Effect of ovulation rate and timing of ovulation after different hormone treatments on pregnancy rate in dairy cows.

Primiparous and multiparous lactating crossbred dairy cows with a mature corpus luteum and a follicle with >10 mm in diameter were treated with cloprostenol. Those cows that showed oestrus within 5 days after treatment were inseminated (Group P). The other cows (Group PG) were treated with GnRH 2 days after cloprostenol treatment and timed artificial insemination (AI) was performed on the consecutive day, or were inseminated (Group G) after detected oestrus and treated with GnRH immediately after AI. The control cows (Group C) after detected oestrus were only inseminated. All of the AIs using frozen semen were done between 6 and 7 a.m. while the ultrasonographic examinations after AI were performed between 4 to 6 p.m. The ovaries of each cow were scanned by means of transrectal ultrasonography from the day of AI until ovulation. Daily blood samples were collected for progesterone measurements. The ovulation and pregnancy rates among the groups changed between 84.6% and 95.5%, as well as 44.4% and 60%, respectively, however the differences were not statistically significant. All the cows were evaluated according to date of ovulation after AI and the pregnancy rate was 55.4% (Group 1: ovulation occurred between AI and 9-11 h after AI), 54.5% (Group 2: ovulation occurred between 9-11 h and 33-35 h after AI) and 35.5% (Group 3: ovulation occurred between 33-35 h and 57-59 h after AI), respectively. There was a trend (P=0.087) for 2.2 greater odds of staying open among cows inseminated between 33 to 35 h and 57 to 59 h before ovulation compared to cows inseminated within 9 to 11 h before ovulation. If ovulation occurred before AI, the pregnancy rate was only 22.2%, therefore determination of optimal time for AI is of great importance.

Co-infection with Bovine Herpesvirus 4 and Histophilus somni Significantly Extends the Service Period in Dairy Cattle with Purulent Vaginal Discharge.

The aim of the study was to investigate the effect of Bovine Herpesvirus 4 (BoHV-4) and Histophilus (H.) somni on fertility rate of cows in a Hungarian Holstein-Friesian dairy herd with purulent vaginal discharge (PVD). Non-pregnant cows (n = 188) with mature corpus luteum were treated with cloprostenol and 3 days later if they did not show oestrus, were examined by rectal palpation. Animals showing PVD (n = 60/31.9%/) and 14 controls with normal vaginal discharge (Score 0) were randomly selected and further examined by ultrasonography and blood samples were collected for detecting BoHV-4 DNA and transcervical guarded swabs were collected from the uterus for bacteriological examination. Although the majority of the examined animals were infected with BoHV-4 and H. somni including the control animals as well, in group of animals with PVD score 3, fewer animals became pregnant and the duration between the first treatment to pregnancy was significantly extended. Based on these clinical and comparative data, our results confirm that these two microorganisms together may impair important reproductive parameters which may cause large economic losses to dairy farms.

Heart rate and heart rate variability in multiparous dairy cows with unassisted calvings in the periparturient period.

Behavioural changes before calving can be monitored on farms; however, predicting the onset of calving is sometimes difficult based only on clinical signs. Heart rate (HR) and heart rate variability (HRV) as non-invasive measures of autonomic nervous system (ANS) activity were investigated in Holstein-Friesian cows (N=20) with unassisted calvings in the periparturient period to predict the onset of calving and assess the stress associated with calving. R-R-intervals were analysed in 5-min time windows during the following three main periods of measurement: 1) between 0 and 96 h before the onset of calving restlessness (prepartum period); 2) during four stages of calving: (I) early first stage; between the onset of calving restlessness and the first abdominal contractions; (II) late first stage (between the first abdominal contractions and the appearance of the amniotic sac); (III) early second stage (between the appearance of the amniotic sac and the appearance of the foetal hooves); (IV) late second stage (between the appearance of the foetal hooves and delivery of the calf), and 3) over 48 h following calving (postpartum period). Data collected between 72 and 96 h before calving restlessness was used as baseline. Besides HR, Poincaré measures [standard deviation 1 (SD1) and 2 (SD2) and SD2/SD1 ratio], the root mean square of successive differences (RMSSD) in R-R intervals, the high-frequency (HF) component of HRV and the ratio between the low-frequency (LF) and the HF components (LF/HF ratio) were calculated. Heart rate increased only following the onset of the behavioural signs, peaked before delivery of the calf, then decreased immediately after calving. Parasympathetic indices of HRV (RMSSD, HFnorm and SD1) decreased, whereas sympathovagal indices (LF/HF ratio and SD2/SD1 ratio) increased significantly from baseline between 12 and 24 before the onset of calving restlessness. The same pattern was observed between 0 and 1h before calving restlessness. Following the onset of behavioural signs, parasympathetic activity increased gradually with a parallel shift in sympathovagal balance towards parasympathetic tone, which was possibly a consequence of oxytocin release, which induces an increase in vagus nerve activity. Parasympathetic activity decreased rapidly between 0 and 0.5h following calving and was lower than measured during all other stages of the study, while sympathetic activity peaked during this stage and was higher than measured during any other stages. Between 0 and 4h after calving vagal tone was lower than baseline, whereas sympathovagal balance was higher, reflecting a prolonged physiological challenge caused by calving. Vagal activity decreased, whereas sympathovagal balance shifted towards sympathetic tone with increased live body weight of the calf during the late second stage of calving, suggesting higher levels of stress associated with the higher body weight of calves. All HRV indices, measured either at the late second stage of calving and between 12 and 24h after calving, were affected by the duration of calving. Our results indicate that ANS activity measured by HRV indices is a more immediate indicator of the onset of calving than behaviour or HR, as it changed earlier than when restlessness or elevation in HR could be observed. However, because of the possible effects of other physiological mechanisms (e.g. oxytocin release) on ANS activity it seems to be difficult to measure stress associated with calving by means of HRV between the onset of calving restlessness and delivery. Further research is needed to enable more precise interpretation of the prepartum changes in HR and HRV in dairy cattle.

