.3, 33.4, and 31.7 °C, respectively [14]). Therefore both the scrotum and the testis are warmest at the origin of their blood supply (top of scrotum and bottom of testis), but they both get cooler distal to that point (i.e. bottom of scrotum, top of testis). Remarkably, these opposing temperature gradients collectively result in a nearly uniform intratesticular temperature in situ [15].

      In beef bulls, internal temperatures of the caput, corpus, and cauda epididymis averaged 35.6, 34.6, and 33.1 °C (gradient, 2.5 °C), respectively [12]. That the caput was warmer than the testicular parenchyma at the top of the testis was attributed to the proximity of the caput to the testicular vascular cone. Furthermore, it was noteworthy that the cauda, critical in sperm storage and maturation, was cooler than testicular parenchyma.

      Bulls fed moderate‐energy diets after weaning have better semen quality than those fed high‐energy diets. In one study, beef bulls fed a moderate‐ versus high‐energy diet for 168 days after weaning had a larger scrotal surface temperature gradient (3.9 vs 3.4 °C, P < 0.02), more morphologically normal sperm (68.8 vs 62.5%, P < 0.01), and a higher proportion of progressively motile sperm (53.4 vs 44.5%, P < 0.006) [16]. Perhaps increased dietary energy reduced heat loss, thereby increasing temperatures of the testes and scrotum.

      Testicular blood flow and O2 uptake were measured in eight Angus bulls to determine the relative importance of blood flow versus metabolism as sources of testicular heat [17]. Blood flow in the testicular artery averaged 12.4 ml/min. Arterial blood was warmer (39.2 vs 36.9 °C, P < 0.001) and had more hemoglobin saturated with O2 than blood in the testicular vein (95.3 vs 42.0%, P < 0.001). Based on blood flow and hemoglobin saturation, the O2 used by one testis (1.2 ml/min) was calculated to produce 5.8 cal of heat per minute, compared to 28.3 cal/min attributed to blood flow. Therefore blood flow is the major source of testicular heat.

      Pathogenesis of Heat‐Induced Changes in Sperm Morphology

      There is a long‐standing paradigm that testes operate in near hypoxia, blood flow does not significantly increase as testes are warmed, and hypoxia disrupts spermatogenesis after increased testicular temperature [18]. However, this had apparently never been rigorously examined until we conducted two studies to test the following hypotheses: (i) hypoxia disrupts sperm quality and production; and (ii) hyperoxia prevents hyperthermia‐induced reductions in sperm quality and production.

      In one study [19], we exposed 18 rams (nine had an insulated scrotum) to air containing 14, 21, or 85% O2 for approximately 30 hours. In that study, scrotal insulation (to increase testicular temperature) substantially reduced sperm motility (from 58 to 30%) and proportion of morphologically normal sperm (from 87 to 30%), but effects due to O2 were minimal. In a second study [20], 96 male CD‐1 mice were maintained at 20 vs 36 °C, exposed to 13, 21, or 95% O2 twice for 12‐hour intervals (separated by 12 hours at room temperature and 21% O2), and euthanized 14 or 20 days after exposure. Interestingly, sperm morphology and specific stages of sperm cell development were altered in mice exposed to 36 °C, including increases in percentage of sperm with defective heads (P < 0.0001) or tails (P < 0.001) and percentage of altered elongated spermatids (P < 0.001). Regarding effects due to O2 variations, seminiferous tubule diameter and epididymal sperm reserves were reduced in the 13% O2 group, but sperm quality and production were not consistently disrupted by hypoxia. In addition, no hyperthermia‐induced disruptions were prevented by hyperoxia, indicating a major role of increased temperature, but not hypoxia. There were primarily main effects of temperature; mice exposed to 36 °C had smaller testes, fewer morphologically normal sperm, and histologically increased altered spermatids and altered germ cells compared to mice exposed to 20 °C. In both studies, our hypotheses were not supported; sperm quality and production were not consistently disrupted by hypoxia and hyperoxia did not protect against hyperthermia in mice.

Schematic illustration of mean (and SEM) blood flow, O2 delivery, and metabolic rate in testes of 18 bulls (Nelore and Angus) sequentially exposed to three plateaus of testicular temperature (33-35, 37, and 40 °C).

      Our

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