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Institute for Cardiovascular Research, The School of Medicine, University of Leeds, Leeds LS2 9JT, UK
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Abstract |
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-chloralose, a cardiopulmonary bypass was established, and the pulmonary trunk and its main branches as far as the first lobar arteries were vascularly isolated and perfused with venous blood. The chest was closed following connection to the perfusion circuit and pressures distending the aortic arch, carotid sinus and coronary artery baroreceptors were controlled. Changes in the descending aortic (systemic) perfusion pressure (SPP; flow constant) were used to assess changes in systemic vascular resistance. Values of SPP were plotted against mean pulmonary arterial pressure (PAP) and sigmoid functions applied. From these curves we derived the threshold pressures (corresponding to 5% of the overall response of SPP), the maximum slopes (equivalent to peak gain) and the corresponding PAP (equivalent to ‘set point’). Stimulus–response curves were compared between data obtained with intrathoracic pressure at atmospheric and with a phasic intrathoracic pressure ranging from atmospheric to around -10 mmHg (18 cycles min-1). Results were obtained from seven dogs and are given as means ±S.E.M. Compared to the values obtained when intrathoracic pressure was at atmospheric, the phasic intrathoracic pressure decreased the pulmonary arterial threshold pressure in five dogs; average change from 28.4 ± 5.9 to 19.3 ± 5.9 mmHg (P > 0.05). The inflexion pressure was significantly reduced from 37.8 ± 4.8 to 27.4 ± 4.0 mmHg (P < 0.03), but the slopes of the curves were not consistently changed. These results have shown that a phasic intrathoracic pressure, which simulates respiratory oscillations, displaces the stimulus–response curve of the pulmonary arterial baroreceptors to lower pressures so that it lies within a physiological range of pressures.
(Received 19 November 2003;
accepted after revision 5 January 2004;
first published online 14 January 2004)
Corresponding author M. J. Drinkhill: Institute for Cardiovascular Research, School of Medicine, University of Leeds, Leeds LS2 9JT, UK. Email: cvsmjd{at}leeds.ac.uk
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Introduction |
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The responses elicited by stimulation of pulmonary arterial baroreceptors in these early studies and the pulmonary pressures required to induce them may have been confounded by changes in the stimuli to other reflexogenic areas that would be likely to have buffered the primary responses. Regions that could be affected include the arterial baroreceptors and the various cardiac receptors described by Hainsworth (1991). In an attempt to prevent ‘buffering’ of the reflex responses, we (McMahon et al. 2000) developed a preparation involving a cardiopulmonary bypass and careful control of the major cardiovascular reflexogenic areas. Using this preparation, we found that reflex systemic vasoconstriction occurred in response to pulmonary artery distension with pressures that were considerably lower than those previously reported. Nevertheless, the pressures were still unphysiologically high.
We considered that another possible explanation for the very high pressures previously required may have been a result of the unphysiological nature of the open-chest preparations in these experiments. Instead, we felt that if we applied pulsatile pressures to the pulmonary arterial baroreceptors and we used a closed-chest preparation in which physiological phasic negative intrathoracic pressures were applied, the operating range of the pulmonary arterial baroreceptor reflex would be likely to be reduced.
In the accompanying paper we reported experiments in which the stimulus–response characteristics of pulmonary arterial afferents were shown to be enhanced by application of phasic negative pressures to the resealed chest cavity (Moore et al. 2004). In these experiments, the threshold and inflexion pressures from the relationship between pulmonary arterial pressure and vagal afferent discharge were displaced so that they occurred at the pressures normally prevailing in the pulmonary artery.
The present investigation was therefore undertaken to further resolve the question as to whether pulmonary baroreceptors could be involved in normal cardiovascular control. In order to evaluate the likely physiological importance of these receptors, we compared the vascular responses to increases in pulsatile pulmonary arterial pressures in a closed-chest preparation in the presence and absence of phasic negative intrathoracic pressures.
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Methods |
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Local ethical committee approval was obtained and all experiments were conducted in accordance with the Animals (Scientific Procedures) Act, 1986. At the end of the experimental procedures animals were killed by exsanguination while under deep anaesthesia.
