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PubMed1978

Factors influencing the quantity and quality of semen harvested from bulls, rams, boars and stallions.

Several inherited conditions associated with testicular defects, abnormal spermatogenesis and morphologically abnormal sperm have been found. These usually are controlled by single gene pairs. A notable exception is testicular size, with heritability in young bulls ranging from .42 to .88. Testicular size directly affects sperm output potential. The major contributor to variation in semen quality is the environment. Environmental effects may be temporary or permanent. Permanent effects occurring during prenatal and prepubertal periods and temporary or permanent factors acting after spermatogenesis is initiated can alter semen quality. Semen quality improves during the first few months after puberty and declines in old age. Malnutrition and the ingestion of toxic materials can have a major effect on testicular development and spermatogenesis, but the reproductive system has considerable regenerative capacity unless the dietary deficiencies are severe and prolonged. Elevated testicular temperatures resulting from incomplete descent of the testes (cryptorchidism), high environmental temperatures or inflammation are detrimental to spermatogenesis in all scrotal mammals. Cold temperatures appear to be innocuous unless actual freezing of tissue occurs. During periods of decreasing daylight semen quality declines in stallions and improves in seasonally breeding sheep. The time required to form and transport sperm in bulls, rams, boars and stallions is about 64, 56, 47 and 59 days. Therefore, a considerable potential lag may exist between a testicular event responsible for a change in semen quality and the time that this change is evident in ejaculated semen. Conditions imposed at the time of semen collection such as frequency of ejaculation, degree of sexual preparation and type of semen collection may influence the quality of semen harvested. Finally, certain semen characteristics are more variable than others and investigators should utilize suitable existing data to design the most effective least-cost experiments.

Animals↗
PubMed2002

Temperature and mortality in 11 cities of the eastern United States.

Episodes of extremely hot or cold temperatures are associated with increased mortality. Time-series analyses show an association between temperature and mortality across a range of less extreme temperatures. In this paper, the authors describe the temperature-mortality association for 11 large eastern US cities in 1973-1994 by estimating the relative risks of mortality using log-linear regression analysis for time-series data and by exploring city characteristics associated with variations in this temperature-mortality relation. Current and recent days' temperatures were the weather components most strongly predictive of mortality, and mortality risk generally decreased as temperature increased from the coldest days to a certain threshold temperature, which varied by latitude, above which mortality risk increased as temperature increased. The authors also found a strong association of the temperature-mortality relation with latitude, with a greater effect of colder temperatures on mortality risk in more-southern cities and of warmer temperatures in more-northern cities. The percentage of households with air conditioners in the south and heaters in the north, which serve as indicators of socioeconomic status of the city population, also predicted weather-related mortality. The model developed in this analysis is potentially useful for projecting the consequences of climate-change scenarios and offering insights into susceptibility to the adverse effects of weather.

Climate↗
PubMed1985

Pulmonary vascular responsiveness in cold-exposed calves.

The pulmonary vascular responses to acute hypoxia and to infusions of histamine and 5-hydroxytryptamine (5-HT) were recorded in unanesthetized standing bull calves under neutral (16-18 degrees C) and cold (3-5 degrees C) temperature conditions. Cold exposure alone resulted in a significant increase in pulmonary arterial wedge pressure from 10.2 +/- 3.5 to 15.9 +/- 4.9 Torr (1 Torr = 133.322 Pa). Resistance to blood flow between the pulmonary wedge and the left atrium significantly increased from 0.50 +/- 0.51 to 1.21 +/- 0.78 mmHg . L-1 . min-1 (1 mmHg = 133.322 Pa) with cold exposure. This apparent pulmonary venoconstrictor response to cold exposure was further evaluated to determine if hypoxia, histamine, or 5-HT responsiveness was altered by cold exposure. Twelve minutes of hypoxia increased pulmonary arterial and systemic arterial pressures, heart rate, and respiratory rate similarly in cold and neutral temperatures. Cold exposure did not alter the dose-related reductions of systemic arterial and pulmonary arterial pressures in response to histamine. Similarly, the decreases in systemic arterial pressure and heart rate and increases in pulmonary arterial and left atrial pressures in response to 5-HT were not significantly different in cold and neutral conditions. It was concluded that acute, mild cold exposure results in an increase in resistance to blood flow in the pulmonary venous circulation without a general increase in pulmonary vascular reactivity, as measured by responses to hypoxia, histamine, and 5-HT.

