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Biomedical subjects

A M Sessler

Publications and source records attributed to A M Sessler.

7 recordsLinked to original sources
PubMed1996

Regulation of stearoyl-CoA desaturase 1 mRNA stability by polyunsaturated fatty acids in 3T3-L1 adipocytes.

The effects of arachidonic acid (20:4, n-6) and other fatty acids on the expression of stearoyl-CoA desaturase gene 1 were investigated in fully differentiated 3T3-L1 adipocytes. Treatment of 3T3-L1 adipocytes with arachidonic acid resulted in a decrease in stearoyl-CoA desaturase (Scd) enzyme activity and scd1 mRNA. Arachidonic acid did not alter the transcription of the scd1 gene, whereas the half-life of the scd1 mRNA was reduced from 25.1 to 8.5 h. Blocking the conversion of arachidonic acid to eicosanoids by pretreatment of the cells with cyclooxygenase, lipoxygenase, or cytochrome P-450 epoxygenase inhibitors did not reverse the inhibition caused by arachidonic acid, indicating that eicosanoid synthesis is not necessary for the repression of scd1 mRNA expression. Treatment of adipocytes with linoleic (18:2, n-6) and linolenic (18:3, n-3) acids also resulted in inhibition of scd1 mRNA accumulation. By contrast, oleic acid (18:1, n-9) and stearic acid (18:0) had no effect on scd1 mRNA levels. Taken together, these results suggest that polyunsaturated fatty acids repress the expression of the scd1 gene in mature adipocytes by reducing the stability of scd1 mRNA.

3T3 Cells↗
PubMed1996

A model cell line to study regulation of stearoyl-CoA desaturase gene 1 expression by insulin and polyunsaturated fatty acids.

Insulin and polyunsaturated fatty acids (PUFAs) regulate the expression of SCD1 gene in mouse liver. Accordingly, we examined the insulin and PUFA regulation of SCD1 gene expression in H2.35 cells. The levels of SCD1 mRNA in H2.35 cells increased at the restrictive temperature of 39 degrees C, when the glucose-containing medium was supplemented with insulin. The insulin-stimulated expression of SCD1 mRNA was significantly blunted when the induction medium was supplemented with linolenic acid (18:2n-3) and arachidonic acid (20:4n-6). Stearic acid (18:0n-9) and oleic acid (18:1n-9) were without dramatic effects. The effect of insulin and PUFAs on a transfected SCD1 fusion gene (SCD1.CAT4.3) was also examined in H2.35 cells. Whereas insulin stimulated SCD1.CAT4.3 expression, arachidonic acid significantly decreased SCD1.CAT4.3 activity. These studies suggest that insulin and PUFAs regulate SCD1 gene transcription via regulatory DNA sequences flanking the 5' end of the gene.

Actins↗
PubMed1995

Heat flow and distribution during induction of general anesthesia.

BACKGROUND: Core hypothermia after induction of general anesthesia results from an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution. METHODS: Six minimally clothed male volunteers in an approximately 22 degrees C environment were evaluated for 2.5 control hours before induction of general anesthesia and for 3 subsequent hours. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in distal esophageal (core) temperature, leaving the core hypothermia specifically resulting from redistribution. RESULTS: Core temperature was nearly constant during the control period but decreased 1.6 +/- 0.3 degree C in the first hour of anesthesia. Redistribution contributed 81% to this initial decrease and required transfer of 46 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 1.1 +/- 0.3 degree C, with redistribution contributing only 43%. Thus, only 17 kcal was redistributed during the second and third hours of anesthesia. Redistribution therefore contributed 65% to the entire 2.8 +/- 0.5 degree C decrease in core temperature during the 3 h of anesthesia. Proximal extremity heat content decreased slightly after induction of anesthesia, but distal heat content increased markedly. The distal extremities thus contributed most to core cooling. Although the arms constituted only a fifth of extremity mass, redistribution increased arm heat content nearly as much as leg heat content. Distal extremity heat content increased approximately 40 kcal during the first hour of anesthesia and remained elevated for the duration of the study. CONCLUSIONS: The arms and legs are both important components of the peripheral thermal compartment, but distal segments contribute most. Core hypothermia during the first hour after induction resulted largely from redistribution of body heat, and redistribution remained the major cause even after 3 h of anesthesia.

Adult↗
PubMed1993

Leg heat content continues to decrease during the core temperature plateau in humans anesthetized with isoflurane.

BACKGROUND: Sufficient hypothermia during anesthesia provokes thermoregulatory responses, but the clinical significance of these responses remains unknown. Nonshivering thermogenesis does not increase metabolic heat production in anesthetized adults. Vasoconstriction reduces cutaneous heat loss, but the initial decrease appears insufficient to cause a thermal steady state (heat production equaling heat loss). Accordingly, the authors tested the hypotheses that: 1) thermoregulatory vasoconstriction prevents further core hypothermia; and 2) the resulting stable core temperature is not a thermal steady state, but, instead, is accompanied for several hours by a continued reduction in body heat content. METHODS: Six healthy volunteers were anesthetized with isoflurane (0.8%) and paralyzed with vecuronium. Core hypothermia was induced by fan cooling, and continued for 3 h after vasoconstriction in the legs was detected. Leg heat content was calculated from six needle thermocouples and skin temperature, by integrating the resulting parabolic regression over volume. RESULTS: Core temperature decreased 1.0 +/- 0.2 degrees C in the 1 h before vasoconstriction, but only 0.4 +/- 0.3 degrees C in the subsequent 3 h. This temperature decrease, evenly distributed throughout the body, would reduce leg heat content 10 kcal. However, measured leg heat content decreased 49 +/- 18 kcal in the 3 h after vasoconstriction. CONCLUSIONS: These data thus indicate that thermoregulatory vasoconstriction produces a clinically important reduction in the rate of core cooling. This core temperature plateau resulted, at least in part, from sequestration of metabolic heat to the core which allowed core temperature to remain nearly constant, despite a continually decreasing body heat content.

Anesthesia, Inhalation↗
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↗
PubMed1991

Perioperative thermal insulation.

To determine the efficacy of passive insulators advocated for prevention of cutaneous heat loss, we determined heat loss in unanesthetized volunteers covered by one of the following: a cloth "split sheet" surgical drape; a Convertors disposable-paper split sheet; a Thermadrape disposable laparotomy sheet; an unheated Bair Hugger patient-warming blanket; 1.5-mil-thick plastic hamper bags; and a prewarmed, cotton hospital blanket. Cutaneous heat loss was measured using 10 area-weighted thermal flux transducers while volunteers were exposed to a 20.6 degrees C environment for 1 h. Heat loss decreased significantly from 100 +/- 3 W during the control periods to 69 +/- 6 W (average of all covers) after 1 h of treatment. Heat losses from volunteers insulated by the Thermadrape (61 +/- 6 W) and Bair Hugger covers (64 +/- 5 W) were significantly less than losses from those insulated by plastic bags (77 +/- 11 W). The paper drape (67 +/- 7 W) provided slightly, but not significantly, better insulation than the cloth drape (70 +/- 4 W). Coverage by prewarmed cotton blankets initially resulted in the least heat loss (58 +/- 8 W), but after 40 min, resulted in heat loss significantly greater than that for the Thermadrape (71 +/- 7 W). Regional heat loss was roughly proportional to surface area, and the distribution of regional heat loss remained similar with all covers. These data suggest that cost and convenience should be major factors when choosing among passive perioperative insulating covers. It is likely that the amount of skin surface covered is more important than the choice of skin region covered or the choice of insulating material.

Adult↗