Adult female beagle dogs were anaesthetized with -chloralose (100 mg kg-1I.V. in saline, Vickers Laboratories Ltd, Leeds, UK), infused through a catheter inserted under local anaesthesia (2% lidocaine hydrochloride, Phoenix Pharma Ltd, Gloucester, UK) through the right saphenous vein, so that its tip lay in the inferior vena cava. Surgical anaesthesia was maintained throughout the duration of the experiments by a continuous infusion of chloralose (0.5–1.0 mg kg-1 min-1). Alfentanyl (30 µg kg-1I.V. Janssen-Cilag Ltd, High Wycombe, UK) was administered over 10 min prior to major surgical procedures. During surgery, it was infused continuously at 2.5 µg kg -1 min-1, and this infusion was terminated 60 min prior to the start of the experimental protocol. At intervals throughout the experiment, the appropriate depth of anaesthesia was assessed from the stability of blood pressure and heart rate, and by observing only a small contraction of the limbs in response to toe pinch or to a sharp tap on the surgical table.
Following induction of anaesthesia, a longitudinal mid-line incision was made in the neck, the trachea intubated and the lungs artificially ventilated with a mixture of 40% oxygen in room air using a Starling ‘Ideal’ pump, initially set at 17 ml kg-1 and 18 strokes min-1. Arterial blood PO2, PCO2 and pH were monitored frequently using a pH/blood gas analyser (Instrumentation Laboratory, model IL 1610, Lexington, MA, USA) and maintained within normal limits by adjustments of the stroke of the respiratory pump, the rate of oxygen inflow, and infusions of molar sodium bicarbonate solution, as required.
Both carotid sinus regions were prepared by ligating all branches arising from the carotid bifurcations, except the external carotid and lingual arteries, which were used for subsequent perfusion.
The sternum was split along the midline and each side of the chest was divided between the 4th and 5th ribs. Once the pleural cavity was opened, the expiratory output from the pump was immersed in 3 cm of water to prevent lung collapse. The 2nd to 7th pairs of intercostal arteries were tied and then divided to mobilize a length (approximately 5 cm) of the descending aorta. The inferior vena cava was mobilized immediately above the diaphragm and a loose thread placed around it. To allow the creation of a pulmonary arterial pouch, both pulmonary arteries were dissected free to the points of their first branches and loose threads placed around them. Extreme care was taken to avoid damage to nerves running over the lung roots. The pericardium was opened to expose the right atrium and right ventricle for subsequent cannulation.
Heparin (500 i.u. kg-1 i.v.; Leo Laboratories Ltd, Princes Risborough, UK) was administered to the animal immediately prior to cannulation. The perfusion circuit (Fig. 1) was partially filled with a heparinized mixture of equal parts of mammalian Ringer solution and dextran in dextrose solution. The total volume of the circuit was approximately 1 litre. Following this, a cardiopulmonary bypass was established by inserting a cannula into the right atrium, via its appendage, and another into the inferior vena cava (7 and 10 mm i.d.) to drain blood into an open reservoir (A in Fig. 1). The blood from reservoir A was pumped through a membrane gas exchange unit (Sorin Biomedica Cardio, Saluggia, Italy) to the main reservoir B which was maintained at a constant pressure. The central end of the thoracic aorta was cannulated (7 mm i.d.) and perfused with blood from B at constant pressure. This pressure determined the pressure perfusing the aortic arch and the coronary and cephalic circulations. The descending aorta was cannulated (7 mm i.d.) immediately above the diaphragm and a pump (Model 603 U, Watson-Marlow, Falmouth, UK) perfused blood from reservoir B at a constant flow to the subdiaphragmatic circulation. The pump rate was initially set to give a systemic perfusion pressure of 120 mmHg.
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The left and right common carotid arteries were cannulated, perfused at a constant pressure (see C in Fig. 1) and drained, by cannulae inserted into the central ends of both linguinal arteries, into reservoir A.
All tubing connected to cannulae in the chest were externalized through the chest wall and the chest resealed by strapping the ribs and sternum together, then the overlying muscle and skin were tightly sutured together. Two tubes from the chest were connected to a vacuum source which was used to apply a controlled phasic negative intrathoracic pressure. Intrathoracic pressure was measured by an air-filled catheter positioned inside the chest cavity attached to a strain gauge transducer.
