In the resting awake dog a continuous-wave Doppler flow transducer on the right bronchoesophageal artery inscribes a sharp early systolic spike and low flow in late systole and throughout diastole, indicating a highly resistive bed. An analysis of autonomic factors using intravenous, cumulative, and randomly applied cholinoceptor, beta 1- and beta 2-adrenoceptor, and alpha 1- and alpha 2-adrenoceptor antagonists indicates that the low vascular conductance is due to cholinoceptor and alpha 1- and alpha 2-adrenoceptor effects in a ratio 3.6:1. No beta-adrenoceptor tone is present. Sighing behavior invokes a transient (< 2 s) fall in intrapleural pressure (and thus rise in bronchovascular transmural pressure) of 10-30 mmHg, which is followed by a two- to threefold increase over 30 s in bronchial flow and conductance, an effect simulated in 50% of dogs when bronchovascular transmural pressure is acutely raised and maintained over 40-60 s by inflating an intra-aortic balloon distal to the origin of the bronchial artery. Autonomic blockade has no effect on bronchovascular dilatation evoked either by sighing or by balloon inflation. It is concluded that, in the resting bronchial circulation, there exists strong cholinoceptor and alpha-adrenoceptor-based vasoconstrictor activity which can be overpowered by strong nonadrenergic noncholinergic local vasodilator reflexes evoked by sudden changes in intrathoracic transmural pressure possibly acting on stretch-sensitive sensory nerve endings containing substance P, calcitonin gene-related peptide, and neurokinins. The tonic vasoconstrictor but not the sigh-evoked vasodilator effects are sensitive to pentobarbital sodium anesthesia.

SUMMARY1. The effects of arterial hypoxia on muscle blood flow were examined in normal unanaesthetized rabbits in relation to simultaneously determined changes in cardiac output, arterial pressure and heart rate. Muscle blood flow was estimated from the difference between total limb flow (local thermodilution) and the estimated skin flow (using a calibrated heat conductivity method). The role of the arterial chemoreceptors and baroreceptors in the control of muscle blood flow was examined and the nature of the sympathetic efferent discharge analysed. followed by a return to control values paralleling the changes in cardiac output. In severe arterial hypoxia (Po2 < 30 mm Hg) the initial vasoconstriction was less marked, and during the 'steady state' there was a large vasodilatation and increase in muscle blood flow, at a time when the cardiac output was not elevated.3. The early vasoconstriction in arterial hypoxia is mediated mainly through sympathetic vasoconstrictor nerves as a result of strong arterial chemoreceptor stimulation.4. Increased secretion of adrenaline is an important factor in restoring muscle blood flow to control values during moderate arterial hypoxia, and in elevating the muscle blood flow above these values in severe hypoxia.The peripheral dilator (,8-) effects of adrenaline oppose the peripheral constrictor (a-) effects resulting from increased activation of sympathetic constrictor nerves during arterial hypoxia.

OBERG, B. and S. WHITE. Circulatory effects of interruption and stimulation of cardiac uagal afferents. Acta physiol. scand. 1970. 80. 383-394.The influence of the rhythmic activity in cardiac vagal afferents on the circulation was analyzed in chloralose-anrsthetized cats by observing the cardiovascular responses to sudden interruption of this activity 2nd to afferent stimulation of the cardiac nerves. The evoked responses were compared with those produced by "unloading" and stimulation of arterial baroreceptors. -Elimination of the impulse traffic in vagal afferents produced a blood pressure rise, a tachycardia and vasoconstrictions in skeletal muscle, intestine and kidney, indicating a tonic restraint of these afferents on the medullary vasomotor centre. The responses were generally moderate in the presence of normally functioning arterial baroreceptors but were pronounced after elimination of "buffering" influences from these receptors. -Comparisons of the inhibitory influences from vaKal cardiac afferents and baroreceptor afferents, respectively, on the vasomotor centre indicated that the former were preferentially directed to neurons controlling the efferent discharge to the heart and the renal vessels. There was no evidence for a particularly strong engagement of the capacitance vessels in reflex patterns mediated through cardiac afferents. -Low frequency afferent stimulation of the cardiac nerves generally induced a profound bradycardia, which was probably due to stimulation of fibres not normally tonically active. 7-70303'3. Act4 phyrid. s c a d VoE. 80: 3

SUMMARY1. The respiratory and circulatory effects of graded arterial hypoxia, alone or with superadded hypercapnia, were studied in four groups of unanaesthetized rabbits including normal animals and those with selective section of the aortic nerves, selective section of the carotid sinus nerves and section of both sets of nerves.2. When measured 2-4 days after selective section of the carotid sinus nerves the resting respiratory minute volume and arterial Po, were lower and the Pco, higher than normal. These effects were not observed after selective section of the aortic nerves. Selective aortic nerve section, and selective carotid sinus nerve section each produced a similar increase in the resting arterial pressure and heart rate, but were without effect on the resting cardiac output.3. During arterial hypoxia reflex respiratory and circulatory effects ascribable to arterial chemoreceptor stimulation (hyperventilation, bradycardia, vasoconstriction) were mediated for the most part through the carotid sinus nerve. In animals with only the aortic nerves intact the circulatory response was determined largely by the opposing effects of aortic baroreceptor reflexes and the local peripheral dilator action of hypoxia.4. The circulatory effects of hyperventilation induced by hypercapnia during arterial hypoxia, in animals with both aortic and carotid sinus nerves cut were small. 5. The results suggest that relatively few chemoreceptor fibres originate from the aortic region in the rabbit, though the carotid sinus and aortic nerves both contain baroreceptor fibres.

