Acute stress triggers peripheral vasoconstriction, causing a rapid, short-term drop in skin temperature in homeotherms. We tested, for the first time, whether this response has the potential to quantify stress, by exhibiting proportionality with stressor intensity. We used established behavioural and hormonal markers: activity level and corticosterone level, to validate a mild and more severe form of an acute restraint stressor in hens (Gallus gallus domesticus). We then used infrared thermography (IRT) to non-invasively collect continuous temperature measurements following exposure to these two intensities of acute handling stress. In the comb and wattle, two skin regions with a known thermoregulatory role, stressor intensity predicted the extent of initial skin cooling, and also the occurrence of a more delayed skin warming, providing two opportunities to quantify stress. With the present, cost-effective availability of IRT technology, this non-invasive and continuous method of stress assessment in unrestrained animals has the potential to become common practice in pure and applied research.

1 Isoprenaline (10-9-10' M) relaxed rat isolated mesenteric resistance arteries pre-contracted with K+ (30-60 mM) (p EC50 (M) 8.03 + 0.40; maximum relaxation 66.79 ± 2.43%, n = 7). This relaxation was partially attenuated by the nitric oxide (NO) synthase inibitor Nw-nitro-L-arginine methyl ester (L-NAME, 10-4 M).2 The P2-adrenoceptor agonist, salbutamol (10-9-1iO-M), produced a modest maximum relaxation (35.93 ± 2.93%), which was not sensitive to L-NAME.3 The PI-adrenoceptor agonist, dobutamine (l0-9-l0-5M), relaxed arteries precontracted with K+.This relaxation was abolished by L-NAME (10-4 M) and also by propranolol (10-6 M), but not affected by D-NAME (10-4 M). The inhibition by L-NAME was partially reversed by L-arginine (l0-3 M).Removal of the endothelium severely attenuated relaxation to dobutamine. 4 Contractile responses to depolarizing K+ solutions were enhanced by the addition of L-NAME, and also by removal of the endothelium.5 The above findings demonstrate that P1-adrenoceptor activation causes relaxation via NO release from the endothelium of rat mesenteric resistance arteries. In addition, contraction to K+ is modified by release of NO from the endothelium, possibly in response to tension development.

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B-mode ultrasound was used to measure fat and muscle thicknesses on 30 subjects (17 men, 13 women, age = 20-37 yr) at 14 sites (triceps, biceps, forearm, chest [males only], subscapular, axilla, abdomen, suprailium, lumbar, quadriceps, suprapatellar, hamstrings, medial calf, and posterior calf) on two different days. Quadruplicate photographic images (trials) were printed from a single measurement at each site on each day. Two investigators each measured two of the images from each site. Each thickness was measured to the nearest 0.05 mm with a vernier caliper. Generalizability theory was used to determine the relative contribution of subjects, investigators, days, and trials to the total measurement variability. Subjects accounted for 84-96% of the variance in the muscle measurements and for 79-97% of the variance in the fat measurements. A subjects-by-day interaction accounted for 2-13% of the variance in muscle measurements and 2-12% of the variance in fat measurements. The contribution by investigators and trials to the variance was less than 1%. Generalizability coefficients (G) exceeding 0.92 were obtained for all sites for muscle measurements, while G for fat measurements exceeded 0.90 for all but the axilla site (G = 0.88). These results indicate that B-mode ultrasound is a highly reliable method for the measurement of both fat and muscle thicknesses in young males and females. © 1992 Wiley-Liss, Inc.

