The role of the cervical sympathetic nerve in the regulation of oxygen consumption of the carotid body of the cat

1. Carotid body blood flow (c.b.f.) and carotid arterial-carotid body venous oxygen (A-V O(2)) difference were measured and carotid body oxygen consumption calculated in twenty-six cats anaesthetized with pentobarbitone sodium, paralysed with gallamine triethiodide and ventilated mechanically.2. With the sinus nerves intact and with blood gas tensions and carotid sinus pressure within physiological limits, section of either the pre- or post-ganglionic cervical sympathetic nerve on the same side caused an average rise in c.b.f. of 9.2 mul./min, in A-V O(2) difference of 0.09 ml./100 ml. and in carotid body oxygen consumption of 0.075 mul./min.3. When the pre- or post-ganglionic cervical sympathetic nerves were stimulated, c.b.f. and A-V O(2) difference fell. The fall in c.b.f. was enhanced at high P(a, CO2); the fall in A-V O(2) difference and in calculated oxygen consumption was enhanced at low mean arterial pressure (M.A.P.) or P(a, O2).4. Following sympathectomy, a reduction of M.A.P. at constant P(a, O2) and P(a, CO2) caused a fall in c.b.f. and a commensurate rise in A-V O(2) difference so that carotid body oxygen consumption remained approximately constant.5. When P(a, O2) was altered over the range 35 to > 400 mm Hg, or P(a, CO2) over the range 27-70 mm Hg at constant M.A.P., c.b.f. changed by amounts which were similar to those observed when the sympathetic nerves were intact and A-V O(2) difference changed in the opposite direction so that carotid body oxygen consumption similarly remained constant.6. Comparison of these results with those observed when the sympathetic nerves were intact indicates that the sympathetic nerves exert a vasoconstrictor effect upon carotid body blood vessels over a wide range of blood gas tensions and arterial pressure and that they also tend to diminish the rate of carotid body oxygen consumption. The mechanisms which may be involved in this regulation are discussed.     

The carotid body in the duck and the consequences of its denervation upon the cardiac responses to immersion

1. The anatomy of the carotid body and its afferent nerve supply was studied in the duck and a method of denervating the carotid body which ensures a satisfactory post-operative course is described.2. The effect of denervating the carotid body upon the cardiac response to immersion of the head in water was studied in ten ducks which at the time of the test were unanaesthetized.3. When the nerves were intact, immersion of the head caused a fall in heart rate after a latent period of between 1 and 9 sec to an average of 24% of the resting rate after 30 sec. Simultaneous measurement of arterial oxygen tension (P(a, O2)) in the brachiocephalic artery showed a rapid initial fall during the initial 10 sec from control levels, 93-103 mm Hg, to between 42 and 47 mm Hg, followed by a gradual fall of 3-5 mm Hg for each subsequent 30 sec period of submergence.4. Following carotid body denervation, the latent period before heart rate started to fall was no different from control but the average fall in heart rate was now to 90% of the resting rate and brachiocephalic P(a. O2) continued to fall steadily during submergence reaching levels of between 10 and 21 mm Hg by the end of the second minute.5. Stimulation of the central end of branches of the IXth (glossopharyngeal) nerve supplying the glottis caused apnoea and bradycardia.6. It is concluded that apnoea and bradycardia during submergence in the duck is initiated reflexly from receptors in the nares, pharynx and glottis but that the profound degree of bradycardia and mechanisms which maintain a relatively high P(a, O2) are regulated by peripheral chemoreceptor activity.     

The Relationship between Arterial PO2 and Cerebral Blood Flow in Hypoxic Hypoxia

The relationship between arterial oxygen tension (Pa_O2) and cerebral blood flow (CBF) in hypoxic hypoxia was studied in artificially ventilated and normocapnic rats. Changes in CBF were evaluated from arterio-venous differences in oxygen content after 2, 5, 15 and 30 min exposure to Pa_O2 85, 75, 55, 45, 35 and 25 mm Hg. In separate experiments the Pa_O2 was decreased to 25 mm Hg for 1, 2, 5, 15 and 30 min in animals in which Pa_CO2 was allowed to fall by 5–10 mm Hg. There was a small, gradual increase in CBF when Pao, was lowered in steps from 130 to 55 mm Hg, and a more pronounced increase at P_O2 values below 50 mm Hg. At Pa_O2 25 mm Hg CBF increased to values of 500% of normal. Significant increases in CBF were recorded at Pa_O2 values of 85 and 75 mm Hg in spite of the fact that previous studies have failed to record an elevatad tissue lactate content at these P_O2 levels, and in spite of an unchanged cerebral venous P_O2. When the Pa_O2 was reduced to 25 mm Hg CBF increased markedly already at 1 and 2 min, and this increase in CBF occurred even if Pa_CO2 was allowed to fall by 5–10 mm Hg. Previous results have shown that in such short periods enough lactic acid is not formed to induce a net tissue acidosis. The results thus give no support to the hypothesis that cerebral hyperemia in hypoxia is coupled to accumulation of lactic acid in the tissue.     