Blood pressures were recorded using saline-filled nylon catheters attached to strain gauge transducers (Gould-Statham P23Gb, Oxnard, CA, USA), connected to: the right carotid cannula (carotid sinus pressure); the left pulmonary cannula (pulmonary arterial pouch pressure); a cannula passed via the central end of the left carotid artery into the aortic arch (thoracic aortic, coronary arterial and cerebral perfusion pressures); and, the abdominal aorta (systemic arterial perfusion pressure). Pressure signals were amplified (EMMA system, SE Laboratories, Feltham, UK) and recorded on a computerized data acquisition system (Fastdaq, Lectromed, Letchworth, UK), VHS tape (Racal V-store, Racal Recorders Ltd, Southampton, UK) and a direct-writing electrostatic recorder (Model ES 1000, Gould Electronics, France). Signals of pressures and nerve activity were amplified (EMMA system). Before each experiment the pressure transducers were calibrated against a mercury column.
The temperature of the animals was monitored using a thermistor probe placed in the oesophagus and this was maintained between 37 and 39°C by use of heat exchangers incorporated into the perfusion circuit and by heaters under the animal table.
Experimental protocol
The responsiveness of the preparation was assessed by changing carotid sinus pressure in a single step from 60 to 210 mmHg. This was repeated at regular intervals during the experiments.
The vascular responses to pulmonary artery distension were determined as follows. Pulmonary arterial pressure was increased in small increments and the pressure stimulus was held constant at each step until steady-state responses were seen (about 60 s). The steady-state data were collected and analysed on-line. Each test commenced at the lowest attainable pulmonary arterial pouch pressure, which was around 5 mmHg; this acted as a control period for the test.
Pulmonary pressure tests were undertaken under two conditions: (1) with atmospheric pressure in the resealed chest, and (2) in the presence of phasic negative intrathoracic pressures with an amplitude around 10–15 mmHg and frequency of 18 cycles min-1. The sequence of tests was randomized.
Data analysis
Data were digitized at 1 kHz with signal processing software (Fastdaq, Lectromed) and analysed off-line. Vascular responses were accepted for analysis from those animals in which pulmonary pressure tests resulted in an increase of systemic vascular resistance by at least 10%. Pulmonary baroreflex control of vascular resistance was determined from the relation between pulmonary arterial pressure and systemic perfusion pressure. Stimulus–response curves were created using a curve-fitting computer software package (GraphPad version 4.0, GraphPad Software Inc., San Diego, CA, USA) to fit a sigmoid regression curve to the data points. From each curve, various parameters were derived. Threshold pressure was taken as the pulmonary arterial pressure corresponding to 5% of the overall systemic perfusion pressure response. The maximal slope of the curve was determined from the first derivative of the fitted sigmoid function, and the inflexion point was the pulmonary pressure that corresponded to the maximal slope.
All data were normally distributed therefore data are presented as means ±S.E.M. Between conditions comparisons were performed by Student's paired t tests and by two-way repeated measures ANOVA with post hoc Bonferroni tests where appropriate. Statistical significance was accepted at P < 0.05.
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Results |
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The responsiveness of preparations to carotid sinus pressure was assessed at intervals during experimentation. An increase in carotid sinus pressure from 61.0 ± 0.7 to 214.5 ± 14.2 mmHg decreased systemic perfusion pressure from 138.3 ± 10.6 to 100.0 ± 5.9 mmHg (-27.0 ± 7.0%; Student's paired t test, P < 0.05). During pulmonary artery distension, pressures perfusing the carotid sinuses were held constant at 60.1 ± 0.5 mmHg ; the pressure to the aortic arch, coronary arteries and cephalic circulation was held constant at 124.4 ± 5.1 mmHg .
Examples of pressure traces recorded during pulmonary baroreceptor stimulation with (A) atmospheric intrathoracic pressure and (B) phasic negative intrathoracic pressure are shown in Fig. 2. An example from another animal of the systemic perfusion pressure–pulmonary arterial pressure relationship under each of the two conditions in of chest pressure is shown in Fig. 3. This shows the sigmoid plots fitted to the actual data to enable determination of the threshold pressure, the maximum slope and inflexion point. In this example, during phasic negative intrathoracic pressure there was a decrease in the pulmonary pressure corresponding to the inflexion point of the curve and an approximate doubling of the maximal slope.
