Experimental Physiology (1995), 80, 255-263
 Printed in Gr)eat Br-itain

                                           BEATA WYPYCH
   Department of Neurophysiology, PAS Medical Research Centre, 3 Dworkowa Street, 00-784 Warsaw, Poland
                      (MANUSCRIPT RECEIVED 13 JULY 1994, ACCEPTED I NOVEMBER 1994)

    The contribution of sympathetic and vagal inputs to ventilatory depression induced by dopamine
    was studied in eighteen anaesthetized, spontaneously breathing, normoxic cats. Breathing was
    via a tracheostomy. Dopamine (20 jug (kg body wt)-') was injected intravenously in the intact
    animal, then after section of the cervical sympathetic trunks, and finally after midcervical
    vagotomy. Dopamine, injected as a bolus, induced depression of ventilation, affecting
    predominantly the volume component of the breathing pattern at all experimental stages. The
    extent of volume reduction was larger and different from that in intact animals following section
    of sympathetic (P < 0.05) and vagal trunks (P < 0.01). The respiratory cycle was significantly
    prolonged (P < 0.01) prior to vagotomy, due entirely to the increase in the expiratory time (TE).
    Bilateral section of the carotid sinus nerves performed in six cats virtually abolished post-
    dopamine ventilatory depression.

 Dopamine is normally present in the carotid body of the cat (Ciocchio, Biscardi & Tremazzani,
 1966; Zapata, Hess, Bliss & Eyzaguirre, 1969; Mir, Al-Neamy, Pallot & Nahorski, 1982).
 Bolus injection of dopamine in this species inhibits carotid chemoreceptor discharge in vivo
 (Black, Comroe & Jacobs, 1972; Sampson, Aminoff, Jaffe & Vidruk, 1976; Docherty &
 McQueen, 1978; Lahiri, Nishino, Mokashi & Mulligan, 1980; Folgering, Ponte & Sadig,
 1982) and in vitro (Zapata, 1975; Llados & Zapata, 1978; Monti-Bloch & Eyzaguirre, 1980).
 The inhibitory effect of intravenous dopamine on carotid chemoreceptor activity was found
 to be greater at moderate levels of hypoxic and hypercapnic stimuli (Lahiri et al. 1980;
 Nishino & Lahiri, 1981). It is also present in hyperoxic conditions (Zapata & Zuazo, 1980).
   Dopamine does not cross the blood-brain barrier. Its action is mainly on peripheral chemo-
 receptors. Transient depression of ventilation induced by dopamine affects the tidal volume
 and, less consistently, the timing component of the breathing pattern and is abolished by
 bilateral section of the carotid sinus nerves (Black et al. 1972; Zapata & Zuazo, 1980, 1982;
 Nishino & Lahiri, 1981).
   This chemoreflex effect on ventilation raised the question of whether and how the sensory
 inputs controlling respiratory feedback reflexes contribute to the decreased drive to breathe.
 Both components of the respiratory pattern affected by the ventilatory depression are
 regulated by two mechanisms: the volume feedback from the lungs and the activity of the
 bulbopontine structures (Sant'Ambrogio & Remmers, 1985).

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    Our objective in the present study was to determine if the sympathetic and vagal pathways
  contribute to the respiratory depression following dopamine challenge. So far as we are
  aware there has been no such study. We reasoned that the respiratory oscillations in the
  sympathetic nervous system, and vagal facilitatory influences, could participate in a post-
  dopamine decrease in ventilatory drive. We hypothesized that the sympathetic and vagal
  pathways provide a major stabilizing influence that minimizes the reduction of tidal volume
  in response to exogenous dopamine.
    A preliminary summary of the results has been published (Wypych, 1993).