The relationship between arterial po2 and cerebral blood flow in hypoxic hypoxia.

The relationship between arterial oxygen tension (PaO2) and cerebral blood flow (CBF) in hypoxic hypoxia was studied in artificially ventilated and normocapnic rats. Changes in CBF were evaluated from arteriovenous differences in oxygen content after 2, 5, 15 and 30 min exposure to PaO2 85, 75, 55, 45, 35, and 25 mm Hg. In separate experiments the PaO2 was decreased to 25 mm Hg for 1, 2, 5, 15 and 30 min in animals in which PaCO2 was allowed to fall by 5-10 mm Hg. There was a small, gradual increase in CBF when PaO2 was lowered in steps from 130 to 55 mm Hg, and a more pronounced increase at PO2 values below 50 mm Hg. At PaO2 25 mm Hg CBF increased to values of 500% of normal. Significant increased in CBF were recorded at PaO2 values of 85 and 75 mm Hg in spite of the fact that previous studies have failed to record an elevated tissue lactate content at these po2 levels, and in spite of an unchanged cerebral venous PO2. When the PaO2 was reduced to 25 mm Hg CBF increased markedly already at 1 and 2 min, and this increase in CBF occurred even if PaCO2 was allowed to fall by 5-10 mm Hg. Previous results have shown that in such short periods enough lactic acid is not formed to induce a net tissue acidosis. The results thus give no support to the hypothesis that cerebral hyperemia in hypoxia is coupled to accumulation of lactic acid in the tissue.     

AMP-activated protein kinase underpins hypoxic pulmonary vasoconstriction and carotid body excitation by hypoxia in mammals

In order to maintain tissue partial pressure of oxygen (P(O(2))) within physiological limits, vital homeostatic mechanisms monitor O(2) supply and respond to a fall in P(O(2)) by altering respiratory and circulatory function, and the capacity of the blood to transport O(2). Two systems that are key to this process in the acute phase are the pulmonary arteries and the carotid bodies. Hypoxic pulmonary vasoconstriction is driven by mechanisms intrinsic to the pulmonary arterial smooth muscle and endothelial cells, and aids ventilation-perfusion matching in the lung by diverting blood flow from areas with an O(2) deficit to those that are rich in O(2). By contrast, a fall in arterial P(O(2)) precipitates excitation-secretion coupling in carotid body type I cells, increases sensory afferent discharge from the carotid body and thereby elicits corrective changes in breathing patterns via the brainstem. There is a general consensus that hypoxia inhibits mitochondrial oxidative phosphorylation in these O(2)-sensing cells over a range of P(O(2)) values that has no such effect on other cell types. However, the question remains as to the identity of the mechanism that underpins hypoxia-response coupling in O(2)-sensing cells. Here, I lay out the case in support of a primary role for AMP-activated protein kinase in mediating chemotransduction by hypoxia.     

Early effects of abrupt reduction of local pressure on the forearm and its circulation

