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Biomedical subjects

P Lomax

Publications and source records attributed to P Lomax.

At least 55 records · Page 3Linked to original sources
PubMed1981

Objective techniques for the assessment of postmenopausal hot flashes.

The present study was undertaken to evaluate objective methods of monitoring postmenopausal hot flashes. Continuous recordings of finger and core temperature and sternal skin conductance were carried out in 8 postmenopausal and 4 premenopausal women. Four postmenopausal patients were studied a second time following 30 days of daily oral administration of ethinyl estradiol 0.05 mg. One hundred twenty flashes were subjectively noted and recorded during 104 hours of study in the postmenopausal women. Eighty-two, 98, and 81% of subjective flashes were associated with changes in finger temperature, skin conductance, and core temperature, respectively. The rate of occurrence and magnitude of changes of physiologic markers were significantly greater (P less than .01) in postmenopausal than premenopausal women. Estrogen replacement therapy not only eliminated the subjective sensations but also significantly reduced (P less than .02) the frequency and magnitude of the changes in physiologic function measured by finger temperature. Measurement of skin conductance changes was the single most sensitive and specific indicator of hot flashes. The simultaneous change of both skin conductance and finger temperature, although less sensitive, was a very specific indicator of a hot flash. These results support the concept that the measurement of physiologic changes can be used to assess objectively the occurrence of this symptom complex.

Adult↗
PubMed1980

Postmenopausal hot flushes: a disorder of thermoregulation.

The changes in cutaneous and body temperature and cutaneous conductance during hot flushes in eight postmenopausal women were studied. The vasomotor changes occurred approx. 45 sec after the patients experienced the initial subjective symptoms of the attacks. The rise in skin conductance appeared to be a more reliable index of the flushing episode than did the change in skin temperature. On the basis of the changes recorded it is suggested that the hot flush syndrome may represent a specific thermoregulatory disorder rather than being due to a non-specific central autonomic discharge. The episodes may be triggered by a neuroendocrine imbalance following the disruption of ovarian function and fall in estrogen production. In assessing the frequency and severity of hot flushes, and the effects of treatment, objective measurements of skin and core temperature and skin conductance should replace subjective criteria.

Adult↗
PubMed1980

Comparison of nine brands of membrane filter and the most-probable-number methods for total coliform enumeration in sewage-contaminated drinking water.

Nine different brands of membrane filter were compared in the membrane filtration (MF) method, and those with the highest yields were compared against the most-probable-number (MPN) multiple-tube method for total coliform enumeration in simulated sewage-contaminated tap water. The water was chlorinated for 30 min to subject the organisms to stresses similar to those encountered during treatment and distribution of drinking water. Significant differences were observed among membranes in four of the six experiments, with two- to four-times-higher recoveries between the membranes at each extreme of recovery. When results from the membranes with the highest total coliform recovery rate were compared with the MPN results, the MF results were found significantly higher in one experiment and equivalent to the MPN results in the other five experiments. A comparison was made of the species enumerated by these methods; in general the two methods enumerated a similar spectrum of organisms, with some indication that the MF method was subject to greater interference by Aeromonas.

Chlorine↗
PubMed1980

Ethanol-induced hypothermia in the rat.

Ethanol (0.5-3.2g x kg-1 i.p.) caused a dose-dependent fall in body temperature in rats. A dose of 1.5g x kg-1 i.p. led to a fall of 1.6 +/- 0.20 degrees C over 60 min at an environmental temperature of 18 +/- 1 degrees C. There was no evidence of acute tolerance when the hypothermic response was elicited by the same dose of ethanol (0.7--20.0g x kg-1 i.p.) 24 h later; indeed the second response was consistently, although not significantly, greater than the first. Behavioral thermoregulatory studies indicated that the fall in temperature after ethanol is due, at least in part, to a downward setting in the thermoregulatory set point. These results suggest that the rat may be a suitable animal model for a study of accidental hypothermia following ethanol ingestion and exposure to low environmental temperatures.

Animals↗
PubMed1977

Dopaminergic mechanisms in precipitated withdrawal in morphine-dependent rats.

Rats were made dependent on morphine by implantation of a pellet and withdrawal was precipitated by the injection of naloxone 72 hours later. Withdrawal was assessed by scoring each of the following signs individually: chewing, licking, teeth chattering, facial tremor, grooming, writhing, diarrhea, weight loss, wet dog shakes, head shakes and hypothermia. The role of dopamine in withdrawal was determined by pretreating the animals with apomorphine or pimozide. Apomorphine in the lower dose range (0.625-1.25 mg/kg) produced a significant decrease in teeth chattering, writhing, weight loss and wet dog shakes. The high dose of apomorphine (2.5 mg/kg) significantly inhibited all features of the withdrawal except writhing and weight loss. Pimozide caused a significant increase in chewing, writhing and head shakes, but only with the highest dose used (0.5 mg/kg). Pimozide (0.5 mg/kg) significantly reduced withdrawal hypothermia, but apomorphine had no effect on this sign except at the highest dose when withdrawal hypothermia was increased.

Animals↗
PubMed1976

Naltrexone-induced hypothermia in the rat.

Naltrexone, in relatively high doses, has been reported to cause a fall in body temperature in human ex-heroin addicts who had been abstinent for at least 6 weeks. The underlying mechanism of this hypothermic effect has been investigated in rats. The first consideration was that the temperature change was a reflection of delayed withdrawal but rats implanted with a morphine pellet 45 days earlier showed no significant change in temperature after a dose of naltrexone that caused marked withdrawal hypothermia in dependent rats implanted 3 days previously. A fall in core temperature was only induced in rats after doses of 80 and 160 mg/kg i.p. of naltrexone. Behavioral thermoregulatory studies revealed that the animals correct the falling body temperature by increased exposure to a radiant heat source indicating that the central thermostats had not been significantly affected by the drug. These data suggest that the major component in the hypothermic effect of naltrexone is activation of efferent heat loss pathways or peripheral heat loss mechanisms. Due to current suggestions that opiate receptors might represent the receptors for an endogenous transmitter the results are discussed in relation to this consideration. When compared to the sites and mechanism of action of opiates on thermoregulation the results with naltrexone lend little support to the hypothesis that the fall in temperature is due to displacement of an endogenous substance from central opiate receptors.

Animals↗
PubMed1976

Morphine hyperthermia in the rat: an action on the central thermostats.

The mechanism underlying the hyperthermic response to low doses of morphine has been investigated in rats. Doses of morphine sulfate less than 10 mg/kg i.p. caused a rise in body temperature accompanied by vasoconstriction of the cutaneous blood vessels of the tail. This hyperthermia, unlike the hypothermia following higher doses of morphine was not blocked by naloxone nor did tolerance develop to the response. Injections directly into the hypothalamus suggested that, as with the fall in temperature after high doses of morphine, the hyperthermic effect is also due to an action on the preoptic/anterior hypothalamic thermoregulatory centers. Experiments measuring thermoregulatory behavior showed that rats delayed escaping from a heat load after low doses of morphine even though their core temperature was rising. These results suggest that low doses of morphine raise the set point of the central thermostats in rats resulting in a hyperthermia mediated, at least in part, by decreased cutaneous heat loss.

Animals↗