Effects of repeated surgical stress on daily changes of body core temperature in mice.

Daily body core temperature rhythm has been known to become blunted for several days following intra-abdominal implantation of biotelemetry transmitters in small rodents and about a week is required for re-establishment of stable body core temperature oscillation. In the present study carried out on mice it was found that a repetition of the same minor surgical intervention (laparotomy) several days apart could speed up the stabilization of body temperature oscillations. Melatonin supplied with the drinking water continuously was found to speed up the return of stable daily body temperature rhythm further on consecutive laparotomies, while daily injections of methylprednisolone resulted in some delay in the development of stable body core temperature oscillations. It is concluded that in C57BL/6 mice possessing low plasma levels of melatonin exhibit an adaptive response to repeated stresses influencing the dynamics of daily body temperature rhythm.

Energetics of fasting heterothermia in TRPV1-KO and wild type mice.

To learn the possible role of TRPV1 in the changes of temperature regulation induced by short-term energy lack, TRPV1-KO and wild type mice were exposed to complete fasting for 2 or 3 days while their core temperature and locomotor activity were recorded using a biotelemetry method. In both types of mice, fasting led to progressive daytime hypothermia with night-time core temperature being maintained at normothermia (collectively called heterothermia). During fasting rises of locomotor activity were observed parallel to night-time normothermia with occasional increases of both parameters recorded every 2 to 3 hours (ultradian rhythms). The daytime fall of core temperature was significantly greater in wild type than in TRPV1-KO mice, in the former an advance of the temperature/activity rhythm having been observed in spite of the presence of a 12/12 hour light/darkness schedule. Re-feeding applied at the beginning of the light-period led to rapid reappearance of normothermia in both types of mice without a large increase in locomotor activity. It is concluded that the TRPV1-gene may have a role in the development of adaptive daytime hypothermia (and hence saving some energy) in mice during complete fasting but still allowing normothermia maintained at night, a strategy probably serving survival under natural conditions in small size rodents such as the mouse. The possible role of muscle thermogenesis either with or without gross bodily movement during fasting or on re-feeding, respectively, may be based on different mechanisms yet to be clarified.

Regulation of energy balance by peptides: a review.

Regulation of energy balance consists of two intertwined circuitries: food intake-- metabolic rate--body weight, vs. metabolic rate--heat loss--body temperature. Metabolic rate serves interaction between the two. Some peptides influence individual components of energy homeostasis, without having coordinated anabolic or catabolic properties. Anabolic and catabolic peptides function with redundancy, and also show specific features. They all influence ingestive behavior vs. metabolic rate and temperature, but do not necessarily act directly at central thermoregulatory pathways. Most of them alter metabolic rate (but not heat loss) through the ventromedial nucleus, while consequent moderate changes in thermal signals can influence function of the preoptic/anterior hypothalamic region and initiate compensating regulatory steps to restore temperature. Thus, besides ingestion, these peptides influence metabolic rate, whereas the passive temperature changes will only be obvious as long as environmental circumstances allow. Other substances cause coordinated central regulatory changes resembling fever (e.g. cholecystokinin), anapyrexia, or cold-defense: they primarily affect body temperature, and then the temperature-dependent changes in catabolic/anabolic peptide functions alter feeding behavior. Such arrangement can secure relative independence of the two regulatory circles, allowing for minimization of depression in metabolic rate and body temperature during starvation (despite elevated anabolic activity), or for increased food intake with lack of hypothermia in cold adaptation (despite high anabolic activity), or for normal body temperature in overfed states (despite enhanced catabolic activity), etc. However, the independence is relative since the two systems interact in the overall regulation of energy homeostasis: neuropeptides influence body temperature and temperature modifies peptide actions.

