COMPARISON OF THE REFLEX EFFECTS OF ARTERIAL BARORECEPTORS AND CARDIAC RECEPTORS ON THE HEART RATE OF CONSCIOUS RABBITS

1. The reflex effects on heart rate (HR) of presumptive cardiac receptors have been differentiated from those of the arterial baroreceptors in conscious rabbits by inflating cuffs on the ascending aorta, descending aorta, inferior vena cava and pulmonary artery. 2. When the outflow from the right ventricle was progressively impeded the accompanying increase in HR was entirely explicable by unloading of the arterial baroreceptors. 3. As the outflow from the left ventricle was progressively impeded there was an initial increase in HR due to unloading of the arterial baroreceptors, followed by a progressive decline. This decline was attributed to a reflex arising from vagallyinnervated receptors in the left side of the heart. The threshold of this cardiac receptor-HR reflex occurred at a higher level of mean aortic pressure than that at which the effects of the arterial baroreceptors on HR were maximal. Cholinergic (vagal) efferent nerves were responsible for two-thirds of the decline in HR caused by the reflex. 4. The properties of the cardiac receptor-HR reflex were altered by drugs that affect myocardial contractility. Isoprenaline raised the mean aortic pressure at which the threshold occurred, but lowered the corresponding level of left ventricular end-diastolic pressure. Propranolol virtually abolished the reflex, even though left ventricular end-diastolic pressure reached a high level. 5. It is concluded that in the conscious rabbit the arterial baroreceptor reflexes normally prevent the threshold of the cardiac receptor-HR reflex from being attained.     

DOES THE HAEMODYNAMIC RESPONSE TO ACUTE CENTRAL HYPOVOLAEMIA DEPEND ON THE RATE OF FALL OF CARDIAC OUTPUT?

1. In published studies of the effects of acute blood loss in conscious rabbits, the rates of haemorrhage have ranged for 3-9% of blood volume/min. This is potentially a confounding factor when it comes to comparing the results of different studies. We have therefore tested whether the haemodynamic response to acute central hypovolaemia depends on the rate of fall of cardiac output. 2. Cardiac output in six conscious rabbits was reduced by 4, 8 and 12% of baseline levels per min by gradual inflation of a cuff around the thoracic inferior vena cava. These rates correspond approximately to blood loss at rates of 3, 6 and 9% of blood volume/min. 3. The haemodynamic responses were biphasic. In Phase I (compensatory) there was progressive systemic vasoconstriction and tachycardia, and only a small fall in blood pressure. In Phase II (decompensatory), systemic vasoconstriction failed abruptly, arterial pressure plummeted and heart rate declined. 4. We could detect no effect of rate of fall of cardiac output on the pattern of the haemodynamic responses in either Phase I or Phase II. 5. We conclude that the rate of blood loss in different studies of haemorrhage in conscious rabbits, within the range 3 to 9 per cent of blood volume per minute, need not be regarded as a confounding factor when it comes to interpreting the results. It is likely that this conclusion can be generalized to studies of haemorrhage in other mammalian species.     

FACTORS INFLUENCING THE EFFECTS OF INTRAVENOUS NALOXONE ON ARTERIAL PRESSURE AND HEART RATE AFTER HAEMORRHAGE IN CONSCIOUS RABBITS

The circulatory responses to different intravenous doses of naloxone were studied in conscious rabbits before and after haemorrhage, under different conditions including prior ganglion blockade. Unless there had been blood loss, naloxone elicited no pressor response, even in high dose. After bleeding so that arterial pressure fell to 40 mmHg, the dose-response relationship for naloxone had two components. Over a low-dose range (threshold 0.3 mg/kg) naloxone had a modest pressor effect but did not affect heart rate. Over a much higher dose range (threshold 0.6 mg/kg) naloxone caused a marked rise in arterial pressure and a profound bradycardia. The highest dose of naloxone examined (25 mg/kg) caused a rise in arterial pressure of 70 mmHg and a reduction in heart rate of 160 beats/min. The pressor and bradycardic effects of naloxone were the same whether post-haemorrhagic hypotension lasted 5, 10, 20 or 30 min. The responses to naloxone in low or high dose depended much more closely on the volume of blood removed than on the level to which arterial pressure fell. Even after non-hypotensive haemorrhage a high dose of naloxone had marked pressor and bradycardic effects. Ganglion blockade prior to haemorrhage abolished the pressor response to a low, but not to a high, dose of naloxone. It was concluded that prolonged and severe hypotension are not necessary to 'prime' the cardiovascular system to respond to naloxone after haemorrhage. In a high dose its pressor effects appear to be mediated post-ganglionically, but in a low dose it may act within the central nervous system.     