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Individual and group average values for the threshold pressures, the maximal slopes, and the inflexion points for the stimulus–response relationships under each condition are listed in Table 1. Values for the threshold pressure were lower in five of seven experiments when the phasic intrathoracic pressure was applied. The inflexion pressure, however, was lower in all seven experiments. These are summarized in Fig. 5 and overall the value was significantly lower with a negative intrathoracic pressure compared to atmospheric pressure (27.4 ± 4.0 vs. 37.8 ± 4.8 mmHg; P < 0.03) . No consistent effect of negative intrathoracic pressure was observed on the maximal slopes, although on average, the slope was nearly doubled during phasic intrathoracic pressure. Of the seven animals studied, the gain was doubled in four and decreased in three. The animals showing decreases were those with the smallest slopes.
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Discussion |
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Previous work has demonstrated that distension of the vascularly isolated pulmonary artery with a sufficiently high pressure can result in reflex vasoconstriction and an increase in respiratory activity. However, the physiological significance of these results is doubtful due to the excessively high pressures required to induce a response. For example, Ledsome and coworkers reported small but consistent increases in systemic vascular resistance when the pulmonary arterial pouch is distended with blood at around 30–40 mmHg (Ledsome & Kan, 1977; Kan et al. 1979; Ledsome et al. 1981). In contrast, Coleridge & Kidd (1963) had observed hypotension in some of their experiments when pulmonary arterial pressure was increased within the range 20–60 mmHg but an increase in systemic pressure when distension pressures in excess of 80 mmHg were used.
The reason for these divergent responses is unclear. However, one factor common to these experiments is that no attempt was made to ensure that ‘buffering’ by the various baroreceptors and other cardiac mechanoreceptors could not have masked the response. Another possible explanation for the high pressures required to induce a response may relate to a number of differences between experimental studies and the intact animal. In the intact animal: (1) pulmonary pressure has a phasic character, varying with the cardiac cycle; (2) the chest is closed; and (3) intrathoracic pressure is normally negative and varies throughout the respiratory cycle.
In our earlier report (McMahon et al. 2000), we addressed the issue of ‘buffering’ by controlling pressures to all other reflexogenic regions in an open-chest preparation. In these experiments, we found greater increases in vascular resistance at lower pulmonary distension pressures, although these were still at the upper end and beyond the limit of those normally encountered in the pulmonary artery. In three experiments, the chest cavity was resealed following connection to the perfusion circuit and it was observed that a static negative intrathoracic pressure enhanced the responses to pulmonary artery distension. This led to our hypothesis that the pulmonary baroreflex may be more effective in intact closed-chest animals with phasic negative pressure changes. We tested this in our recent study of pulmonary vagal afferent fibres (Moore et al. 2004). In these experiments we observed that the threshold and inflexion pressures of the pressure–discharge relationship were within the physiological range when a phasic negative pressure was applied to the resealed chest.
The experiments described here are the first in which the vascular responses to stimulation of pulmonary baroreceptors over a physiological range are investigated in a closed-chest preparation. Stimulus–response curves were defined during the following conditions: (1) atmospheric pressure in the closed chest; and (2) phasic negative intrathoracic pressure changes of around -10 mmHg at a frequency of 18 cycles min-1.
During phasic negative intrathoracic pressure changes, the threshold pressure (corresponding to 5% of the overall response of SPP) was lower in more than two-thirds of the experiments; however, the effect was variable and overall there was no statistically significant change in this parameter. Differentiation of the stimulus–response curves, however, revealed a significant reduction in the inflexion pressure (‘set point’), by almost one-third, during phasic intrathoracic pressure changes. There was no consistent effect on the maximal slope of the curve, although most experiments did show an increase. These results indicate that phasic negative intrathoracic pressures lower the operating pressure of the pulmonary arterial baroreflex with no consistent effect on the maximal gain. This finding is the first to highlight the importance of phasic changes in intrathoracic pressure on the effectiveness of the vascular response to pulmonary baroreceptor stimulation and supports our view (Moore et al. 2004) that pulmonary vagal afferents are responsive at pressures prevailing in the pulmonary arteries under normal conditions.