Acute, subacute and chronic effects of central neuropeptide Y on energy balance in rats.

Central neuropeptide Y (NPY) injection has been reported to cause hyperphagia and in some cases also hypometabolism or hypothermia. Chronic central administration induced a moderate rise of short duration in body weight, without consistent metabolic/thermal changes. In the present studies the acute and subsequent subacute ingestive and metabolic/thermal changes were studied following intracerebroventricular (i.c.v.) injections of NPY in cold-adapted and non-adapted rats, or the corresponding chronic changes following i.c.v. NPY infusion. Besides confirming basic earlier data, we demonstrated novel findings: a temporal relationship for the orexigenic and metabolic/thermal effects, and differences of coordination in acute/subacute/chronic phases or states. The acute phase (30-60 min after injection) was anabolic: coordinated hyperphagia and hypometabolism/hypothermia. NPY evoked a hypothermia by suppressing any (hyper)metabolism in excess of basal metabolic rate, without enhancing heat loss. Thus, acute hypothermia was observed in sub-thermoneutral but not thermoneutral environments. The subsequent subacute catabolic phase exhibited opposite effects: slight increase in metabolic rate, rise in body temperature, reaching a plateau within 3-4 h after injection -- this was maintained for at least 24 h; meanwhile the food intake decreased and the normal daily weight gain stopped. This rebound is only indirectly related to NPY. Chronic (7-day long) i.c.v. NPY infusion induced an anabolic phase for 2-3 days, followed by a catabolic phase and fever, despite continued infusion. In cold-adaptation environment the primary metabolic effect of the infusion induced a moderate hypothermia with lower daytime nadirs and nocturnal peaks of the circadian temperature rhythm, while at near-thermoneutral environments in non-adapted rats the infusion attenuated only the nocturnal temperature rise by suppressing night-time hypermetabolism. Further finding is that in cold-adapted animals, the early feeding effect of NPY-infusion was enhanced, whereas the early hypothermic effect in cold was limited by interference with competing thermoregulatory mechanisms.

Daily body temperature rhythm and heat tolerance in TRPV1 knockout and capsaicin pretreated mice.

Daily body temperature (DBT) rhythm of mice lacking one of the transient receptor potential (TRP) family of proteins, the capsaicin receptor or TRPV1, was recorded by biotelemetry and found to have significantly higher amplitude than that of wild-type mice. Capsaicin-desensitized wild-mice exhibited an even higher DBT amplitude than did TRPV1 deficient mice. A standard heat load (radiant temperature of 36-37 degrees C) resulted in similar rises in body core temperature in wild-type mice and in TRPV1 deficient mice, while capsaicin-desensitized wild-type mice exhibited a robust heat-intolerance. The lack of TRPV1 slightly modifies amplitude of daily body temperature rhythm but does not seem to influence physiological heat defence in mice. In vivo evidence for a TRP protein functioning in the physiological heat-defence range is still lacking.

Low physical performance in obese adolescent boys with metabolic syndrome.

OBJECTIVE: To assess cardiorespiratory exercise function in obese children with and without metabolic syndrome (MS). DESIGN: Comparing three groups of subjects with different cardiovascular risk profiles. SUBJECTS: Twenty-two MS (body weight (mean+/-s.d.) 97.3+/-15.3 kg; age (mean+/-s.d.) 14.2+/-1.9 y), 17 obese (82.6+/-15.7 kg; 14.2+/-2.6 y) and 29 normal weight control (64.3+/-8.5 kg; 15.3+/-1.0 y) boys. MEASUREMENTS: Exercise duration (ED), resting heart rate (HR(0)), peak heart rate (HR(peak)), physical working capacity at 170 beat/min (PWC-170), peak oxygen consumption (VO(2peak)) and the lactic acidosis threshold (LAT) were determined on treadmill, using a continuous ramp protocol. RESULTS: ED (MS (mean+/-s.d.); 655+/-86 s; obese 703+/-64 s; control 750+/-0 s) in absolute value and PWC-170 normalised for body weight (139+/-40 w; 177+/-40 w; 211+/-40 w) were significantly shorter and lower in the MS group, as compared to obese and control groups (P<0.05). VO(2peak) (2.2+/-0.4 l/min; 2.4+/-0.5 l/min; 2.9+/-0.4 l/min) and LAT (1.3+/-0.4 l/min; 1.5+/-0.4 l/ min; 1.8+/-0.4 l/min) normalised for body weight, were significantly shorter and lower in the MS group, as compared to control group (P<0.05). HR(0) was significantly higher (P<0.05) in MS group than in obese and control groups (88+/-12 bpm; obese 78+/-10 bpm; 73+/-10 bpm). CONCLUSION: Cardiorespiratory exercise performance capacity in MS boys are reduced. It still remains to be elucidated whether the metabolic alterations or the decreased physical activity is responsible for the observed reduction in cardiorespiratory performance.