THE EFFECTS OF MECLOFENAMATE ON RENAL AND PERIPHERAL VASCULAR BEDS IN CONSCIOUS RABBITS

1. Meclofenamate caused a dose-dependent increase in renovascular resistance in conscious rabbits. 2. This effect was greatest in inner cortical zones at the highest dose (6 mg/kg) but at the lowest dose (0-75 mg/kg) vascular resistance in the outer cortex was preferentially increased. 3. In contrast, meclofenamate increased cerebral perfusion and the proportion of cardiac output received by the testis. No effect was demonstrated on other organs studied. 4. The results suggest a local vasodilator influence of renal prostaglandins in normal conscious rabbits.     

EFFECTS OF ENDOTHELIN-1 ON ARTERIAL PRESSURE AND MYOCARDIAL CONTRACTILITY IN THE CONSCIOUS NORMOTENSIVE RABBIT

1. We studied the effects of an intravenous bolus of endothelin-1 on arterial pressure and myocardial contractility in the conscious rabbit. 2. Endothelin produced an initial fall in arterial pressure accompanied by an increase in heart rate. This was followed by a dose-dependent increase in arterial pressure, peaking about 7 min after injection, accompanied by a reciprocal fall in heart rate. 3. Left ventricular rate of change of pressure (LV dP dt) increased with endothelin except at higher doses (0.8 and 1.6 nmol/kg), where in some animals it decreased.     

EFFECTS OF ENDOTHELIN-1 ON ARTERIAL PRESSURE: A COMPARISON OF INTRAVENOUS AND INTRA-ARTERIAL ADMINISTRATION IN CONSCIOUS RABBITS

1. Intravenous endothelin-1 releases endothelium-derived relaxing factor (EDRF) and prostacyclin from the lungs, and substantial pulmonary clearance is claimed. Since these vaso-active substances could alter the haemodynamic effects of endothelin-1, the effects of boluses of endothelin-1 injected intravenously and into the left ventricle (intra-arterial) were compared, measuring arterial pressure and heart rate in conscious male New Zealand rabbits. The pulmonary clearance of endothelin-1-like immunoreactivity (Et-1LI) and initial plasma half-life were measured in anaesthetized rabbits during and after intravenous infusion of endothelin-1. 2. The effects of intravenous and intra-arterial routes of administration were not significantly different. Arterial pressure decreased (intravenous: 21.6, intra-arterial: 24.2 mmHg, P= 0.12, n= 10, t-test, 9 d.f.), then increased (intravenous: 21.2, intra-arterial: 16.4 mmHg, P= 0.33), while heart rate increased (intravenous: 66, intra-arterial: 53 beats/min, P = 0.09), then decreased (intravenous: 50, intra-arterial: 54 beats/min, P= 0.30). 3. Arterial and venous plasma levels of Et-1LI were not significantly different, venous levels increasing from 30 ± 3 pg/ mL (12 ± 1 pmol/ L) at 1 pmol/ kg per min to 770 ± 78 pg/ mL (308 ± 31 pmol/L) at 16 pmol/kg per min (n = 5). Mean initial plasma half-life was 0.6 min (range: 0.25–1.1 min). 4. It was concluded that there is no significant net pulmonary clearance of exogenously administered endothelin-1 in the conscious rabbit, and that any vaso-active factors released in the lungs by endothelin-1 do not have a significant effect on systemic arterial pressure.     