  Eighteen adult cats of either gender (weight 2.5-4-7 kg) were anaesthetized with 30 mg kg-' sodium
  pentobarbitone (Sagatal, May and Baker Ltd, UK) injected intraperitoneally and later supplemented
  with 16mg kg-' a-chloralose (Fluka AG, Switzerland) injected intravenously. Cats were placed supine
  on a heated operating table and allowed to breathe room air spontaneously. A femoral vein and a
  femoral artery were catheterized for further injections and to monitor blood pressure, respectively. The
  trachea was cannulated and the tracheal tube connected to a pneumotachograph. The C4-C5 root of the
  right phrenic nerve was cleared, cut, desheathed and prepared for recording. The cervical sympathetic
  trunks and the cervical vagi were separated, isolated and encircled with loose ligatures for section later
  in the experiment.
     Arterial blood pressure was measured with a pressure transducer (C.K. 01, Mera-Tronik, Warsaw,
  Poland) and blood pressure monitor (4011S, MCK, Warsaw, Poland). Volume signals were recorded
  from a pneumotachograph (Electrospirometer CS6, Mercury, Glasgow, UK). End-tidal CO2 was
  measured with a capnograph (Engstrom Eliza plus, Gambro, Bromma, Sweden). Action potentials of
  the phrenic nerve were amplified (Tektronix 3A3, USA) and integrated (type 464, Medipan, Poland).
  The time constant of the integrator was 100 ms. All recordings were registered with an Omnilight
  Recorder 8M36 (Honeywell, Japan). Rectal temperature was 37-39 °C throughout the experiment.
     Dopamine (3-hydroxytyramine hydrochloride, crystalline; Sigma) was administered intravenously
  (20 ug kg-') as a bolus injection. The respiratory effects of dopamine were recorded (1) in intact
  animals, (2) following section of the cervical sympathetic trunks and (3) after subsequent midcervical
  vagotomy. At the end of the experiment, the carotid sinus nerves were cut in six of the cats. Inspiratory
  time (TI) and expiratory time (TE) were determined, respectively, from the start and the peak of the
  phrenic neurogram and breathing frequency was computed. Minute ventilation was computed from the
  tidal volume (VT) and breath duration.
     The responses of ventilatory variables were assessed by comparing the mean of five breaths following
  the dopamine injection that showed a maximal decrease in VT with the mean of five breaths before
  injection (control). Student's paired t test was used to compare absolute values following dopamine
  injection with control values, and the difference between the mean values obtained for each
  experimental condition. All results were calculated as means and standard deviations. A difference was
  considered significant if P < 0.05.

  The initial values for tidal volume were: 38.9 + 10 1 ml in intact cats, 43-2 + 10.3 ml after
  section of the cervical sympathetic trunks and 54.2 + 12.9 ml after subsequent vagotomy
  (n= 18).
    The mean values for the respiratory cycle duration (TTOt) were: 2 91 + 0 62 s in intact cats,
  3.6 + 1.41 s after section of cervical sympathetic trunks and 5*7 + 2.2 s following vagotomy
  (n= 18).

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                          Vr (MI)



                                                Intact        Sympathetic         Vagi cut
                                                               trunks cut

 Fig. 1. Mean decreases in tidal volume (VT) subsequent to dopamine (O) administration in intact animals and those with
   sympathetic and vagal trunks cut. CL, control. Data are presented as means + S.D. *** P < 0-001 compared with pre-
   dopamine values, n = 18.

   In our experiments I.V. bolus injection of 20 ,ug kg-' of dopamine led to a decrease in VT
 between 1 and 10 s after administration at all experimental stages. When an equal volume of
 0 9 % saline was injected into the femoral vein, it failed to produce any respiratory changes.
   The effects usually consisted of a reduction in amplitude of several respiratory cycles over
 a variable period. Responses in intact cats lasted no longer than 27 s; those following section
 of the sympathetic trunks lasted at most 36-5 s and, after subsequent vagotomy, the effect
 persisted for up to 41 s. Ventilation usually returned to control values within 1 min. The
 respiratory changes were accompanied by slight increases in systemic blood pressure. Both
 systolic and diastolic pressures increased significantly (P <0001), by 5 and 3 25 kPa,
 respectively, in all experimental conditions (n = 15).
   The injection of dopamine reduced tidal volume in all animals studied. Figure 1 shows the
 mean fall in tidal volume in response to i.v. injection of dopamine in eighteen cats initially
 intact, and then sympathectomized and subsequently vagotomized.
   The mean decrease in tidal volume induced by dopamine was highly significant in each
 neural state compared with pre-drug controls (P <0.01). The volume effects were
 accompanied before vagotomy by prolongation of the respiratory cycle (TTOt). In intact cats
 TTot increased by 0-4 s (P < 0.01), and in those with section of cervical sympathetic trunks,
 by 0 8 s (P < 0.01) following dopamine injection.
   Since the inspiratory time (TI) showed no appreciable change, the increase was attributable
 entirely to the significant prolongation of expiratory time (TE) in intact cats (P < 0.01) and
 those with sectioned sympathetic trunks (P < 0.05). As illustrated in Fig. 2, after midcervical
 vagotomy cats did not show a significant change in expiratory time.