1. The pressure at the surface of a segment of forearm enclosed in a plethysmograph was abruptly reduced from atmospheric to -20 to -120 mm Hg.2. Forearm circumference (equivalent to the volume of a small segment of forearm (V(f))) was measured with a strain gauge. Pressure was measured in the plethysmograph (P(p)), in veins exposed (P(ve)) and not exposed (P(vne)) to suction, in the brachial artery not exposed to suction (P(bane)) and in forearm tissue (P(t)).3. Reduction of P(p) caused increase of V(f). This was not due to gas evolution, since bubbles would not be liberated at the pressures employed. Nor was increase of V(f) due to venous backflow since P(ve) fell, but P(vne) did not, even with upper arm circulation occluded or when P(vne) was raised by venous occlusion prior to reduction of P(p).4. Reduction of P(p) temporarily arrested venous outflow since P(ve) < P(vne) < P(bane) for 30 sec. With reduction of P(p) 30 sec after occlusion of the upper-arm circulation, P(ve) < P(vne) for > 1 min, indicating that arterial inflow was then minimal.5. Increase of V(f), following reduction of P(p), was therefore due to inflow of arterial blood, of soft tissue or interstitial fluid. Interstitial fluid could flow from regions external to the plethysmograph, or enter as the result of filtration across capillaries. Occlusion of the upper arm circulation was not expected to interfere with motion of forearm soft tissue or the intratissue flow of interstitial fluid. It appears that capillary filtration is small compared with observed blood flow. Therefore subtraction of V(foccl) measured at intervals after reduction of P(p) (upper arm circulation occluded) from V(f) similarly obtained (but upper arm circulation free) appeared to give change of forearm volume due to inflow of arterial blood (DeltaV(b)). V(b), the volume inflow rate of arterial blood during suction, was then obtained.6. Resting forearm flow was 1.8 ml./min/100 ml. in seven normal subjects (average mean arterial blood pressure 86 mm Hg). With P(p) = -90 mm Hg, V(b) was 10.2 ml./min/100 ml. Suction therefore reduced vascular resistance, measured as (P(bane)-P(ve)) /V(b).     

Effects of graded pulsatile pressure on the reflex vasomotor responses elicited by changes of mean pressure in the perfused carotid sinus-aortic arch regions of the dog

1. In the anaesthetized dog, the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. We have confirmed our previous observations that under steadystate conditions the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in carotid sinus pulse pressure, whereas those evoked by changes of mean aortic arch pressure are only weakly affected by modifications of aortic pulse pressure.3. When the carotid sinus and aortic arch regions are perfused in combination at constant pulse frequency (110 c/min), the relationship between mean carotid sinus-aortic arch pressure and systemic arterial perfusion pressure is dependent on the size of the pulse pressure.4. Increasing the pulse pressure alters the curve relating the mean carotid sinus-aortic arch pressure to systemic arterial perfusion pressure in such a way that the perfusion pressure is lower at a given carotid sinus-aortic arch pressure within the range 80-150 mm Hg. The larger the pulse pressure, up to about 60 mm Hg, the greater the fall in systemic arterial perfusion pressure. Above a mean carotid sinus-aortic arch pressure of about 150 mm Hg, alterations of pulse pressure have little effect.5. There is a family of curves representing the relation between mean carotid sinus-aortic arch pressure and systemic vascular resistance, depending on the pulse pressure.     

The effect of hypercapnia on myocardial blood flow and metabolism

1. In closed-chest dogs anaesthetized with trichlorethylene, the inhalation of carbon dioxide sufficient to increase the arterial P(CO2) from 40 to about 100 mm Hg, increased myocardial blood flow (measured using a (133)Xe clearance technique) and right atrial pressure. There were no consistent changes in mean arterial blood pressure, heart rate or cardiac output.2. The effect of hypercapnia on myocardial blood flow was not influenced by the previous administration of atropine and propranolol or of bretylium. It can be concluded, therefore, that the elevated arterial P(CO2) has a direct vasodilator effect on the myocardial microcirculation.3. During hypercapnia the coronary sinus P(O2) was increased and the coronary arteriovenous oxygen content difference, and calculated myocardial oxygen consumption, reduced. It is suggested that this latter effect may be the result of myocardial depression produced by the decrease in arterial blood pH.4. There was no evidence of myocardial glucose uptake either before or during hypercapnia. The myocardial extraction of lactate and pyruvate at rest varied between 0 and 55%. During acute hypercapnia the extraction of lactate usually fell.5. When the arterial P(CO2) was maintained at 100 mm Hg for a period of 1 hr the effects on myocardial blood flow and on oxygen consumption were not sustained.6. Stepwise increments and decrements in arterial P(CO2) of 10-20 mm Hg produced corresponding increases and decreases in myocardial blood flow and demonstrated that changes in arterial P(CO2) of 20-30 mm Hg can markedly affect blood flow in the myocardium.     

Circulatory responses of supine subjects to the exposure of parts of the body below the xiphisternum to subatmospheric pressure

1. Observations are reported on the effects of exposure of parts of the body below the level of the xiphisternum of supine subjects to a pressure 70 mm Hg below atmospheric for 1 min.