OBERG: B. and S. WHITE. T h e role of vagal cardiac nerves and arterial baroreceptors in the circulatory adjustments to hemorrhage in the cat. Acta physiol. scand. 1970. 80. 395-403.The relative importance of arterial baroreceptors and receptors with afferent fibres in the cardiac nerves, respectively, in producing compensatory circulatory adjustments in moderate hemorrhage was analyzed in chloralose-anesthetized cats. -The effects of standardized hemorrhage on blood pressure, heart rate and renal and skeletal muscle blood flows were observed before and after section of respective receptor afferents. Both groups of receptors, when operating in the absence of the other, were capable of producing tachycardia and vasoconstriction during a blood loss, but the pattern of response, elicited via the two sets of afferents, differed. Compensation via cardiac nerve afferents thus implied a particularly strong engagement of vasomotor neurons, controlling the heart and the renal vessels, while the arterial baroreceptor adjustments seemed to involve a more uniform exitation of all vasomotor centre neurons. Very rapid hemorrhages often produced a pronounced bradycardia, resembling that seen in the "vaso-vagal" syncope in man. This response was found to he mediated through a vago-vagal reflex arch, and probably constitutes a protective mechanism, causing a break on the heart in situations of extremely poor diastolic filling.

SUMMARY1. The circulatory response following acute loss of 26 % of the blood volume was examined in unanaesthetized rabbits. The groups of animals studied were normal rabbits; adrenalectomized rabbits; animals subjected to prolonged treatment with guanethidine in which peripheral adrenergic nerve transmission is blocked, but which can reflexly liberate adrenal medullary hormones; animals subjected to combined adrenalectomy and guanethidine treatment with no functional adrenergic effectors; in each case with or without administration of atropine. The responses of animals with section of the carotid sinus and aortic nerves were also examined.2. The spontaneous rate of replacement of the blood volume after haemorrhage by reabsorption of extravascular fluid was the same in all the above preparations, the blood volume returning to normal 3-4 hr after bleeding.3. The 'passive' effects of haemorrhage were examined in animals without functioning autonomic effectors and include a large fall in right atrial pressure and cardiac output, arterial hypotension, no significant change in total peripheral resistance, and a bradycardia of gradual onset.

A B S T R A C T The peripheral vascular response to severe exercise was studied in 11 healthy conscious dogs instrumented with Doppler ultrasonic flow probes on the mesenteric, renal, and iliac arteries, and miniature pressure gauges in the aorta. The response to severe exercise was restudied in six of these dogs after recovery from a second operation producing complete heart block by the injection of formalin into the atrioventricular (AV) node. Three of these dogs also exercised while their ventricles were paced at rates of 100/min and 200/min. The untethered normal dogs ran at speeds of 15-25 miles/hr behind a mobile recording unit for a distance averaging 1.5 miles, while continuous measurements of arterial blood pressure and blood flow were telemetered and recorded on magnetic tape. Severe exercise in normal dogs increased heart rate from 84 to 259/min, arterial pressure from 89 to 140 mm Hg, flow resistance in the mesenteric and renal beds by 59 and 52% respectively, and iliac blood flow 479% above control, while mesenteric and renal blood flows remained constant and iliac resistance decreased by 73%.In dogs with complete AV block, severe exercise at speeds of 10-18 miles/hr increased heart rate from 47 to 78/min, mean arterial pressure from 81 to 89 mm Hg, iliac flow 224%, resistance in the renal bed by 273%, and mesenteric bed by 222% while it decreased blood flow in mesenteric and renal beds by 61 and 65% respectively, and iliac resistance by 62%. A similar response occurred during exercise with pacing at 100/min,

DJOJOWGITO,A. M., B. FOLKOW, B. UBERG and S. W. WHITE. A comparison of blood viscosity measured in vitro and in a vascular bed. Acta physiol. scand. 1970. 78. 70-84.Blood viscosity in vivo ("apparent viscosity") and its variations with flow rate was analyzed in the maximally dilated calf muscle vascular bed of the cat by comparing pressure-flow relationships for blood and a Newtonian fluid (dextran-Tyrode) over a flow range between 60 and 0.2 ml/min x 100 g tissue. Viscosity in vitro for the same perfusates was measured in a cone-plate viscometer.-Apparent viscosity was much lower (approximately 50 76 ) than iii vitro values at high shear rates, with less variation between animals. I t increased with decreased flow but was as a maximum only doubled, which occurred at flows around 0.5 ml/min x 100 g. Since such small flows normally occur in constricted vessels with higher flow velocities than at maximal dilatation, the range of viscosity changes with flow in the intact circulation is probably decidedly smaller. The steep rise of viscosity in vitro at quite low shear rates had no counterpart in vivo; in fact, viscosity then tended to fall again. The discrepancies between blood viscosity in vivo and in vitro seem to be related to vascular dimensions, favour-