Middle cardiac nerve section alters ventilatory response to PaCO2 in the cockerel.

To determine whether afferents in the middle cardiac nerves (MCN) contribute to extrapulmonary PaCO2 sensitivity, we did the following: we anesthetized six cockerels with sodium pentobarbital (25-35 mg/kg), and cannulated the cutaneous ulnar vein, and the carotid and brachial arteries. The thorax was opened and each lung unidirectionally ventilated from separate gas delivery systems. A ligature, which temporarily occluded blood flow, was placed around the right pulmonary artery. Both cardiac sympathetic nerves were cut, as well as the left vagus just above the level of the recurrent branch. We exposed the non-perfused right lung to 105 Torr PCO, to silence intrapulmonary chemoreceptors (IPC). We measured blood pressure, heart rate and ventilatory movements while the denervated left lung was used to fix PaCO2 at seven levels ranging from 7-140 Torr. As arterial PCO2 increased, ventilatory amplitude increased from 0.3 mm to 3.6 mm, while frequency decreased from 140 to 24 per min. After cutting the MCN, ventilatory movements were less responsive to PaCO2 changes. Ventilatory amplitude was 3.0 mm at the lowest PaCO2 and increased to 4.0 at the highest PaCO2. We conclude that: 1) when IPC discharge is low, afferents in the MCN inhibit ventilatory movements during hypocapnia, and 2) these afferents may contribute to systemic CO2 sensitivity.

Cardiac receptors evoke ventilatory response with increased venous PCO2 at constant arterial PCO2.

The effects of elevated venous PCO2 and denervation of the cardiac ventricles on ventilation were studied in 20 anesthetized open-chest unidirectionally ventilated White Leghorn cockerels. Venous PCO2 was increased by insufflating the gut with high CO2 while recording changes in the amplitude of the sternal movements. Arterial blood gases were held constant by unidirectionally ventilating the lungs with gas flows approximately five times the animal's resting minute volume. Insufflating the gut with 90% N2-10% O2 did not change the level of ventilation, whereas with 90% CO2-10% O2 the amplitude of sternal movement increased 500% above that with no gut gas flow. Exchange of N2 for the CO2 was followed by a rapid reduction of ventilatory movements to control levels. Arterial blood gases remained constant during gut gas insufflation, whereas mixed venous PCO2 increased and mixed venous pH decreased when high CO2 was given to the gut. Cutting the middle cardiac nerves, which primarily innervate the ventricles of the heart, reduced the ventilatory response to CO2 gut insufflation by 67%. Sympathetic denervation of the thoracic viscera did not change the responses. It appears that, in the chicken, increasing the mixed venous PCO2 while holding the arterial blood gases constant alters ventilation by an afferent system located in the venous circulation or in the right ventricle which is sensitive to changes in PCO2.

The effect of hypoxia on plasma potassium concentration and the excitation of arterial chemoreceptors in the cat.

Intra-arterial recordings of potassium concentration ([K+]a) and arterial chemoreceptor discharge were made in six anaesthetized cats while tracheal PO2 was stepped every 2 min (end-tidal PO2 ca. 140, 60, 40 and 95 Torr) at constant PCO2 (33 Torr). [K+]a increased hyperbolically from 3.0 mM to 4.5 mM as arterial PO2 was lowered from 95 to 40 Torr. Because the discharge of arterial chemoreceptors is excited by hyperkalaemia as well as hypoxia, the hypoxic discharge of arterial chemoreceptors may have a component mediated by [K+]a. The mechanisms underlying the arterial K+ increase in hypoxia remain unknown.

Effects of potassium, oxygen and carbon dioxide on the steady-state discharge of cat carotid body chemoreceptors.

1. We have studied the effects of intravenous infusions of 0.1 mmol/min KCl (raising arterial potassium from ca. 3.2 to 6.0 mM) on the steady-state responses of carotid body chemoreceptors to end-tidal PCO2 and PO2 in the pentobarbitone-anaesthetized cat. 2. The excitatory effect of these KCl infusions was enhanced by hypoxia and reduced or abolished by hyperoxia. 3. Hypercapnia did not enhance, and usually reduced, excitation by KCl. 4. When similar control discharge frequencies were established by hypoxia or by hypercapnia, a KCl infusion excited the hypoxic discharge by about twice as much as it did the hypercapnic discharge. 5. These observations are not inconsistent with the idea that the mechanism underlying hypoxic excitation of arterial chemoreceptors is one that controls extracellular potassium concentration near the afferent nerve ending. 6. Insofar as potassium-induced excitation of chemoreceptor discharge is abruptly reduced by hyperoxia it behaves like Asmussen and Nielsen's postulated 'anaerobic work substance' and it may therefore contribute to the increased importance of the arterial chemoreflex reported in exercise.