2. The stress on the circulation was greater than when parts below the iliac crests were similarly exposed. Heart rate increased by 15-20 beats/min, there was a sustained fall in arterial blood pressure, and forearm blood flow fell profoundly and in some subjects was reduced to below 0·1 ml./100 ml. min.

3. In arms that were sympathectomized, or had received an intraarterial infusion of an adrenergic blocking drug, the fall in forearm blood flow was much less and could be related to the fall in arterial pressure.

4. When the suction was released there was a brief overshoot of arterial blood pressure and brief cardiac slowing. Forearm blood flow rose to reach a peak some 15 sec after the release.

5. In the sympathectomized forearm on release of suction there was an immediate rise in blood flow which was proportionately much greater than the rise in arterial blood pressure.

6. This rise was not due to circulating vasodilator substances or to the activity of cholinergic vasodilator nerves. The possibility that it was the result of a change in the tone of the resistance vessels occurring in response to the sudden change in transmural pressure is discussed.

     

Effects of mecamylamine on responses of carotid body chemoreceptors in vivo to physiological and pharmacological stimuli

1. Effects of mecamylamine on the spontaneous discharge rate of afferent fibres of carotid body chemoreceptors in vivo and their responses to ACh, NaCN, HCl and hypoxia were studied in sixteen cats.2. Cats were anaesthetized with sodium pentobarbitone, paralysed with gallamine triethiodide and artificially ventilated. Chemoreceptor excitants were injected into the common carotid artery; mecamylamine was given intravenously.3. Mecamylamine, 230 mug/kg or greater, failed to diminish either the rate of spontaneous discharge of carotid body chemoreceptors at high arterial oxygen tensions (greater than 130 mm Hg), or the responses of these receptors to NaCN (0.5-25 mug), HCl or hypoxic blood.4. Responses of chemoreceptor afferent fibres to ACh (1.0-50 mug) in the same preparations were either completely abolished or considerably reduced by mecamylamine.5. These data do not support the hypothesis of a cholinergic mechanism for the initiation of chemosensory discharges in the carotid body, either at rest or in response to stimuli such as NaCN, acid or hypoxia.     

The role of arterial oxygen tension in the respiratory response to localized heating of the hypothalamus and to hyperthermia

1. Rectal temperatures, respiratory rates, arterial blood gas tensions, arterial pH and the percentage of red cells in arterial blood have been measured in the unanaesthetized ox in a cool environment (15/12 degrees C, dry bulb/wet bulb [DB/WB]), in a hot, dry environment (40/21 degrees C, DB/WB), during hyperthermia, during infra-red irradiation, and during localized heating of the anterior hypothalamus. In some experiments the gas tensions and pH of mixed venous blood, and the percentage saturation of the arterial blood with oxygen, were also measured.2. In the cool environment at a mean rectal temperature (T(r)) of 38.8 degrees C and a respiratory rate (f) of 28/min the mean values obtained from six animals were: arterial oxygen tension (P(a, O) (2)), 93 mm Hg; arterial carbon dioxide tension (P(a, CO) (2)) 42 mm Hg; arterial pH 7.49; arterial oxygen saturation (S(a, O) (2)) 94%; arterial oxygen capacity (Cap(a, O) (2)) 13.6 vol.%; arterial packed cell volume (P.C.V.) 29%.3. Exposure to the hot, dry environment resulted in a small increase in the rectal temperature and thermal polypnoea, but there were no statistically significant changes in the blood gas tensions.4. During hyperthermia statistically significant increases occurred in rectal temperature, respiratory rate, P(a, O) (2), pH and arterial haematocrit, while the P(a, CO) (2) decreased. The venous oxygen tension (P(v, O) (2)) decreased also, and the tentative conclusion was made that although the oxygenation of arterial blood remained unimpaired during hyperthermia, tissue hypoxia may supervene. At very high levels of deep body temperature, some evidence for a secondary decrease in P(a, O) (2) was obtained.5. Localized heating of the anterior hypothalamus caused an increase in respiratory rate and in P(a, O) (2). The P(v, O) (2) increased also. These changes were considered to be due to increased cardiac output and diversion of blood to the skin.6. During infra-red irradiation of three animals at an environmental temperature of 40/21 degrees C, the respiratory rate increased, but the P(a, O) (2) decreased.     