In intact animals, an increase in phasic intrathoracic pressure produces a simultaneous change in the environment of a number of receptors with potential cardiorespiratory interactions. For example, it has long been known that pulmonary slowly adapting stretch receptor feedback is a potential modifier of reflex circulatory responses (Daly, 1986); however, divergent responses of vascular resistance to lung inflation are reported in anaesthetized animals (Daly & Robinson, 1968; Hainsworth, 1974; Wood et al. 1985). In the present study, pulmonary mechanoreceptors were excluded by tying the lung lobes at their base.
We need now to speculate on what could be the physiological role of pulmonary baroreceptors. The cardiovascular system is controlled by a number of reflex mechanisms. Arterial baroreceptors are the best known and most widely studied of the reflexes (Eckberg & Sleight, 1992). Carotid, aortic and coronary artery baroreceptors function as a negative feedback system and are effective in limiting short-term fluctuations in blood pressure. In contrast, stimulation of pulmonary baroreceptors results in systemic vasoconstriction and an increased respiratory drive. Interestingly, the experiments reported here indicate that pulmonary baroreceptor stimulation in the presence of a physiological change in intrathoracic pressure is more effective in inducing significant vasoconstriction than physiological changes in pulmonary arterial intraluminal pressure alone
The interaction of cardiovascular and respiratory variables constitutes an important influence on autonomic cardiovascular and respiratory control. One possible role for pulmonary arterial baroreceptors is that they are involved in the cardiorespiratory adjustments during exercise. It is reported that exercise hyperventilation is capable of producing a phasic intrathoracic pressure of -23 mmHg during inspiration and 4–23 mmHg during expiration (Janicki et al. 1996). It is very likely therefore that during exercise the combined stimulus of an increase in right ventricular outflow and an increase in respiratory effort, resulting in greater pulmonary artery transmural pressure, would lead to greater stimulation of pulmonary arterial baroreceptors. Such an increased stimulation of pulmonary baroreceptors would be likely to contribute to the generalized vasoconstriction that is known to divert blood to metabolically active tissue during exercise (Rowell et al. 1996). Furthermore, it is possible that pulmonary baroreceptor feedback contributes to the changes in autonomic outflow that are believed to contribute to classic baroreceptor reflex resetting observed during exercise (Raven et al. 1997). Another response to stimulation of pulmonary arterial baroreceptors is to increase respiratory activity (Kan et al. 1979; McMahon et al. 2000). It is likely therefore that a feed-forward mechanism originating from pulmonary artery baroreceptors could provide the increased respiratory drive that contributes to hyperpnoea at the onset of exercise, resulting in even greater reflex stimulation. Such a mechanism may explain previous suggestions that acute hyperpnoea at the onset of exercise is secondary to an increase in cardiac output (Wasserman et al. 1986).
Another possible situation where it might be expected that pulmonary arterial baroreceptor stimulation could be involved is where venous return, and therefore right ventricular outflow, decreases. This would be relevant in orthostatic stress, including simulated orthostatic stress as during application of lower body negative pressure. These situations are associated with vasoconstriction and increased baroreceptor sensitivity (Pawelczyk & Raven, 1989; Cooper & Hainsworth, 2001). Unloading of pulmonary baroreceptors, however, would be expected to result in the opposite responses. This would suggest either that during these conditions other mechanisms such as splanchnic distension (Doe et al. 1996) may exert more powerful effects, or that the more important stimulus to pulmonary arterial baroreceptors is exerted through the changes in intrathoracic pressure, and hence transmural pressure, rather than the pulmonary arterial pressure per se.
In conclusion, this study has established that the reflex vasoconstriction occurring in response to stimulation of pulmonary baroreceptors can be obtained at the arterial pressures normally prevailing in the pulmonary circulation. However, responses at physiological pulmonary pressures are dependent upon a more physiological environment, i.e. closed chest and phasic negative intrathoracic pressure changes. This is probably due to the effect of the negative intrathoracic pressure on transmural pulmonary arterial pressure. The principal physiological role of pulmonary baroreceptors might be in mediating cardiorespiratory responses to increases in cardiac output and pulmonary arterial pressure during exercise. Also, they would be strongly stimulated in diseases of the lung including pulmonary hypertension.
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References |
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) and phasic negative intrathoracic (
) pressures in the closed chest. Dashed and continuous lines represent the fitted logistic function. Right panel, the dashed line represents the first differential of the stimulus–response curves with atmospheric chest pressure. The continuous line represents the first differential with phasic negative intrathoracic pressures.
