Читать книгу Bovine Reproduction - Группа авторов - Страница 74

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.

We recently conducted two studies in rams under general anesthesia to determine effects of hypoxia and of testicular hyperthermia on testicular blood flow, and O₂ delivery and uptake. In the first study [21], eight rams were exposed to successive decreases in O₂ concentration in inspired air (100, 21, and 13%; 45 minutes at each concentration). As O₂ concentration decreased (100 to 13%), testicular blood flow increased (9.6 vs 12.9 ml/min/100 g of testis, P < 0.05). Increased testicular blood flow maintained O₂ delivery and increased testicular temperature by ~1 °C. In the second experiment [22], testicular temperatures of nine crossbred rams were sequentially maintained at 33–35, 37, and 40 °C (45 minutes at each temperature). As testicular temperature increased from 33–35 to 40 °C, there were increases in mean testicular blood flow (9.8 vs 12.2 ml/min/100 g of testes, P < 0.05), O₂ extraction (31.2 vs 47.3%, P < 0.0001), and O₂ use (0.35 vs 0.64 ml/min/100 g of testes, P < 0.0001). In both experiments, there was no evidence of anaerobic metabolism, based on no significant difference in lactate, pH, HCO₃ ^–, and base excess.

Following our studies in rams, we conducted another study to determine the effects of short‐term testicular hyperthermia on testicular blood flow, O₂ delivery and uptake, and evidence of testicular hypoxia in pubertal Angus (B. taurus) and Nelore (B. indicus) bulls (nine per breed) under isoflurane anesthesia [23]. As testes were warmed from 34 to 40 °C, there were increases (P < 0.0001, but no breed effects) in testicular blood flow (mean ± SEM, 9.59 ± 0.10 vs 17.67 ± 0.29 ml/min/100 g, respectively), O₂ delivery (1.79 ± 0.06 vs 3.44 ± 0.11 ml O₂/min/100 g), and O₂ consumption (0.69 ± 0.07 vs 1.25 ± 0.54 ml O₂/min/100 g), but no indications of testicular hypoxia (Figure 4.1). Our hypothesis that Angus bulls have a greater relative increase in testicular blood flow than Nelore in response to increased testicular temperature was not supported, as there was no significant breed difference.

Figure 4.1 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). Assessment of blood flow and sample collection were done four times at 15‐minute intervals and then the testes warmed to reach the next temperature plateau. For each end point, there was a difference (P < 0.001) between all temperature plateaus. Testicular temperature increased testicular metabolism; however, testicular blood flow nearly doubled, providing ample O₂ to meet metabolic demands, with no evidence of hypoxia.

Our studies in conscious rams and mice, as well as in anesthetized rams and bulls, challenged the classical paradigm regarding scrotal/testicular thermoregulation, as acute testicular hyperthermia caused increases in blood flow and in delivery and uptake of O₂, with no indications of hypoxia. In contrast to the long‐standing paradigm, our data were evidence that effects of increased testicular temperature were due to testicular temperature per se and not secondary hypoxia.