The separate and combined influences of common carotid occlusion and nonhypotensive hemorrhage on kidney blood flow

The separate and combined effects of bilateral common carotid occlusion (C.C.O.) and hemorrhage on renal blood flow (R.B.F.) were studied in 11 unanesthetized dogs.C.C.O. increased arterial blood pressure (4.4 kPa; 33 mm Hg) and heart rate (10 beats/min) while R.B.F. remained unchanged. When kidney perfusion pressure was maintained at its resting level during C.C.O. (implanted pneumatic cuff) there was also no change in R.B.F.After cutting the aortic nerves in 2 dogs the increase in blood pressure and heart rate with C.C.O. was greater (10.6 kPa; 80 mm Hg and 72 beats/min); however, there was no change in R.B.F.A blood loss of 16% (13.6 ml/kg) reduced central venous pressure (0.3 kPa; 2 mm Hg), increased heart rate (8–14 beats/min) and decreased arterial mean pressure by a maximum of 0.7 kPa (5 mm Hg) (nonhypotensive hemorrhage, N.H.H.). R.B.F. showed a tendency to rise and 90 min after the onset of bleeding was slightly increased (12% of control).After N.H.H. carotid occlusion had no effect on R.B.F. when kidney perfusion pressure increased; when perfusion pressure was controlled during C.C.O. the maximum observed decrease of R.B.F. was 15 ml/min (5% of control).It is concluded that the control of R.B.F. during the baroreceptor reflex under normovolemia and after a blood loss of 16% in the conscious dog at rest does not involve sympathetic vasoconstrictor effects which result in a significant changes in total blood flow.This study was supported by the German Research Foundation within the S.F.B. 90, Heidelberg     

The frequency of nerve impulses in single carotid body chemoreceptor afferent fibres recorded in vivo with intact circulation

1. The responses of single afferent fibres of carotid body chemoreceptors to independent changes in arterial O(2) and CO(2) tensions and pH were studied in the cat in vivo.2. The response curve obtained relating chemoreceptor activity to changes in arterial P(O2) was similar to an hyperbola; the frequency of nerve impulses at first decreased rapidly as the P(a,O2) was raised and then more slowly. The arterial P(O2) at which the slow decrease was reached varied among the different fibres; the mean level was 190 mm Hg (S.D. +/- 40 mm Hg).3. Single chemoreceptor afferent fibres continued to discharge even when the arterial P(O2) was more than 600 mm Hg.4. The discharges of single chemoreceptor afferent fibres increased both with increasing P(a,CO2) at constant pH and P(a,O2), and with increasing arterial H(+) at constant P(a,CO2) and P(a,O2).5. It is concluded that single carotid body chemoreceptor afferent fibres of the cat can be activated in vivo by an increase in either arterial H(+) or arterial P(CO2) as well as by a decrease in arterial P(O2).     

The effect of haemorrhage on haemoglobin concentration, blood volume and arterial pressure in kittens and cats

1. The arterial haemoglobin concentration in kittens less than 24 hr old was inversely related to body weight. There was about twice as much haemoglobin/unit body weight at birth as in adult cats. Haemoglobin concentrations were minimal at 3-6 weeks of age.2. In animals lightly anaesthetized with sodium pentobarbitone, arterial pressure rose from 52 mm Hg at birth in kittens to 133 mm Hg in adult cats. Blood volume decreased from 73 ml./kg at birth to 60 ml./kg in adults.3. When kittens less than a fortnight old were subjected to stepwise blood letting, arterial pressure fell proportionately with blood volume; in older kittens and in cats, arterial pressure was less well maintained at similar proportionate reductions of blood volume than in young kittens.4. The responses to haemorrhage of kittens and cats were compared with those of rabbits similarly treated and with those of adult cats anaesthetized with urethane and chloralose reported in the literature.     