Animals↗
PubMed1970

Efeect of temperature on hospital admissions for myocardial infarction in a subarctic area.

In a study of the effect of mean daily temperature on the admission and fatality rates of 771 patients with myocardial infarction the admission rate was found to be significantly higher on cold (temperature below 0 degrees C.) than on warm (temperature above 0 degrees C.) days. The fatality rate was almost equal in cold and warm weather. Thus the seasonal fluctuation in the admission rate of patients with myocardial infarction is probably due to a direct effect of environmental temperature.

Arctic Regions↗
PubMed2000

Effects of thyroxine on rat brown fat and muscle thermogenesis in the cold.

We studied whether the activation of rat brown adipose tissue (BAT) by cold exposure or by the administration of beta-3-noradrenergic agonist CGP-12177 could be prevented by the inhibition of thyroxine (T4) to triiodothyronine (T3) conversion. Hypothyroid rats were treated with replacement doses of T4, T4 plus iopanoic acid (IA) or T3. Groups of rats were placed at 4 degrees C for 24 h or kept at room temperature. Cold exposure induced a significant increase in guanosine diphosphate (GDP) binding to BAT mitochondrial proteins in T4-treated rats, an effect not abolished by IA. No significant changes were seen in T3-treated rats. In rats maintained at room temperature and injected with CGP-12177, T4 induced a significant rise in GDP binding which was not blocked by IA. T3 also induced a significant increase in binding. The study of mitochondrial oxygen consumption in muscle from cold-exposed rats showed a marked decrease in consumption in T3-treated rats as compared to values in the warm. Normal oxygen consumption was restored with 2-fold doses of T3 replacement, whereas 5-fold doses increased consumption above normal. The data suggest that in states with low or absent T3, T4 can stimulate heat production and preserve normothermia.

Adipose Tissue, Brown↗
PubMedDate not supplied

[Gastric emptying in children. I. Influence of the temperature of a hydration solution for oral use].

The effect of temperature of solutions on gastric emptying was studied in sixteen children (8 infants and 8 newborns). At the time of the study all of them were being fed by nasogastric tube. Each baby had measured its gastric emptying for two different temperature solutions, approximately 27 degrees C and 4 degrees C, room and cold temperature. The gastric retention was calculated by knowing the injected volume, of about 20 ml per kilo of weight, the aspirated volume after 10 minutes and the obtained concentration of phenol red used as marker. The results showed a significant larger gastric retention for low temperature one. Possibly, low temperature solutions decrease the gastric peristalsis in accordance with hypothesis that low temperature solutions may inhibit vomiting.

Female↗
PubMed2006

Hypothermia-related deaths--United States, 1999-2002 and 2005.

Hypothermia, defined as a core body temperature of <95 degrees F (<35 degrees C), is preventable. Excessive exposure to cold temperatures leads to potentially fatal central nervous system depression, arrhythmias, and renal failure. Advanced age, chronic medical conditions, substance abuse, and homelessness are among risk factors for hypothermia-related death. This report describes three hypothermia-related deaths that occurred during 2005 and reviews CDC data on hypothermia-related deaths during 1999-2002 in the United States. Public health strategies should target U.S. populations at increased risk for exposure to excessive cold and recommend behavior modification (e.g., dressing warmly, modifying activity levels, or avoiding alcohol) to help reduce mortality and morbidity from hypothermia.