THE EFFECTS OF CENTRAL ADMINISTRATION OF ω-CONOTOXIN GVIA ON CARDIOVASCULAR PARAMETERS AND AUTONOMIC REFLEXES IN CONSCIOUS RABBITS

1. The effects of central administration of ω-conotoxin GVIA (ω-CTX), an N-type calcium channel blocker, were examined in conscious rabbits implanted with lateral intracerebroventricular (i.c.v.) cannulae. 2. Experiments were performed over 4 consecutive days. On day 1, the baroreceptor heart rate (induced by glyceryl trinitrate and phenylephrine) and Bezold-Jarisch like (elicited by serotonin) reflexes were measured before (0 h) and 2 h after central administration of ω-CTX (3 or 30 pmol/ kg, i.c.v.) or vehicle. On days 2–4, resting parameters and reflexes were again monitored but no further ω-CTX was administered. 3. No change in heart rate (HR) was observed in any rabbit treatment group during the experimental period. In the vehicle (n= 6) and ω-CTX 3 pmol/kg (n = 6) groups, small falls in mean arterial pressure (MAP) of 6 ± 2 and 10 ± 3 mmHg, respectively, occurred between 0 and 24 h; MAP then remained stable. Baroreceptor-heart rate reflex curve parameters did not change in either of these groups during the 4 day period. 4. Following administration of w-CTX 30 pmol/kg (n = 7), MAP decreased progressively and by 48 h had fallen by 19 ± 4 mmHg. Also at 48 h, a 20% decrease in HR range of the baroreceptor-heart rate reflex curve was seen without any change in the lower HR plateau from the 0 h control. This indicates that there was an attenuation of the sympathetically mediated upper component of the curve while the vagally mediated component was unaffected. 5. The Bezold-Jarisch like reflex-induced bradycardia, mediated by the efferent vagus nerve, was unaffected by i.c.v. administration of vehicle or either dose of ω-CTX. 6. Therefore, central administration of ω-CTX resulted in a slowly developing hypotensive response consistent with a sympatholytic action while vagally mediated reflexes were unaffected.     

DA-1 RECEPTORS MEDIATE RENAL EFFECTS OF THE DOPAMINE PRODRUG, GLUDOPA, IN CONSCIOUS RABBITS

1. Eight male rabbits were implanted with Doppler flow probes around the lower abdominal aorta and left renal artery. A 2 week recovery period was allowed prior to the experiment. 2. Normal saline, gludopa at 25 micrograms/kg per min and at 100 micrograms/kg per min were each infused i.v. for 60 min. One week later the same protocol was administered to four of these animals in addition to DA-1 antagonist SCH 23390 (0.3 mg/kg i.v.) before gludopa infusion. 3. Gludopa elicited significant increases in urine flow, urinary sodium excretion and renal blood flow, and decreased renal vascular resistance. These changes were abolished by the DA-1 antagonist. Blood pressure, heart rate and hindlimb blood flow remained unchanged. 4. Urine dopamine excretion was increased 1200-fold and 7800-fold after gludopa administration at 25 micrograms/kg per min and 100 micrograms/kg per min, respectively, while plasma dopamine concentration and plasma renin activity (PRA) were not significantly altered. However, PRA was elevated by gludopa with DA-1 antagonism. 5. The renal vasodilation, natriuresis and diuresis produced by gludopa in conscious rabbits appears to be mediated by locally generated dopamine via DA-1 receptors.     

ARTERIAL PRESSURE AND HEART PERIOD IN THE CONSCIOUS RABBIT: DIURNAL RHYTHM AND INFLUENCE OF ACTIVITY

Mean-arterial pressure (MAP), heart period (HP) and the level of physical activity were measured in conscious rabbits and averaged over one-hour periods during 14 consecutive days. Serial autocorrelation coefficients and serial crosscorrelation coefficients were computed, to analyse periodicity. Measurements were started immediately after implantation of the cannula (group A, n = 11) or 10-46 days after implantation of the cannula (group B, n = 6). In the course of 14 days, in group A, MAP decreased 9 mmHg and HP increased 21 ms (P less than 0.05). In group B, MAP decreased and HP increased in a similar way. Percentage activity did not show a trend. Significant diurnal rhythms were found. MAP and percentage activity reached the lowest values at noon, and the highest late in the evening. HP reached the highest values at noon and the lowest late in the evening. MAP and HP fluctuated exactly in antiphase. This suggests a common origin for both rhythms. During physical activity MAP was 10-15 mmHg higher and HP was 35-40 ms shorter than during rest. These differences did not show a trend or a diurnal variation. In individual animals MAP and HP varied greatly from hour to hour. These biological variations in MAP and HP as well as the influence of activity should be taken into account when conclusions are drawn from short-term measurements.     