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  258                          B. WYPYCH AND M. SZEREDA-PRZESTASZEWSKA

            4                                                             8
             3                                                            6
                                         n.s.                      5*
    T1 (s) 2              n.s.                                     TE (s) 4
                                               1                          ~~~~~~~~~~~~~~2

             0                                     -                      0
                      Intact      Sympathetic      Vagi cut                         Intact        Sympathetic    Vagi cut
                                   trunks cut                                                      trunks cut
        Fig. 2. The effect (means + S.D.) of dopamine (1) on inspiratory time (TI) and expiratory time (TE). O. control.
                                     *** P < 0-001, * P < 0-05; n.s., not significant; n = 13.

                                        1100 _
                                        1000 _

                          (ml mmin ')   60i

                                                      Intact         Sympathetic            Vagi cut
                                                                      trunks cut

          Fig. 3. Mean values + S.D. of minute ventilation (VE) at each experimental stage. 0, dopamine; E, control.
                                                     ***P<000 1,n= 18.
    Dopamine depressed minute ventilation in each experimental condition (Fig. 3). These
  decreases involved both reduced tidal volume and prolonged respiratory cycle. The decrease
  in minute ventilation was significantly larger in cats with sectioned sympathetic trunks than in
  intact animals (P < 0.05, n = 13).
    The reduction in tidal volume, calculated as the difference between control values and
  values after dopamine, differed significantly between the experimental conditions. As shown

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                                            -20 _

                               A VT (ml)


                                                       |\   \   '\   \ \ \ \

                                                                                      Sy mpathetic
                                                                                       truinks cut
                                                                                                          Vaoi cut

  Fig. 4.   Mealn   decreases in   tidail olumne (AVT) calcuilated as diilerenices between pre- and post-dopamiine xalues             in   each
                                          experimnenital conditioni. P < 0 05, P < 001,1         18.




                              Al (ml)       -1c5



                                                                     Vagi      CLut          Certical   sinius
                                                                                                nerv es cut

      Fig. 5. Mean ( + S.D.) doparminc-indUCcd rcdiCtions in tidal V olIme (Al"T) calculated iil Fig. 4          as   in %   agotomnizcd cats
                              before and after sectionl of both catrotid sinus nersves. P < 0-01, = 6.

 in Fig. 4, the reduction of tidal volume becamie larger following the consecutive section of
 sympathetic and vagal trunks.
   Bilateral section of the carotid sinus nerves abolished the decrease in tidal volume
 following dopamine administration (Fig. 5).

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                                            DISCUSS ION
  The results of this study are in general agreement with the reports of other investigators in
  that bolus injection of dopamine in the cat transiently depresses ventilation. The drug is
  effective whether injected into the carotid artery (Black et al. 1972) or intravenously (Zapata
  & Zuazo, 1980). The carotid sinus and aortic nerves are the main afferent pathways involved
  in the respiratory response to dopamine (Nishino & Lahiri, 1981; Smatresk & Lahiri, 1982).
  In all reports describing the respiratory depression due to dopamine in cats, these
  chemoafferent nerves, initially preserved intact, were interrupted in various experimental
  schemes to characterize the diminution of the respiratory effects of dopamine. In our
  experiments the carotid sinus nerves were preserved throughout the whole experimental
  protocol and finally cut in six cats.
     We have focused our interest on the role of sympathetic and vagal contributions to the
  hypoventilatory effects of dopamine. In our cats, with afferent inputs initially preserved, the
  same dose of dopamine (20 jug kg-') reduced the tidal volume less than reported by Zapata &
  Zuazo (1980). However, this amount of dopamine induced larger reductions with
  progressive sections (see Figs 1 and 4). This brief chemodeafferentation produced by intra-
  venous injection of dopamine silences the sensory impulses arriving at the nucleus of the
  solitary tract from the carotid nerves and induces the decrease in tidal volume. Activity in the
  sympathetic and vagal trunks may mask the effects of dopamine-induced inhibition of
  afferent impulses passing from chemoreceptors to the bulbopontine structures.
     In the current experiments the timing component of the respiratory pattern was
  significantly affected by dopamine-induced ventilatory depression. It was not apparent as
  described by Zapata & Zuazo (1980), but consistent and reproducible in all animals. The
  slowing was entirely due to an appreciable prolongation of TE, which is in line with the
  finding of Nishino & Lahiri (1981). Changes in breathing rate due to peripheral ventilatory
  chemosensory drive were shown to be mainly contributed by the aortic bodies (Eugenin,
  Larrin & Zapata, 1989, 1990). Vagotomy performed at midcervical level in cats also causes
  aortic neurotomy (Ito & Sher, 1974). Following this procedure our cats were deprived of
  sensory input from aortic bodies affected by dopamine, and also of the vagal effects on
  respiratory cycle duration.
     Our results showing a marked reduction in minute ventilation following dopamine
  administration are in line with other findings (Nishino & Lahiri, 1981; Zapata & Zuazo,
   1982). They are reinforced by additional evidence that dopamine agonists similarly depress
  minute ventilation (Zapata & Zuazo, 1982; Bonora & Gautier, 1988).
     The inhibitory effect of dopamine upon ventilatory drive seems to occur independently of
  its hypertensive effects, as tidal volume always decreased before increases in blood pressure.
  Moreover, Iturriaga, Alcayaga & Zapata (1988) have shown that the hypertensive responses
  evoked by unilateral common carotid occlusion were not associated with significant changes
  in ventilation.
     The present study demonstrates two further findings on the hypoventilatory response to
  dopamine, namely that the fall in tidal volume is increased progressively by exclusion of the
  cervical sympathetic trunk and of the lung vagi. Dopamine was shown to inhibit not only the
  carotid nerve chemosensory activity, but also impulses in the cervical preganglionic
  sympathetic nerve (Matsumoto, Mokashi & Lahiri, 1987).

