Cardiac output (CO) and the fractional distribution (FD) of γ-labeled plastic microspheres (15 ± 5 μm) injected into the left ventricle were used to calculate blood flow to organs and tissues of barbital-sedated warm-acclimated (WA) or cold-acclimated (CA) white rats at rest and then during their maximal calorigenic response to infused noradrenaline (NA). Flow to the major masses of brown adipose tissue (BAT) increased in WA rats from a mean of 0.81 ml/min (0.92% of CO) at rest to 13.5 ml/min (11.4% of CO) during calorigenesis; it increased in CA rats from 2.3 ml/min (2.6% of CO) to 57.2 ml/min (33.5% of CO). Flow to skeletal muscle increased in WA rats from 12.0 ml/min at rest to 15.1 ml/min during calorigenesis; it increased in CA rats from 9.9 ml/min to 14.5 ml/min. Flow to heart and to muscles involved in respiratory movements was two to five times greater during calorigenesis. Flow to most other tissues and organs increased or decreased by less than 40%.Arteriovenous differences in blood oxygen [Formula: see text] across interscapular BAT (IBAT) during rest and during calorigenesis together with measurements of blood flow established that IBAT alone accounted for 14% of the extra O2 used by CA rats during NA-induced calorigenesis. If during calorigenesis other masses of BAT have an [Formula: see text] as great as that for IBAT, the major masses of BAT together would account for 60% of the calorigenic response of the CA rat. In contrast, even if the skeletal muscle of the CA rat used all the O2 in the blood flowing through it during calorigenesis, it could not have been responsible for more than 12% of the calorigenic response.The rat, long considered to exemplify major participation of skeletal muscle in nonshivering thermogenesis (NST), now becomes just one of a growing list of species for which there is explicit or circumstantial evidence that NST occurs principally in BAT. It thus becomes reasonable to propose as a general principle that BAT is the primary anatomical site of the NST that is characteristic of many small mammals: CA adults, newborns, and hibernators alike.

Radioactive microspheres (12–16 μm) were used to measure cardiac output (CO), its fractional distribution, and hence tissue blood flow in conscious, warm-acclimated (WA) or cold-acclimated (CA) white rats exposed to temperatures of 25, 21, 6, −6, and −19 °C, the objective being to assess the tissue distribution of cold-induced thermogenesis. Total oxygen consumption was also measured. CA rats at 25 °C (CA25) had elevated arteriovenous shunting and other signs of heat stress. CA21 proved more suitable controls for the CA group. The cold-induced changes in blood flow to total skeletal muscle not involved in respiratory movements (M) and to the major masses of brown adipose tissue (BAT) were quantitatively very different in the two acclimation groups: in WA25 and CA21 flows to M were 31 (0.24 CO) and 27 (0.17 CO) mL/min, respectively, while flows to BAT were 2.1 and 9.7 mL/min; in WA−19 and CA−19 flows to M were 62 (0.32 CO) and 35 (0.16 CO) mL/min, respectively, while flows to BAT were 25 and 56 mL/min. In contrast, the effects of cold exposure on flows to other tissues and organs were remarkably alike in the two acclimation groups: e.g., flows to heart, ribcage, and diaphragm increased about three times between 25 and −19 °C, flow to the skin fell about 50%, and flows to the hepatosplanchnic region and kidneys were little or not at all affected by cold exposure. Estimates of the contributions of different tissues and organs to cold-induced thermogenesis were made on the basis of the relative changes in blood flow. It is concluded that BAT is by far the dominant anatomical site of the increased heat production of cold-exposed CA rats, and that nonshivering thermogenesis in BAT supplements considerably the shivering thermogenesis of cold-exposed WA rats.

Twenty patients with enzymatically proven glycogen storage disease type III (GSD III) aged 3-30 years underwent cardiological evaluation. Seventeen showed subclinical evidence of cardiac involvement in form of ventricular hypertrophy on ECG. Of 16 patients in whom an ECG examination was performed, 13 had abnormal echocardiographic features. Only 2 patients had cardiomegaly on X-ray. The cardiac findings in 1 of the patients, a 25-year-old female with clinically evident cardiomyopathy are described in detail. In view of our findings, patients with established GSD III, should not only be investigated regarding their muscular involvement, but should also undergo a detailed evaluation of their cardiac status.

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Barbital-sedated, cold-acclimated (CA) or warm-acclimated (WA) rats were given different doses and combinations of noradrenaline, theophylline, and the adrenergic-blocking agents propranolol and phentolamine, to stimulate or inhibit calorigenesis in various ways. To see whether the effects of these drugs on calorigenesis could be ascribed to effects on the adenylate cyclase (EC 4.6.1.1) - cyclic AMP system, and to try to assess thereby the significance of this system in the regulation of nonshivering thermogenesis (NST), changes in the concentration of plasma cyclic AMP were measured as an index (Broadus, A.E., Hardman, J.G., Kaminsky, N. I., Ball, J. H., Sutherland, E.W., and Liddle, G. W.: 1971. Ann. N.Y. Acad. Sci. 185, 50-60) of changes in tissue levels of cyclic AMP. In CA rats, which have a severalfold greater capacity for NST than WA rats, calorigenic responses to noradrenaline, theophylline, noradrenaline plus theophylline, or phentolamine plus theophylline were as much as four times larger than in WA rats, However, the changes in level of plasma cyclic AMP produced by each of these and other treatments were virtually the same for both groups. It would appear, therefore, that the difference between WA and CA rats in ability to produce heat by NST is not a function of the amplitude of changes in tissue levels of cyclic AMP. Nevertheless, it was also observed, and was particularly striking in CA rats, that when a drug or combination of drugs had a stimulatory, inhibitory, or synergistic effect on calorigenesis, it had a similar effect with respect to elevation of plasma cyclic AMP. Altogether, the results indicate that adenylate cyclase and cyclic AMP are likely to be participants in the regulation of NST in the rat, but that they would be subservient in this regard to whatever factors are responsible for acclimation-related differences in capacity for NST.