INFLUENCE OF CARDIAC AFFERENTS ON TIME-DEPENDENT CHANGES IN THE RENAL SYMPATHETIC BAROREFLEX OF CONSCIOUS RABBITS

1. The stability of the renal sympathetic baroreflex and nasopharyngeal reflex, and the role of cardiac sensory receptors, was studied in conscious rabbits over a 5 h experimental period. 2. Renal sympathetic nerve activity (SNA) was recorded during (i) slow ramp changes in mean arterial pressure (MAP) of 1-2 mmHg/s induced by inflating perivascular balloon cuffs, and (ii) the inhalation of cigarette smoke. Experiments were repeated in other rabbits after blocking cardiac afferents with 5% intrapericardial procaine. 3. Baroreflex responses to the first two caval cuff inflations of the day were significantly greater than subsequent responses. After this, triplicate sets of reflex curves were relatively stable during a 2 h period in the morning. When the experiment was repeated in the afternoon, there was a significant attenuation of baroreflex range and a small fall in resting renal SNA which were abolished by pericardial procaine. 4. Changes in baroreflex properties were minimal when the reflex was assessed only twice, at the beginning and end of a 5 h period. No change was seen in the nasopharyngeal reflex whether the rabbits had been subjected to few or to many cuff inflations. 5. We conclude that time dependent changes can occur in the renal sympathetic baroreflex of conscious rabbits which must be allowed for by appropriate protocol design. These include increasing inhibitory influences from cardiac sensory receptors in experimental situations requiring multiple reflex estimations.     

EFFECTS OF NEUROPEPTIDE Y ON BAROREFLEX CONTROL OF HEART RATE AND MYOCARDIAL CONTRACTILITY IN CONSCIOUS RABBITS

1. The effects of intravenous (i.v.) neuropeptide Y (NPY, 10 micrograms/kg bolus) on the stimulus-response curves relating changes in heart period (HP) and in peak left ventricular (LV) dP/dt to acute changes in mean arterial pressure (MAP) were determined in conscious, normotensive rabbits. 2. The relationship between increases and decreases in MAP and the subsequent changes in HP were represented by a sigmoid-shaped curve described by a logistic function. Following NPY administration there was a baroreflex-dependent increase in the maximum slope (sensitivity) at the midpoint of this MAP-HP curve from 7.0 +/- 0.5 to 10.6 +/- 1.3 ms/mmHg (P less than 0.05). NPY caused an upward shift in the whole curve which reflected the NPY-induced bradycardia and was independent of baroreflexes. 3. The relationship between increases in MAP and decreases in peak LV dP/dt was determined during fixed-rate atrial pacing to prevent the effects of the accompanying bradycardia. Increases in MAP and the corresponding reductions in peak LV dP/dt were represented by an exponential function. The slope of the curve, measured at its origin 5-15 min after NPY administration, was reduced from -0.9 +/- 0.2 to -0.4 +/- 0.1 units (P less than 0.05). 4. The effects of NPY are consistent with an action on efferent connections of the arterial baroreceptor reflex, mediated through a reduction in cardiac beta-adrenergic tone. They would also be explained through actions on the afferent or central neural connections of the baroreflex.     

间尼索地平与尼索地平对清醒兔血流动力学和局部血流量的影响

应用放射性生物微球技术观察间尼索地平(m-Nis)和尼索地平(Nis)对清醒兔血流动力学和局部血流量的影响。m-Nis 1μg/kg·min~(-1)×10min iv显著增加清醒兔CO、CI、SV和LVSW;等剂量Nis增加CO及CI不显著;两药对清醒兔MABP、HR和脑、心、肾、脾等局部血流量影响相似,对这些器官的血流分布及心输出量分布无明显影响。     