Cholecystokinin and thermoregulation--a minireview.

Thermoregulatory effects of cholecystokinin (CCK) peptides are reviewed with special emphasis on two types of responses, that is hypothermia or hyperthermia. In rodents exposed to cold a dose-dependent hypothermia has been observed on peripheral injection of CCK probably acting on CCKA receptors. Central microinjection of CCK in rats induced a thermogenic response that could be attenuated by CCKB receptor antagonists, but some authors observed a hypothermia. It is suggested that neuronal CCK may have a specific role in the development of hyperthermia, and endogenous CCK-ergic mechanisms could contribute to the mediation of fever. Possible connections between thermoregulatory and other autonomic functional changes induced by CCK are discussed.

Central thermoregulatory effects of neuropeptide Y and orexin A in rats.

Orexin A and neuropeptide Y that are known to induce a feeding response when applied centrally, in the present studies also caused hypothermia. Neuropeptide Y elicited hypothermia by depressing metabolic rate (without affecting heat loss mechanisms), while orexin A acted through enhancing peripheral heat loss (without affecting metabolic rate). Neither peptide induced coordinated thermoregulatory changes, both of them appeared to influence thermoregulation via different effector mechanisms.

Neuroglia: possible role in thermogenesis and body temperature control.

The neuroglia, especially astrocytes, constitute a cell mass capable of adaptive heat production, since both the metabolic substrates and the biochemical machinery for energy production and its regulation seem to be available in these cells. Earlier physiological studies from this laboratory have provided circumstantial evidence that rodents such as rats and rabbits may indeed be capable of increasing their cerebral heat production during acute cold exposure. Recent relevant literature on the ability of neuroglia of the mammalian CNS to synthesize and release different transmitters and modulators and to communicate mutually with neuronal elements is discussed in support of the idea that different glial cell types could also contribute to the central regulation of body temperature in addition to the more established similar function of the neuronal pathways. The present hypothesis may have relevance to changes in glial cell mass and activity that occur in patients during the course of aging, or in gliosis with a consequent tendency for epilepsy caused by head trauma, with a consequent decrease or increase of intracranial metabolic rate, respectively. Also, the possibility for glial contribution to the thermoregulatory changes seen in psychoses is discussed.

Systemic but not central administration of tumor necrosis factor-alpha attenuates LPS-induced fever in rats.

The purpose of this study was to test the hypothesis that tumor necrosis factor-alpha (TNF) limits fever induced by lipopolysaccharide (LPS) in rats and to determine whether such antipyretic action of this cytokine is outside or inside the central nervous system (CNS). The CNS effects on LPS-induced fever were tested by injecting a subpyrogenic amount (0.20 microgram) of human recombinant TNF (hrTNF) intracerebroventricularly or by slowly infusing into the anterior hypothalamus an amount previously measured in this brain region during LPS fever (0.24 U in 0.13 microliter of artificial cerebrospinal fluid/min). The peripheral effects of this cytokine on LPS fever were tested by injecting 1 micrograms/kg of hrTNF intraperitoneally or by intraperitoneal administration of 300 micrograms/kg of the hrTNF soluble receptor p80 (hrTNFsr). The core temperature (measured by biotelemetry) during LPS fever was not significantly affected by administration of hrTNF intracerebroventricularly or intrahypothalamically. An intraperitoneal injection of hrTNF (1 microgram/kg) had a significant antipyretic effect on febrile response to LPS (mean temperature 2-8 h after injections was 37.28 +/- 0.12 degrees C in rats injected with hrTNF and LPS vs. 38.73 +/- 0.04 degrees C in rats injected with saline and LPS; analysis of variance among groups, P = 0.0001; Fisher's protected least significant difference, P < 0.05). When rats were injected intraperitoneally with hrTNFsr, the febrile response to LPS was enhanced (analysis of variance among groups, P = 0.0001; Fisher's protected least significant difference, P < 0.05). These results support the hypothesis that TNF acts to limit the magnitude of LPS-induced fever and that this action occurs outside the CNS.