The effect of variations in heart rate and regional distribution of blood flow on the normal pressor response to diving in ducks

1. During a 2 min period of submersion of normal ducks, sciatic artery blood flow fell to 10 +/- 1.5% control and carotid artery blood flow was reduced to 71 +/- 7% control. Mean arterial blood pressure (M.A.P.), however, was maintained at 83 +/- 3.5% of control. The whole animal showed a constrictor response during submersion, with the sciatic vascular bed showing average constriction. Both resistance to flow and yield pressure increased in the sciatic bed but changed little in the carotid bed. After 1 min submersion P(a,O2) was 52 +/- 1 mm Hg.2. Upon emersion, as soon as ventilation commenced, the whole animal showed a dilator response. The carotid bed exhibited marked vasodilatation whereas the sciatic bed returned to its control level.3. After alpha-receptor blockade, ducks were submerged for 1 min. During this time M.A.P. fell to 64 +/- 5.6% of control and heart rate was reduced to 49 +/- 8.3% of control. Blood flow through the sciatic and carotid arteries also fell to values of 41 +/- 6.9% of control and 91 +/- 13% of control respectively. There was little change in either resistance to flow or yield pressure in the sciatic bed compared to normal ducks, and the carotid bed showed reductions in resistance to flow and yield pressure during submersion. P(a,O2) after 1 min under water was 41 +/- 1.1 mm Hg.4. beta-receptor blockade had no effect on any of the measured variables during submersion. Upon surfacing, however, although the whole animal response was one of dilatation, the carotid bed was less dilated than in normal ducks at this time and the sciatic bed was more constricted.5. Injection of atropine not only abolished the bradycardia during submersion but also caused a rise in M.A.P. and sciatic blood flow during the period under water. After 1 min submersion P(a,O2) was 30 +/- 1.2 mm Hg.6. It is concluded that stimulation of adrenergic alpha-receptors is responsible for the increase in resistance to flow through the sciatic artery and the maintenance of blood pressure during submersion in the normal animals. This selective constrictor activity and the resulting ischaemia is important in the maintenance of P(a,O2) during submersion. Adrenergic beta-receptors (cardiac and/or peripheral) are involved, to a small extent, in the blood pressure and blood flow changes that occur when ventilation commences upon emersion.     

The blood flow and oxygen consumption of brown adipose tissue in the new-born rabbit

1. A direct method for measuring venous outflow from brown adipose tissue in anaesthetized new-born rabbits is described.

2. During noradrenaline infusion the mean blood flow through brown adipose tissue increased from 87 to 360 ml./100 g tissue (wet wt.).min, and the mean rate of oxygen consumption of brown adipose tissue rose from 9·3 to 60 ml. O₂/100 g tissue.min.

3. During cold exposure the mean blood flow through brown adipose tissue increased from 90 to 304 ml./100 g tissue.min.

4. The mean cardiac output was 266 ml./kg body weight.min; during noradrenaline infusion it was 405 ml./kg body weight.min. At rest about one tenth, and during noradrenaline infusion about one quarter of the cardiac output went to brown adipose tissue.

5. It was calculated that most of the extra oxygen consumed during the metabolic response of the anaesthetized new-born rabbit to noradrenaline infusion or cold exposure was consumed by brown adipose tissue.

6. Hypoxia (breathing 10% O₂ in N₂) greatly reduced the increase in oxygen consumption but not the increase in blood flow in brown adipose tissue caused by noradrenaline infusion.

     

Maternal hyperventilation and foetal hypocapnia in sheep

1. In anaesthetized foetal lambs near term, hypocapnia induced by maternal hyperventilation abolished the rise of arterial pressure and femoral vasoconstriction caused by hypoxaemia. This is consistent with interaction of P_CO2 and P_O2 on the foetal aortic bodies.

2. In immature lambs (0·6-0·77 of term) maternal hyperventilation caused a fall in foetal carotid P_CO2 commensurate with that in the maternal blood. In mature lambs (at 0·9 or more of term) the fall in foetal carotid P_CO2 was less than that in maternal blood, whether the foetus was exteriorized or in utero.

3. The mean transplacental gradient for P_CO2 (maternal arterial-umbilical vascular), when the foetus was replaced with a mechanical pump recirculating foetal blood, was 6·3 mm Hg. This is attributed to placental CO₂ production, and is nearly half the mean P_CO2 gradient (maternal artery-foetal carotid) of about 14 mm Hg during normal maternal ventilation.

4. The mean maternal-umbilical transcotyledonary venous gradients (avoiding vascular shunts through the myometrium and intercotyledonary chorion) were for P_CO2 1·7 mm Hg and for P_O2 13·4 mm Hg.

5. Maternal hyperventilation (P_{a, CO2} ~ 20 mm Hg) caused a small fall in mean foetal carotid P_O2 (5 mm Hg), which was readily reversible with no evidence of progressive acidaemia.