Adult↗
PubMed1992

[Cytophotometric and electrophysiologic analysis of the role of the celiac plexus in maintaining temperature homeostasis in cold stress in rats].

The role of the celiac plexus in maintaining temperature homeostasis in rats during cold stress was studied histochemically, ultrastructurally, and electrophysiologically. Inhibition on efferent impulses in preganglionic (splanchnic) nerves and facilitation in postganglionic (superior mesenteric) nerves during a short-term cold exposure leading to slight hypothermia were found. In cold-exposed animals after the celiac plexus decentralization, the neurons showed an increase in the fluorescence intensity and activity of energy metabolism enzymes, hyperplasia of fine structures responsible for protein synthesis and energy supply of cells. It is suggested that during cold stress when efferent impulse flow in preganglionic nerves markedly decreases, the celiac plexus becomes a regulatory centre for autonomic functions involved in the maintenance of temperature homeostasis.

Animals↗
PubMed1993

Heat loss during surgical skin preparation.

BACKGROUND: Hypothermia develops rapidly during the 1st h of anesthesia and results in part from evaporative heat loss during surgical skin preparation. The authors tested the hypothesis that evaporation of skin preparation solution contributes significantly to hypothermia. METHODS: Five healthy, unanesthetized volunteers were studied in a 22 +/- 0.4 degrees C environment. One thigh of each volunteer was washed for 10 min, using each of the following representative solutions: (1) water; (2) 50% ethanol in water (EtOH/H2O; similar to tincture of iodine); and (3) povidone-iodine gel. Water and EtOH/H2O each were tested at ambient temperature (cold), warmed to 40 degrees C before application (warm), and with radiant heating of the skin, and gel only at ambient temperatures, resulting in seven study states. Heat loss and skin temperatures on the washed thighs were measured using thermal flux transducers, and values compared with the data obtained from the contralateral unwashed thighs. Change in mean body temperature (per 70 kg) due to washing was calculated by integrating measured heat loss over time and multiplying by the specific heat of human tissue. A mathematical model was developed to predict cutaneous heat loss using only skin temperature, independent of the type and temperature of skin-preparation solution or the use of radiant heating during preparation. RESULTS: Heat loss from the unwashed thigh was approximately 14 kcal/m2 during radiant warming and approximately 39 kcal/m2 without warming. Net heat loss (increment produced by washing) was approximately 30 kcal/m2 with water and gel without radiant warming, but loss was larger with EtOH/H2O than with water under all study conditions. Radiant warming reduced total heat loss (increment produced by washing and environment) during both the EtOH/H2O and water trials, compared with warm or cold EtOH/H2O and water alone. The calculated decreases in mean body temperature per 70 kg ranged from -0.2 to -0.7 degree C/m2. The smallest decrease occurred during radiant warming and washing with water, and the largest decreases during warm or cold EtOH/H2O. CONCLUSIONS: Heat loss was significantly less with water-based than with alcohol-based solutions. Though heating the solutions and radiant warming decreased heat loss, such loss under each tested condition, even per square meter of washed surface, was small compared to other causes of perioperative hypothermia. Consequently, the authors recommend that efforts to maintain intraoperative normothermia be directed elsewhere.

Adult↗
PubMed2000

Effects of delayed intraischemic and postischemic hypothermia on a focal model of transient cerebral ischemia in rats.

