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Changes in cardiac output, mean arterial blood pressure, hematocrit ratio, and arterial and venous oxygen content resulting from bilateral carotid occlusion were investigated. Cardiac output exhibited no significant alteration during endosinusal hypotension, and the systemic hypertension engendered was attributed to an increase in vasomotor tone. Arterial and venous oxygen content, as well as hematocrit ratio, increased significantly during the period of carotid occlusion. This increase was ascribed to splenic contraction evoked by carotid occlusion, since no comparable augmentation was observed when the splenic circulation was temporarily interrupted.

Inhibition studies with hydroxycitrate and other substances have demonstrated that, in skin, translocation of acetyl-CoA from the mitochondria to the cytosol is mediated as citrate. Studies with specifically labelled aspartates and glutamates confirm this and demonstrate that the oxaloacetate produced on citrate cleavage is recycled through pyruvate. Hence, the skin is able to generate NADPH 2 by means of isocitrate dehydrogenase and by the malate cycle. In an attempt to assess the magnitude of these pathways, the incorporation of acetate, pyruvate, and L-Iactate in the absence of glucose was studied. All three substances could be incorporated into lipid in the absence of glucose; the rate was lowest for acetate and highest for L-lactate. The incorporation of 14-lactate was unusual, the reaction was concentration dependent and product stimulated, and the rate was almost as high as that for glucose. The skin is thus able to support an active rate at lipogenesis during glucose deprivation when the HMP-shunt is believed to he inactive. In view of this and the high activity of the elongation mechanisms in skin, it is concluded that the HMP-shunt is unable to play a regulatory role in skin. In addition. discrepancy in the measurement of HMP-shunt activity in holocrine tissues has been noted.

When the femoral artery is occluded in the anesthetized dog, the pressure in the distal segment usually declines progressively and approaches a static limit asymptotically. This static limit is independent of the original Degrees of vasomotor tone except under extreme conditions. It is concluded that the rapid supervention of reactive hyperemia in the dog vitiates the static limit as an index of vasomotor tone, unless an instantaneous method is developed for its estimation.

Variations in flow in the presence of a constant arteriovenous pressure difference can only occur when vascular dimensions have been altered, irrespective of the rheological properties of the liquid being perfused. When the vascular bed of the hind leg is subjected to parallel changes in arterial and venous pressures, higher absolute values of pressure result in an enhancement of flow. This constitutes convincing evidence to indicate that certain vessels which offer a significant resistance to blood flow are distensible.

The abrupt rise in mean arterial pressure resulting from elimination of the moderator reflexes is not accompanied by a significant increase in cardiac output. The acute hypertension is therefore attributed to a severe generalized vasoconstriction. The severity of this vasomotor response progressively diminishes during the interval immediately following denervation.

Cardiac output was determined in dogs over a wide range of pressures before and after preclusion of compensatory reflex mechanisms. When the moderator reflexes are functional, total peripheral resistance increases markedly with moderate reductions in arterial pressure. When reflex alterations of vasomotor tone are obviated, pressure and flow usually vary proportionately as arterial pressure is altered. In the average experiment, total peripheral resistance remains relatively constant although appreciable deviations may be observed in individual cases.

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It was the purpose of this investigation to test again the general conclusion that norepinephrine augments cardiac output during experimental hemorrhagic hypotension but has no such effect on normal animals or man. Results are presented which fail to support this differential action in normal and hypotensive dogs and an explanation is offered for failure of the drug to increase cardiac output in human subjects.