COMPARISON OF METHODS FOR ELICITING THE BARORECEPTOR-HEART RATE REFLEX IN CONSCIOUS RABBITS

1. Two methods were used for altering blood pressure in conscious rabbits by up to ± 30 mmHg from the resting level in order to characterize the barorecep-tor-heart rate reflex. These were to inflate descending aortic or inferior vena caval cuffs, or to give brief intravenous infusions of phenylephrine or glycerol trinitrate. The relation of change in blood pressure to change in heart interval was examined, both during the initial ‘ramp’ changes of these variables and when they had reached a ‘steady-state'. 2. Both methods allowed the construction of'steady-state’ sigmoid stimulus-response curves whose parameters were reproducible within animals, and which were attended by a relatively small variance between animals. The inflatable-cuff method gave a higher average value for maximum gain than the vasoactive drug method (10.0 v 5-4 ms/mmHg) and a narrower pressure range between the threshold and saturation points of the response, but values for the other parameters were similar. Corresponding parameters obtained by the two methods correlated closely. 3. After denervating all arterial baroreceptors except one carotid sinus, ‘steady-state’ maximum gain by cuff-inflation was reduced to 3.1 ms/mmHg, and to 2-6 ms/mmHg by the vasoactive drug method. The heart interval range between upper and lower plateau levels was reduced, but the pressure range between threshold and saturation points was widened, with both methods. 4. During the initial ‘ramp’ changes of blood pressure the sensitivity of the reflex was described by the slope of the linear regression of heart interval on ‘mean blood pressure. The slopes obtained by aortic cuff inflation, and by infusion of either vasoactive drug, correlated positively with ‘steady-state’ maximum gain. However, the reproducibility of the ‘ramp’ method was inferior to that of the ‘steady-state’ method with respect to reflex sensitivity, and other parameters of the stimulus-response relation cannot be estimated. 5. Complete baroreceptor denervation virtually eliminated heart rate changes over the range of blood pressures usually employed. However, when blood pressure was increased by more than 40 mmHg a profound reflex bradycardia and hypopnoea were then evoked.     

SYSTEMIC AND REGIONAL HAEMODYNAMICS IN EXPERIMENTAL RENAL HYPERTENSION IN CONSCIOUS RABBITS

1. The radioactive microsphere method was used to measure the distribution of cardiac output, regional flows and resistances in conscious normotensive and hypertensive rabbits implanted with an electromagnetic flow probe on the ascending aorta or pulmonary artery. Hypertension was induced by wrapping one kidney with cellophane and removing the other, and studies were performed about 5 weeks later. 2. Heart rate, stroke volume, cardiac output and total renal mass were reduced in the hypertensive animals, while the weight of, and the cardiac output distribution to left ventricle and the remaining kidney were increased. 3. In renal hypertensive rabbits, the weight normalized regional blood flow was diminished in a number of tissues, including the kidney, and, except for some organs in the splanchnic area (stomach, small intestine, mesentery and pancreas) and the fat, there was a rather uniform increase in tissue vascular resistance.     

间硝苯啶、硝苯啶与尼群的平对动物降压作用的比较性研究

在清醒正常血压大鼠、免以及肾型高血压大鼠,比较了m-nif、nif及nitr的降压强度,和降压的时间动态过程,三药的降压作用与对照组及自身前后对比,统计学上均非常显著。m-nif与nitr降压持续时间较nif长。从清醒正常血压大鼠降压的量效关系比较,m-nif、nif和nitr的ED₅₀)分别为33.7±3.4,45.6±3.6和51.2±4.1 mg/kg(即90±9,132±10,142±11μmol/kg)。按克分子量计算对比m-nif的降压强度最大,nitr最弱。但三药对正常血压及肾型高血压动物的降压作用,按组间对比,无统计学差异。     

VASOPRESSIN RESPONSE TO HAEMORRHAGE IN RATS: EFFECT OF HYPOXIA AND WATER RESTRICTION

1. The aim of the present study was to determine the effect of water restriction and/or hypoxia on the vasopressin response to haemorrhage in conscious rats. 2. Male, Long-Evans rats (n = 39) were prepared with chronically indwelling femoral artery and vein catheters and exposed to 24 h of one of the following: normoxia with ad lib drinking water (N + W); normoxia with water restriction (N - W); hypoxia with ad lib drinking water (H + W); and hypoxia with water restriction (H - W). At the end of 24 h, a 15 mL/kg arterial haemorrhage was performed. 3. Water restricted rats had elevated pre-haemorrhage vasopressin levels. Haemorrhage induced an increase in vasopressin in all groups. Water restriction (N - W) or hypoxia (H + W) each augmented the vasopressin response to haemorrhage. However, the combination of hypoxia and water restriction (H - W) failed to augment the vasopressin response to haemorrhage as compared to normoxic, water replete (N + W) rats. 4. Hypoxia or water restriction per se augment the vasopressin response to haemorrhage. This augmented vasopressin response to haemorrhage is not maintained when hypoxia and water restriction are combined.     