     

Systemic hypoxia and hyperoxia,and liver blood flow and oxygen consumption in the greyhound

The effects of systemic hypoxia upon liver blood flow and oxygen consumption were studied in a group of six pentobarbitone anaesthetised greyhounds. The effect of systemic hyperoxia upon the same factors were also studied in a further group of six greyhounds.Hypoxia studied atPaO₂ tensions of 9.3, 7.3, 5.3 and 3.3 kPa was found to increase mean arterial pressure significantly at eachPaO₂ tension studied immediately the hypoxic gas mixture was introduced but this pressure had returned to control by the time 20 min had passed. At the same time a significant decrease in hepatic arterial blood flow was seen, returning to control by 20 min. No significant changes were seen in portal venous blood flow. Hepatic arterial and mesenteric vascular resistance increased significantly immediately hypoxia was instituted at allPaO₂ tensions.Hepatic oxygen consumption, measured after 20 min, decreased at allPaO₂ tensions, significantly at 3.3 kPa (25 mm Hg). Hepatic venous oxygen content decreased significantly at eachPaO₂, decreasing to 20% of control at 3.3 kPa (25 mm Hg).Hyperoxia studied atPaO₂ tensions of 26.6, 39.9 and 53.2 kPa produced no significant effects upon liver blood flow. However, there was a small increase in hepatic oxygen consumption.     

Carotid body chemoreceptor activity in the new-born lamb

1. Tidal volume, carotid artery oxygen tension (P(a,O2)) and blood pressure and chemoreceptor activity in the sinus nerve have been continuously measured and recorded in nine lambs anaesthetized with pentobarbitone sodium, and varying in age from some minutes after birth to 5 days after birth.2. Inhalation of 100% oxygen caused, after a delay of 3-4 sec, a rise in P(a,O2), a fall in minute ventilation (V) and chemoreceptor activity. The respiratory response was abolished after section of both sinus nerves.3. Inhalation of 10% oxygen in nitrogen caused a fall in carotid P(a,O2), a rise in respiration and in chemoreceptor activity. The respiratory response was abolished after both sinus nerves had been cut.4. Minute ventilation, carotid P(a,O2) and chemoreceptor activity increased on breathing 5% CO(2) in air. Section of both sinus nerves did not affect the maximum increase in ventilation but the lag of the respiratory response approximately doubled while respiration increased more slowly.5. From these results, it was calculated that the chemoreceptors had a latency of 0.25-0.5 sec and the time constant of the rate of change of chemoreceptor activity was 10-15 sec.6. The chemoreceptors responded to changes in P(a,O2) of +/-5-10 mm Hg.7. Comparison of these results with those reported in adult animals suggest that the peripheral chemoreceptors are fully mature at birth, that their response does not differ with the age of the lamb and that the carotid body chemoreceptors are concerned both in the mediation of the hypoxic drive to ventilation and in the respiratory response to inhaled CO(2).     

Variations in carotid arterial compliance during the menstrual cycle in young women

The effect of menstrual cycle phase on arterial elasticity is controversial. In 10 healthy women (20.6+/-1.5 years old, mean+/-s.d.), we investigated the variations in central and peripheral arterial elasticity, blood pressure (carotid and brachial), carotid intima-media thickness (IMT), and serum oestradiol and progesterone concentrations at five points in the menstrual cycle (menstrual, M; follicular, F; ovulatory, O; early luteal, EL; and late luteal, LL). Carotid arterial compliance (simultaneous ultrasound and applanation tonometry) varied cyclically, with significant increases from the values seen in M (0.164+/-0.036 mm2 mmHg-1) and F (0.171+/-0.029 mm2 mmHg-1) to that seen in the O phase (0.184+/-0.029 mm2 mmHg-1). Sharp declines were observed in the EL (0.150+/-0.033 mm2 mmHg-1) and LL phases (0.147+/-0.026 mm2 mmHg-1; F=8.51, P<0.05). Pulse wave velocity in the leg (i.e. peripheral arterial stiffness) did not exhibit any significant changes. Fluctuations in carotid arterial elasticity correlated with the balance between oestradiol and progesterone concentrations. No significant changes were found in carotid and brachial blood pressures, carotid artery lumen diameter, or IMT throughout the menstrual cycle. These data provide evidence that the elastic properties of central, but not peripheral, arteries fluctuate significantly with the phases of the menstrual cycle.