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Regional cerebral blood flow (CBF) was measured by an autoradiographic method in nine adult cats, using antipyrine-(14)C as a diffusible indicator. In seven of the cats, CBF measurements were made during stimulation of a cervical sympathetic trunk. Stimulation caused minor regional decreases of CBF in at least five of these seven cats. The decreases were non-uniform and occurred almost exclusively in cortical structures. Although constriction of cervical arteries probably accounts for some of the effects of sympathetic stimulation, the present study indicates that there is also an effect on cerebral regulatory arterioles. However, there is no convincing evidence that function of the autonomic nervous system is necessary for the normal regulation of the cerebral circulation. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether the level of arterial pressure and degree of baroreceptor activation affect responses to stimulation of chemoreceptors. Chemoreceptors were stimulated by injecting nicotine into the common carotid artery of anesthetized and paralyzed dogs. Responses were observed in the innervated gracilis muscle, perfused at constant flow while perfusion pressure was measured. Arterial pressure was lowered by bleeding the animals and raised by transient occlusion of the descending aorta. Vasoconstrictor responses to stimulation of chemoreceptors were enhanced by hypotension and inhibited by elevation of arterial pressure. Potentiation of the chemoreceptor reflex by hemorrhagic hypotension was not the result of altered vascular resistance in the gracilis muscle, sensitization of chemoreceptors by catecholamines or acidosis, or changes in cerebral perfusion pressure. Additional studies were done in which we excluded the possibility that the changes resulted from direct effects of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were isolated and perfused. On one side, pressure was raised to stimulate the carotid sinus baroreceptors. On the other side, the carotid body chemoreceptors were stimulated by nicotine or by hypoxic and hypercapnic blood. Activation of baroreceptors on one side attenuated the vasoconstrictor response to chemoreceptor stimulation on the other side. This excludes a direct effect of changes in arterial pressure on the chemoreceptors and suggests a central interaction of these reflexes. We conclude that vasoconstrictor responses to stimulation of chemoreceptors are potentiated by hypotension and inhibited by transient hypertension. These effects appear to result at least in part from a central interaction of chemoreceptor and baroreceptor reflexes.

1 A modification of the Folkow Technique for simultaneous measurement of blood flow and capillary filtration coefficient (CFC) in the cat jejunum is described. The modification retained the sympathetic innervation of the preparation, and in the present experiments, drugs were administered intravenously.2 There is evidence that CFC is a cardiovascular quantity independent of blood flow or regional vascular resistance in these preparations. Low doses of drugs may affect CFC without altering the blood pressure, blood flow, or heart rate.3 Under control conditions the CFC, a measure of functional exchange vessel area, was lower than previously reported for similar, but denervated preparations.4 alpha-Adrenoceptor stimulation with phenylephrine (1.0 mug kg(-1) min(-1), i.v.) caused a fall of 75-85% from control values of CFC with concomitant rises in blood pressure of 0-15% and falls in blood flow of 10-40%. The heart rate rose by 0-15%. Phentolamine (0.5-2.0 mg/kg, i.v.) caused a rise in CFC and a slight fall in vascular resistance, and blocked the effects of phenylephrine on this tissue.5 beta-Adrenoceptor stimulation with isoprenaline (0.2 mug kg(-1) min(-1), i.v.) caused a rise in CFC of 75-110%, a fall in blood pressure of 0-10%, a rise in blood flow of 10-60% and a rise in heart rate of up to 35%. Propranolol caused a transient rise in CFC when injected i.v. in a dose of 0.1 mg/kg, which was adequate to block the effects of isoprenaline.6 Angiotensin (25-100 ng kg(-1) min(-1), i.v.) caused falls in CFC of up to 100% and rises in vascular resistance. Aminophylline (0.2-0.4 mg kg(-1) min(-1), i.v.) caused rises in CFC of up to 200% with falls in vascular resistance.7 Histamine (0.01 to 1.0 mug kg(-1) min(-1), i.v.) had little effect on vascular resistance, but 10 and 40 mug kg(-1) min(-1) caused falls in vascular resistance. Doses up to and including 10 mug kg(-1) min(-1) caused falls in CFC, but the higher doses, or smaller doses after histaminase inhibition caused rises in CFC. alpha-Adrenoceptor blockade reversed the fall in CFC caused by small doses of histamine, to a rise. Mepyramine completely blocked the effects of histamine on these preparations.8 5-Hydroxytryptamine (33-100 mug kg(-1) min(-1), i.v.) caused a rise in vascular resistance and a fall in CFC of up to 85%. These effects were blocked by methysergide (250 mug/kg, i.v.).9 Rises in CFC indicate an increase in functional exchange vessel area in the tissue, and falls in CFC a decrease in the area available for vascular exchange. These changes are examined against the possibility of the drugs causing reflex adjustments in sympathetic tone, of systemic deactivation of intravenously administered drugs, and of drug effects on vascular permeability.

1. Thermal stimulation of frog skin produces a discharge in afferents in the dorsocutaneous nerve. The characteristics of this response have been examined with regard to static and dynamic sensitivity to thermal stimuli and to mechanical sensitivity. Frog cutaneous receptors respond only to cooling, with no response to warming through the same thermal range.2. The static temperature at which these receptors are maximally active is about 24 degrees C for Rana pipiens and about 27 degrees C for R. catesbiana.3. The dynamic sensitivity of frog cutaneous receptors is linearly related to both stimulus slope and magnitude. Maximum dynamic sensitivity was between -90 and -120 impulses/ degrees C.sec.4. Antidromic occlusion experiments demonstrate relative insensitivity of these receptors to tonic mechanical stimulation. At high stimulus intensities, however, larger fibres are recruited into the response; this recruitment of action potentials of larger amplitude is a linear function of both stimulus slope and magnitude.5. Spike heights are linearly related to conduction velocities in the dorsocutaneous nerve; tonic mechanoreceptors have a mean spike height of 28.4+/-0.6 muV and conduction velocities about 6-8 m/sec, whereas these temperature sensitive receptors have spike heights 15.8+/-0.4 muV and conduction velocities about 3-4 m/sec.6. Maximum dynamic sensitivity skin is increased following stimulation of the first or second sympathetic ganglion. This increase is both marked and progressive, reaching a maximal enhancement of about 150-160% control at a stimulus rate of 5 stimuli/train, each train delivered once every 5 sec.7. Static sensitivity of the cold receptors is also increased following sympathetic stimulation. This increased sensitivity is shown by both increased discharge rate within the same thermal range and by decreased temperature of maximum static sensitivity.8. Sympathetic modulation of dynamic thermal sensitivity is mimicked by epinephrine and norepinephrine in doses of 10(-6)-10(-7) g/ml. Ephedrine, another adrenergic agonist, also mimics the enhancement of cold receptors by sympathetic stimulation.9. Larger fibres are recruited to account for the increased sensitivity of thermoreceptors following sympathetic stimulation and epinephrine application.10. Propranolol and phentolamine both block the enhancement of the response by sympathetic stimulation, but propranolol blocks the response of the receptor to thermal stimulation as well. Reserpine pre-treatment blocks the effect of sympathetic stimulation on the cold response.