BACKGROUND AND PURPOSE: Intraischemic mild hypothermia has been shown to be neuroprotective in reducing cerebral infarction in transient focal ischemia. As a more clinical relevant issue, we investigated the effect of delayed intraischemic and postischemic hypothermia on cerebral infarction in a rat model of reversible focal ischemia. We also examined the effect of hypothermia on the inflammatory response after ischemia-reperfusion to assess the neuroprotective mechanism of brain hypothermia. METHODS: Rats were subjected to 2 hours of middle cerebral artery occlusion followed by 22 hours of reperfusion under the following protocols: (1) rats were treated with normothermia (37.0 degrees C, 4 hours) and then housed in room temperature (25 degrees C, 18 hours) and (2) rats were treated with hypothermia (33.0 degrees C, 4 hours, brain temperature modulation was started 30 minutes before the reperfusion) and then housed in cold temperature (5 degrees C, 18 hours). Animals were killed 24 hours after the onset of ischemia. The infarct volume was examined with 2,3,5-triphenyl-tetrazolium chloride staining. The accumulation of polymorphonuclear leukocytes (PMNLs) and the expression of intercellular adhesion molecule-1 mRNA were evaluated in both groups. RESULTS: A significant reduction (P<0.05) in infarct volume was found in the hypothermia group compared with the normothermia group. Compared with the normothermia group, hypothermic treatment also significantly reduced the accumulation of PMNLs (P<0.01) and inhibited the overexpression of intercellular adhesion molecule-1 mRNA at 22 hours of reperfusion after 2 hours of ischemia. CONCLUSIONS: Ischemic brain damage can be reduced with delayed intraischemic and prolonged postischemic hypothermia in a focal model of transient cerebral ischemia in rats. The neuroprotective mechanism of hypothermia may be mediated by suppression of PMNL-mediated inflammatory response after ischemia-reperfusion in this model.

Animals↗
PubMed1982

Survival under heat stress of lines selected for fast and slow growth at two temperatures.

Two replicates of four lines of White Leghorn chickens previously selected for fast and slow gain from 5 to 9 weeks of age in a hot (32.2 C) and cold (21.1 C) selection environment were grown from 5 to 9 weeks in the hot and cold temperature environments and then subjected to high temperature stress at 40.6 C. Four different experiments were run. The percent mortality was analyzed when approximately 50% of the birds had died. Birds reared in the cold environment were heavier and consistently had higher mortality than those reared in the hot environment when both were subjected to acute heat stress (40.6 C). The importance of acclimation to mild heat stress on response to acute heat stress was demonstrated by the mortality difference. No significant differences in survival under heat stress were found between lines selected in the hot and the cold selection environments. Lines selected for fast growth had significantly higher mortality rates under high temperature stress than lines selected for slow growth in replicate 1 but not in replicate 2. Estimates of the genetic correlation between weight gain from 5 to 9 weeks of age and percent mortality under heat stress after two generations of selection in replicate 2 was -.004, and after three generations of selection in replicate 1 was +.076.

Animals↗
PubMed2000

The clinical impact of warmed insufflation carbon dioxide gas for laparoscopic cholecystectomy.

BACKGROUND: Reports suggest that the insufflation of cold gas to produce a pneumoperitoneum for laparoscopic surgery can lead to an intraoperative decrease in core body temperature and increased postoperative pain. METHODS: In a randomized controlled trial with 20 patients undergoing laparoscopic cholecystectomy, the effect of insufflation using carbon dioxide gas warmed to 37 degrees C (group W) was compared with insufflation using room-temperature cold (21 degrees C) gas (group C). Intraoperative body core and intra-abdominal temperatures were determined at the beginning and end of surgery. Postoperative pain intensity was evaluated using a visual analog scale and recording the consumption of analgesics. RESULTS: There were no significant group-specific differences during the operation, neither in body temperature (group W: 36.1 +/- 0.4 degrees C vs group C: 35.7 +/- 0.6 degrees C) nor in intra-abdominal temperature (group W: 35.9 +/- 0.3 degrees C vs group C: 35.6 +/- 0. 6 degrees C). Postoperatively, the two groups did not differ in pain susceptibility and need of analgesics. CONCLUSION: The use of carbon dioxide gas warmed to body temperature to produce a pneumoperitoneum during short-term laparoscopic surgery has no clinically important effect.

Aged↗
PubMed2001

Temperature sensing and cold acclimation.

