Bovine Reproduction. Группа авторов
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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.
Sources of Testicular Heat
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.
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.
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