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   The novel aspect of our investigation is the finding that section of the cervical sympathetic
 trunks enhances the fall in tidal volume induced by dopamine. This type of section,
 performed between the superior and medial cervical ganglia, interrupts the sympathetic
 supply to the carotid body, since the preganglionic efferents run in the cervical trunk. The
 ganglioglomerular nerves, branching from the superior cervical ganglion (McQueen, Evrard,
 Gordon & Campbell, 1989; Bee & Howard, 1993), are present, but sympathetic tone and
 drive are absent. Thus the separation of the cervical sympathetic trunk from the thoracic
 sympathetic chain cuts off a large proportion of respiratory-modulated sympathetic discharges,
 which could influence the transient post-dopamine arrest of chemosensory discharges from
 the carotid bodies. The respiratory oscillations inherent in the sympathetic nervous system
 are of variable timing within each phase of individual respiratory cycles and are independent
 of the carotid and vagal inputs (Barman & Gebber, 1976; Bainton, Richter, Seller,
 Ballantyne & Klein, 1985; Huang, Lahiri, Mokashi & Sherpa, 1988; Czyzyk-Krzeska &
 Trzebski, 1990). We cannot exclude the possibility that this central respiratory-activating
 mechanism is likely to be involved in countering the dopamine-induced reduction of tidal
   Central projections of the carotid nerve were shown to terminate within five subnuclei of
 the solitary tract (Nomura & Mizuno, 1982; Torrealba & Claps, 1988), close to the vagal
 afferent projections (Donoghue, Garcia, Jordan & Spyer, 1982). The inhibitory effects of
 chemoreceptor depression on tidal volume and timing components of the breathing pattern
 following dopamine injection could, therefore, be initiated at this site in the bulbopontine
   In our experimental design, preservation of the vagal feedback from the lungs attenuated
 the fall in tidal volume produced by dopamine injection, and midcervical vagotomy
 unmasked its full extent (Fig. 4). Although vagotomy eliminated the prolongation of the
 respiratory cycle, a significant fall in minute ventilation still occurred (Fig. 3). The vagal
 mechanism which minimizes the extent of volume reduction is obscure. One possibility is
 that elimination of the vagal inhibitory effects on tidal volume reveals a synergistic
 dopaminergic inhibition of the latter.
   Bilateral section of the carotid sinus nerves abolished the ventilatory depression following
 dopamine, which corroborates previously published results (Black et al. 1972; Zapata &
 Zuazo, 1980, 1982). We used the same dose of dopamine after final section of the carotid
 sinus nerves and the respiratory response was virtually abolished (Fig. 5). The rise in
 systemic blood pressure was not significant. The larger doses of dopamine used by Zapata &
 Zuazo (1980) in cats with the carotid and aortic nerves cut caused a moderate fall in tidal
 volume, accompanied by hypertensive reactions.
   The results of the present study revealed that ventilatory depression induced by intravenous
 injection of dopamine in cats predominately affects the tidal volume component of the
 breathing pattern. The degree of this respiratory inhibition is enhanced by the consecutive
 exclusion of the sympathetic and vagal inputs. Bilateral section of the carotid sinus nerves
 abolished this chemoreflex.
   In conclusion, our findings support our initial hypothesis. The consecutive divisions of the
 sympathetic and vagal trunks substantially increased the depression of tidal volume induced
 by intravenous administration of dopamine in cats.
 Excellent technical assistance was given by Miss Monika Janisz.

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