Controversies surrounding tympanic temperature (Tty) itself and techniques for measuring it have dampened the potential usefulness of Tty in determining core temperature (operationally defined here as the body temperature taken at a deep body site). The present study was designed to address the following questions. 1) Can a tympanic membrane probe be made that is safer and more reliable than its predecessors? 2) Why is the effect of facial cooling and heating on Tty so inconsistent in reports from different laboratories? 3) Is Tty still useful as a measure of core temperature? Data from this study, obtained with a modified thermocouple probe, suggest that the widely reported facial skin cooling effect on Tty is most probably due to thermal contamination from the surrounding ear canal wall and/or suboptimal contact of the probe sensor with the tympanic membrane because 1) Tty that fell during facial cooling was increased to the precooling level by the repositioning of the probe sensor; 2) Tty determined by using a probe with a larger sensor area (the sensor soldered to a steel wire ring)tended to fall in response to facial cooling, whereas Tty determined with a thermally insulated probe ring did not; and 3) Tty obtained under careful positioning of the insulated probe was relatively insensitive to facial cooling or heating. Because Tty was practically identical to esophageal temperature (Tes) in the steady state, i.e., 36.83 +/- 0.20 (SD) degrees C for Tty and 36.87 +/- 0.16 degrees C for Tes at room temperature (n = 11), and because facial cooling had little effect on both Tty and Tes (36.86 +/- 0.17 degrees C for Tty and 36.86 +/- 0.26 degrees C for Tes during facial or scalp skin cooling), we support the postulate that Tty is a good measure of core temperature. The temperature transient in response to foot warming was detected 5 min (n = 2) faster with Tty than with Tes. Thus, with further improvements in the design of the probe. Tty can become a standard for determination of core body temperature.

Insulin and insulin-like growth factor I (IGF-I) influence numerous metabolic and mitogenic processes; these hormones also have vasoactive properties. This study examined mechanisms involved in insulin- and IGF-I-induced dilation in canine conduit and microvascular coronary segments. Tension of coronary artery segments was measured after constriction with PGF(2alpha). Internal diameter of coronary microvessels (resting diameter = 112.6+/-10.1 microm) was measured after endothelin constriction. Vessels were incubated in control (Krebs) solution and were treated with N(omega)-nitro-L-arginine (L-NA), indomethacin, or K(+) channel inhibitors. After constriction, cumulative doses of insulin or IGF-I (0.1-100 ng/ml) were administered. In conduit arteries, insulin produced modest maximal relaxation (32 +/- 5%) compared with IGF-I (66+/-12%). Vasodilation was attenuated by nitric oxide synthase (NOS) and cyclooxygenase inhibition and was blocked with KCl constriction. Coronary microvascular relaxation to insulin and IGF-I was not altered by L-NA, indomethacin, tetraethylammonium chloride, glibenclamide, charybdotoxin, and apamin; however, tetrabutylammonium chloride attenuated the response. In conclusion, insulin and IGF-I cause vasodilation in canine coronary conduit arteries and microvessels. In conduit vessels, NOS/cyclooxygenase pathways are involved in the vasodilation. In microvessels, relaxation to insulin and IGF-I is not mediated by NOS/cyclooxygenase pathways but rather through K(+)-dependent mechanisms.