The fundamental question in cold acclimation is how do plants perceive the low but nonfreezing temperatures that activate cold acclimation responses. New findings in the past year suggest that changes in membrane fluidity, cytoskeleton rearrangement, and calcium influxes are among the earliest events taking place in plants upon exposure to low nonfreezing temperatures. In the cyanobacterium Synechocystis PCC6803, temperature change is detected by at least two separate sensors. One of these measures membrane fluidity using a classical two-component system involving histidine kinases and a response regulator in a His-to-Asp phosphorelay. Although these Synechocystis results may not be directly relevant to cold acclimation, they can guide our thinking as we search for biological thermometers in higher plants.

Acclimatization↗
PubMed1996

Opioid and nonopioid swim stress-induced analgesia: a parametric analysis in mice.

Environmental stress causes the activation of two types of endogenous pain inhibitory systems in animals: opioid analgesia is antagonized by opiate receptor blockers (e.g., naloxone and naltrexone), whereas analgesia produced by nonopioid systems is insensitive to such antagonism. A large literature documents that the parameters of the laboratory stressor will determine the neurochemical identity of the resultant analgesia. In rats, low severity stressors produce opioid analgesia and higher severity stressors produce nonopioid analgesia. A recent parametric analysis of swim stress-induced analgesia (SSIA) in the female Quackenbush mouse, however, observed the opposite pattern. The present study is a parametric analysis of SSIA using a range of swim temperatures (15-38 degrees C), swim durations (45 s to 7 min), and genetic models [male Swiss-Webster mice, and mice selectively bred from this outbred strain for high (HA), low (LA), or control SSIA]. We find that in nonselected mice low severity swims (i.e., warm temperature, short duration) produce naloxone-sensitive opioid SSIA, whereas high severity swims (i.e., cold temperature, long duration) produce nonopioid SSIA. This pattern is also seen in HA mice displaying very high analgesic magnitudes, but not in LA mice displaying minimal SSIA. In the selectively bred mice, analgesia and hypothermia from forced swimming are positively correlated, but can be dissociated both genetically and neurochemically. Furthermore, swimming in body temperature (38 degrees C) water produces analgesia without concommitant hypothermia, and the increased magnitude of 38 degrees C SSIA displayed by HA mice over control levels is entirely opioid.

Analgesia↗
PubMed2005

Environmental regulation of the anaerobic oxidation of methane: a comparison of ANME-I and ANME-II communities.

The anaerobic oxidation of methane (AOM) is one of the major sinks for methane on earth and is known to be mediated by at least two phylogenetically different groups of anaerobic methanotrophic Archaea (ANME-I and ANME-II). We present the first comparative in vitro study of the environmental regulation and physiology of these two methane-oxidizing communities, which occur naturally enriched in the anoxic Black Sea (ANME-I) and at Hydrate Ridge (ANME-II). Both types of methanotrophic communities are associated with sulfate-reducing-bacteria (SRB) and oxidize methane anaerobically in a 1:1 ratio to sulfate reduction (SR). They responded sensitively to elevated methane partial pressures with increased substrate turnover. The ANME-II-dominated community showed significantly higher cell-specific AOM rates. Besides sulfate, no other electron acceptor was used for AOM. The processes of AOM and SR could not be uncoupled by feeding the SRB with electron donors such as acetate, formate or molecular hydrogen. AOM was completely inhibited by the addition of bromoethanesulfonate in both communities, indicating the participation of methanogenic enzymes in the process. Temperature influenced the intensity of AOM, with ANME-II being more adapted to cold temperatures than ANME-I. The variation of other environmental parameters, such as sulfate concentration, pH and salinity, did not influence the activity of both communities. In conclusion, the ecological niches of methanotrophic Archaea seem to be mainly defined by the availability of methane and sulfate, but it remains open which additional factors lead to the dominance of ANME-I or -II in the environment.

Anaerobiosis↗