Cholecystokinin participates in the mediation of fever.

Cholecystokinin of the central nervous system participates in the pathogenesis of lipopolysaccharide-induced fever in rats, contributing mainly to the first phase rise of this fever. The mediatory role is connected to type-B receptors of cholecystokinin.

Cholecystokinin octapeptide (CCK-8) injected into a cerebral ventricle induces a fever-like thermoregulatory response mediated by type B CCK-receptors in the rat.

In conscious female Wistar rats with chronic lateral cerebroventricular cannula, the thermoregulatory effects of CCK-8, ceruletide and prostaglandin E1 (PGE1) were studied. In addition, the possible involvement of type A or type B receptors of CCK-8 in thermoregulatory effects of PGE1 and CCK-8 was also investigated. In the normothermic rat an intracerebroventricular (i.c.v.) injection of CCK-8 or ceruletide induced a thermogenic response with tail-skin vasoconstriction and a resulting rise in colonic temperature (Tc). There was a significant negative correlation between the starting level of Tc and the extent of rise in Tc following an i.c.v. administration of PGE1, CCK-8 or ceruletide. Subcutaneously injected CCK-8 caused decreases in Tc in a cool ambient temperature as also described by others. The fever-like response to i.c.v. injected CCK-8 was attenuated by a CCK type B receptor blocker, but not by a CCK type A receptor blocker. Conversely, the hypothermic response to peripherally administered CCK-8 was attenuated by a type A receptor blocker, but not by a type B receptor blocker. Neither of these CCK-receptor blockers influenced the fever caused by an i.c.v. injection of PGE1. It is concluded that in normothermic rats the thermogenic response observed after i.c.v. injection of CCK-8 and ceruletide is the most likely central thermoregulatory change mediated by CCK type B receptors, while the well-known hypothermic response observed after peripheral injection of these peptides might also be explained by their direct effect on variables influencing some of the thermoregulatory effector mechanisms at the periphery.

Role of hypothalamic interleukin-6 and tumor necrosis factor-alpha in LPS fever in rat.

The purpose of this study was to determine, using push-pull perfusion, the levels of interleukin (IL)-1-like, IL-6-like, and tumor necrosis factor-alpha (TNF)-like activity in the anterior hypothalamus during lipopolysaccharide (LPS)-induced fever in rats. Additionally, slow anterior hypothalamic infusions of human recombinant IL-6 (hrIL-6) or TNF (hrTNF) for several hours were performed to determine possible febrile effects of these two cytokines. Artificial cerebrospinal fluid (aCSF) was infused as a control. Samples of cerebrospinal fluid were collected 60 min before and 60, 180, 300, and 420 min after the intraperitoneal injection of LPS. A control group was injected intraperitoneally with saline. The core temperature (measured by biotelemetry) of LPS-injected rats was significantly higher (P < 0.05) than the temperature of the rats injected with saline at 180, 300, and 420 min after the injection. The average postinjection IL-6 levels were significantly higher (P < 0.05) in the LPS-injected group. TNF was significantly higher (P < 0.05) than the baseline only at 180 min. There were no changes in levels of IL-1-like activity. Infusion of hrIL-6 at a level similar to the peak IL-6 level measured during LPS-induced fever resulted in a slowly developing and long-lasting increase in core temperature. Infusion of hrTNF at a level corresponding to the peak TNF level measured during LPS-induced fever did not induce a significant increase in core temperature. These results support the hypothesis that elevated hypothalamic concentrations of IL-6 are involved in the induction of fever elicited by peripheral (intraperitoneal) injection of LPS.

[The central thermoregulatory action of cholecystokinin-8 and prostaglandin E1]. / Tsentral'noe termoreguliatornoe deistvie kholetsistokinina-8 i prostaglandina E1.

In unanesthetized rats, the effects of intracerebroventricular injections of prostaglandin E1 (PGE1) and cholecystokinin octapeptide (CCK-8) on body temperature (Tb) regulation were studied. Both PGE1 and CCK-8 evoke hyperthermic responses of short latency and duration. Each substance raises the temperature, irrespective of initial temperature (Tbi). However, the maximal change in Tb and the rate of Tb rise depends on Tbi. A similarity of PGE1 and CCK-8 central thermoregulatory effects and putative roles of these substances in the mechanisms of fever, are discussed.