INTERACTIONS BETWEEN ANGIOTENSIN II AND THE SYMPATHETIC NERVOUS SYSTEM IN THE THE LONG-TERM CONTROL OF ARTERIAL PRESSURE

1. The role of the renin-angiotensin system in long-term control of sympathetic activity and arterial pressure is reviewed. 2. There is evidence that favours a necessary role for the sympathetic nervous system in long-term arterial pressure regulation. First, appropriate changes in sympathetic activity appear to be produced in response to chronic changes in blood volume or blood pressure. Second, prevention of the normal homeostatic decrease in sympathetic activity in response to an increase in sodium intake produces hypertension. 3. Long-term changes in sympathetic activity cannot be mediated by the baroreceptor reflex, because it adapts to sustained changes in pressure. Therefore, an hypothesis is presented that evokes a key role for angiotensin II (AngII) in determining the chronic level of sympathetic activity. The key feature of this model is that the role of AngII is non-adaptive: chronic changes in extracellular fluid volume produce sustained reciprocal changes in AngII, and long-term increases in AngII produce sustained increases in sympathetic activity. 4. Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension.     

EVIDENCE FOR THE INHIBITORY EFFECT OF 5-HYDROXYTRYPTAMINE AT CENTRAL AND PERIPHERAL SITES ON OVULATION IN RABBITS

1. The effect of 5-hydroxytryptamine (5-HT) has been investigated on ovulation per se as well as on induced ovulation in rabbits. 2. 5-HT administered intracerebroventricularly (i.c.v.) did not induce ovulation per se. 3. The ovulation was induced by coitus, subcutaneous administration of progesterone and intravenous administration of cupric acetate. 4. Postcoital and progesterone induced ovulation was found to be blocked by i.c.v. administered 5-HT. 5. Cupric acetate induced ovulation was, however, not found to be blocked by i.c.v. administered 5-HT. 6. Intraperitoneal administration of 5-HT was found to block cupric acetate induced ovulation. 7. It is concluded that 5-HT exerts an inhibitory control over ovulation by acting at central as well as at peripheral sites in rabbits.     

EFFECTS OF HALOTHANE, KETAMINE, PROPOFOL AND ALFENTANIL ANAESTHESIA ON CIRCULATORY CONTROL IN RABBITS

1. We have made a within-rabbit comparison of the effects of four general anaesthetic regimens on the haemodynamic response to acute reduction in central blood volume and on baroreflex control of heart rate. 2. Acute haemorrhage was simulated by gradually inflating a cuff on the inferior vena cava in order to cause cardiac output to fall at a constant rate of 8.5%/min while the responses of systemic vascular resistance, arterial pressure and heart rate were measured. The full range of the baroreceptor-heart rate reflex was elicited by inflating aortic and vena caval cuffs. These indices of circulatory control were repeatedly measured within five protocols, to which each rabbit was exposed in randomized order. 3. In each protocol the rabbit was first studied unanaesthetized. Then a small dose of thiopentone sodium was given (16 mg/kg). In the four main protocols the rabbit was then intubated and ventilated, first with 100% oxygen and then with 50% nitrous oxide, during administration of one of four anaesthetic agents. These were halothane (2.0 and 2.5%), ketamine (2.5 mg/kg per min), propofol (0.83 and 1.25 mg/kg per min) and alfentanil (2.5 and 3.33 micrograms/kg per min). In a sham protocol the effects of 100% oxygen, then those of 50 and 75% nitrous oxide, were studied while the rabbit remained conscious. 4. In unanaesthetized rabbits, in the presence or absence of nitrous oxide, the normal biphasic haemodynamic response to simulated haemorrhage occurred. The first, vasoconstrictor, phase was attenuated by halothane, ketamine and propofol, so that arterial pressure fell more steeply than normal. Not only was the vasoconstrictor phase unaffected by alfentanil but it was extended, so that arterial pressure remained at a normal level even when cardiac output had fallen by 59%. This effect of alfentanil appeared to be mediated centrally, since it could be reproduced by injecting small doses (1.5-7.5 micrograms) into the fourth ventricle. All four anaesthetic agents and nitrous oxide attenuated the baroreceptor control of heart rate. The effect was least with nitrous oxide and alfentanil, greatest with halothane.