Reactive oxygen species mediate arachidonic acid: induced dilation in porcine coronary microvessels. Am J Physiol Heart Circ Physiol 285: H2309-H2315, 2003. First published July 17, 2003 10.1152/ajpheart.00456.2003.-Reactive oxygen species (ROS) have been proposed to mediate vasodilation in the microcirculation. We investigated the role of ROS in arachidonic acid (AA)-induced coronary microvascular dilation. Porcine epicardial coronary arterioles (110 Ϯ 4 m diameter) were mounted onto pipettes in oxygenated Krebs buffer. Vessels were incubated with vehicle or 1 mM Tiron (a nonselective ROS scavenger), 250 U/ml polyethylene-glycolated (PEG)-superoxide dismutase (SOD; an O 2 Ϫ scavenger), 250 U/ml PEG-catalase (a H2O2 scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 M) or diclofenac (10 M) for 30 min. After endothelin constriction (30-60% of resting diameter), cumulative concentrations of AA (10 Ϫ10 -10 Ϫ5 M) were added and internal diameters measured by video microscopy. AA (10 Ϫ7 M) produced 37 Ϯ 6% dilation, which was eliminated by the administration of indomethacin (4 Ϯ 7%, P Ͻ 0.05) or diclofenac (Ϫ8 Ϯ 8%, P Ͻ 0.05), as well as by Tiron (Ϫ4 Ϯ 5%, P Ͻ 0.05), PEG-SOD (Ϫ10 Ϯ 6%, P Ͻ 0.05), or PEG-catalase (1 Ϯ 4%, P Ͻ 0.05). Incubation of small coronary arteries with [ 3 H]AA resulted in the formation of prostaglandins, which was blocked by indomethacin. In separate studies in microvessels, AA induced concentration-dependent increases in fluorescence of the oxidant-sensitive probe dichlorodihydrofluorescein diacetate, which was inhibited by pretreatment with indomethacin or by SOD ϩ catalase. We conclude that in porcine coronary microvessels, COX-derived ROS contribute to AA-induced vasodilation.cyclooxygenase; coronary microcirculation THE VASCULAR ENDOTHELIUM generates a number of vasoactive agents that are important in the regulation of coronary blood flow. These putative agents may be produced through several enzyme pathways, including nitric oxide synthase (NOS), cyclooxygenase (COX), lipoxygenase (LOX), and the cytochrome P-450 monooxygenase (CYP-450) systems. Responses have been determined to be dependent on vessel size, animal species, and regional circulation. Our group reported that in the dog, arachidonic acid (AA)-induced dilatory responses in the coronary microcirculation are mediated through redundant pathways (15). However, Hein and colleagues (7) demonstrated that in the porcine coronary microcirculation, dilation may be mediated through COX.Several groups have proposed that reactive oxygen species (ROS) are mediators of microvascular dilation (1,12,18). Putative ROS mediators include superoxide anions, hydrogen peroxide, and hydroxyl radicals. Metabolism of AA by COX, LOX, or CYP-P450 may be associated with the production of oxygen-derived free radicals (5, 8). In the microcirculation of the brain, ROS derived through metabolism of AA have been suggested to mediate vasodilatory responses to bradykinin (3).Mediators of AA-induced relaxation in the coronary microcirculation rem...

In coronary resistance vessels, endothelium-derived hyperpolarizing factor (EDHF) plays an important role in endothelium-dependent vasodilation. EDHF has been proposed to be formed through cytochrome P-450 monooxygenase metabolism of arachidonic acid (AA). Our hypothesis was that AA-induced coronary microvascular dilation is mediated in part through a cytochrome P-450 pathway. The canine coronary microcirculation was studied in vivo (beating heart preparation) and in vitro (isolated microvessels). Nitric oxide synthase (NOS) (N(omega)-nitro-L-arginine, 100 microM) and cyclooxygenase (indomethacin, 10 microM) or cytochrome P-450 (clotrimazole, 2 microM) inhibition did not alter AA-induced dilation. However, when a Ca(2+)-activated K(+) channel channel or cytochrome P-450 antagonist was used in combination with NOS and cyclooxygenase inhibitors, AA-induced dilation was attenuated. We also show a negative feedback by NO on NOS-cyclooxygenase-resistant AA-induced dilation. We conclude that AA-induced dilation is attenuated by cytochrome P-450 inhibitors, but only when combined with inhibitors of cyclooxygenase and NOS. Therefore, redundant pathways appear to mediate the AA response in the canine coronary microcirculation.

In a series of experiments the effects of colony lighting conditions on homecage aggression were examined, and the relation among measures of homecage aggressive behavior and shock-induced aggression were determined. In each experiment rats were maintained under either a light/dark (LD) cycle or a continuous light (LL) schedule. Experiments IA and IB indicated that for cages of LD rats the highest rates of home-cage aggression occurred during the dark segment of the light cycle whereas the lowest rates of aggression characterized the light segment. In contrast, the rate of home-cage aggression was low and constant across time periods for cages of LL rats. Reflecting these differences between lighting conditions, regression analyses in Experiment IB identified a periodic trend following the fundamental sine curve in the home-cage aggression data from cages of LD rats but not in the data from cages of LL rats. In Experiment 2 the relation between individual differences in home-cage aggression and shock-induced aggression was found to be time dependent for pairs of LD rats. Correlations based on scores of home-cage aggression and shock-induced aggression obtained during the dark segment were positive and statistically significant. Correlations of these two aggressive behaviors based on scores obtained during the light segment were not statistically significant. For pairs of LL rats, no timedependent pattern in the relation of home-cage aggression to shock-induced aggression was observed.The lighting conditions under which laboratory animals are maintained can have significant influences on a range of biologically important behaviors (e.g., Richter, 1965;Wurtman, Axelrod, & Kelly, 1968;Zucker, 1971). In a recent series of experiments Knutson, Hynan, and Kane (1976) demonstrated that shock-induced aggression was also influenced by the colony lighting conditions under which male rats were raised. These experiments indicated that rats maintained on a 12:12 hr light/dark (LD) cycle