1. There is growing evidence that an impairment in the function of nitric oxide synthase may play a role in the vascular complications of diabetes mellitus. The relaxation of resistance arteries from the mesenteric and hindlimb circulations of streptozotocin-induced diabetic rats and age-matched controls were investigated using two endothelium-dependent vasodilators, bradykinin and acetylcholine, and the endothelium-independent vasodilator sodium nitroprusside. The contractile responses to the alpha 1-adrenergic agonist phenylephrine were also studied. 2. Endothelium-dependent relaxation to acetylcholine was impaired in the diabetic rats in arteries from both mesenteric and hindlimb circulations (hindlimb pEC50, 7.93 +/- 0.08 in the control compared with 7.38 +/- 0.10 in the diabetic rat; mesenteric pEC50, 7.47 +/- 0.04 in the control compared with 6.65 +/- 0.06 in the diabetic rat; unpaired t-test P < 0.0001). Bradykinin elicited relaxation in only the mesenteric arteries, and this was not attenuated in the diabetic rats compared with controls. 3. Endothelium-independent relaxation to sodium nitroprusside was similar in the two circulations and was not abnormal in the diabetic rats. There was no significant difference in constrictor responses to phenylephrine between diabetic rats and controls in either the hindlimb or mesenteric arteries, in contrast to an earlier study in which we showed increased sensitivity to noradrenaline. 4. The diabetic rats therefore demonstrated a specific impairment of receptor-mediated endothelium-dependent relaxation to acetylcholine. These results suggest that, in this diabetic model, the ability of the endothelium to relax arteries via nitric oxide may involve a defect of a specific signal transduction pathway, leading to reduced production of nitric oxide.

Hypertensive leg ulcers (Martorell's ulcers) are a unique form of lower extremity ischaemic leg ulcer. First described by Martorell, and Hines and Farber in the 1940s, these ulcers are defined by pain disproportionate to the size of the ulcer, specific location on the lower extremity, female-to-male predominance, association with long-standing, often poorly, controlled hypertension, and healing response to specific antihypertensive

1. The effects of the sodium salt of the weak acid lactate on tension and intracellular pH (pHi) were studied in rat mesenteric small arteries mounted on a wire myograph. Sodium lactate was substituted iso-osmotically for sodium chloride. 2. At a concentration of 50 mm, both L-and D-stereoisomers of lactate markedly relaxed arteries preconstricted with noradrenaline (NA) within 10 min. The concentrationresponse relationship for L-lactate showed that the NA contracture was relaxed by 50 % at approximately 26 mM. L-Lactate did not, however, relax arteries preconstricted with high-K+ (45 mM) solution.3. L-Lactate did not alter extracellular pH (pH.) but caused a small but significant decrease in pH,, measured using the pH-sensitive fluorochrome, 2',7'-bis(carboxyethyl)-5-(6')-carboxyfluorescein (BCECF). Relaxation to L-lactate was unaffected when this change in pHi was offset by the simultaneous addition of NH4Cl to the solution.4. Sodium pyruvate (50 mM) caused a significant intracellular acidosis but did not relax arteries preconstricted with NA. 5. L-Lactate-induced relaxations were unaffected by removal of the endothelium or when the synthesis of nitric oxide (NO) was inhibited by 10-4 M N'-nitro-L-arginine methyl ester (L-NAME).6. The potassium channel blockers glibenclamide (10 /M), 4-aminopyridine (3 mM) and tetraethylammonium chloride (10 mM) did not affect L-lactate-induced relaxation in arteries preconstricted with NA. Inhibition of guanylate cyclase with Methylene Blue, or cyclooxgenase with indomethacin, also did not affect relaxation to L-lactate.

Peroxynitrite-induced relaxation of isolated vessels may involve the formation of S-nitrosothiols. This study characterized the hemodynamic effects of systemically injected peroxynitrite in pentobarbital sodium-anesthetized rats and determined whether these effects were due to the formation of S-nitrosothiols. We utilizedl-penicillamine, which attenuates the hemodynamic effects of systemically injected S-nitrosothiols. The hemodynamic effects of peroxynitrite and the S-nitrosothiolsl- S-nitrosocysteine,l- S-nitrosoglutathione, and S-nitrosoalbumin were determined before and 25 min after the administration ofl-penicillamine or saline. Peroxynitrite and the S-nitrosothiols produced dose-dependent reductions in mean arterial pressure and mesenteric and hindquarter vascular resistances. The hypotensive and vasodilator effects of the S-nitrosothiols were significantly reduced by l-penicillamine. In contrast, the hemodynamic actions of peroxynitrite were unaffected byl-penicillamine. Therefore, peroxynitrite produces hypotensive and vasodilator responses in anesthetized rats that are unlikely to be due to the formation of circulating S-nitrosothiols. The mechanisms by which peroxynitrite produces vasodilatation in vivo remain to be determined.