Effects of altering dead space volume on respiration and air sac gases in geese.

Dead space volume (VD) was altered in spontaneously breathing, anesthetized geese from values far above (about 115 ml) to those far below (about 3 ml) the normal VD (approximately 40 ml). Respiratory gases were measured in cranial (CrS) and caudal air sacs (CdS) and in blood. The major findings were as follows: Ventilation increased linearly with VD, by increases in tidal volume (VT) at constant breathing rate (fresp); effective parabronchial ventilation, (VT-VD) X fresp, remained constant and so did arterial blood gases. No changes occurred in CrS gas composition. CdS PCO2 declined with decreasing VD, and the respiratory exchange ratio increased, reaching values above unity at the lowest VD. The gas composition in CrS, and particularly its relation to end-expired gas composition, is in agreement with current models of the gas flow pattern in the avian lung. The PCO2 values in CdS are higher than expected by simple models, e.g. by dead space re-inhalation. Neopulmonic gas exchange and incomplete gas mixing are suggested to contribute significantly to the gas composition of CdS.

Effect of acute and chronic cardiac denervation on osmotic release of vasotocin in chickens.

Hypo- and hyperosmotic NaCl were infused intravenously to examine osmotic release of arginine vasotocin (AVT) in anesthetized, acutely cardiac-denervated chickens and in conscious, chronically denervated birds. Mean arterial blood pressure was consistently higher in denervated compared to sham-operated chickens but heart rates were similar in experimental and control groups. Plasma AVT concentrations (pAVT) were significantly higher than controls in acutely, but not chronically, denervated chickens. The slope of the regression line relating pAVT to plasma sodium concentration was higher in denervated birds indicating that removal of cardiac receptor activity increases the osmotic sensitivity of the AVT system. The results suggest that cardiac end-net receptor activity may participate in the regulation of blood pressure and can modulate the release of antidiuretic hormone in the chicken.

The effect of CO2 and temperature on respiratory movements in the chicken.

We studied the effect of increasing colonic temperature (Tc) on respiratory amplitude and frequency at different levels of PICO2 in anesthetized, unidirectionally ventilated cockerels. We also evaluated the relationship between PICO2 and PaCO2. Increased PaCO2 augmented respiratory amplitude and decreased frequency at every Tc. Respiratory amplitude increased as Tc rose from 41 to 45 degrees C at each level of PaCO2. During the same rise in Tc, respiratory frequency decreased at the low PaCO2 seen in awake, panting cockerels but increased at eucapnic PaCO2. Tc had no effect on frequency at high PaCO2. Values for respiratory frequency of unidirectionally ventilated cockerels at given Tc and PaCO2 predict those of awake cockerels. We conclude that amplitude of breathing increases in acute hyperthermia unless accompanied by hypocapnia and that without hypocapnia maximal panting frequencies cannot be reached.

The alteration of CO2 respiratory sensitivity in chickens by thoracic visceral denervation.

We measured respiratory movements in nine groups of six cockerels, 20-24 weeks of age. We opened the thorax and all air sacs, and unidirectionally ventilated each lung separately. The right lung received constant P(CO2), while the P(CO2) was altered to the left lung. There were only small differences in response to P(CO2) alterations whether both pulmonary circulations were intact, the left pulmonary circulation was blocked, or the left lung was denervated and the right pulmonary circulation blocked, suggesting (1) that the extrapulonary and pulmonary P(CO2) -sensitive afferents (in one lung) have equivalent influence, and (2) the influences of the two afferent systems are not additive. Respiratory sensitivity after bilateral vagotomy is small despite pulmonary innervation by CO2 -sensitive spinal afferents, perhaps one reason for abnormal respiration after vagotomy. The respiratory influences of pulmonary vagal and spinal CO2-sensitive afferents are also non-additive, suggesting that non-additive interactions among afferents controlling respiration may be common in the chicken. Rates of response to altered intrapulmonary P(CO2) are determined by central mechanisms and not the time for CO2 distribution or receptor response.

Fiber size and sensory endings of the middle cardiac nerve of the domestic fowl (Gallus domesticus).

The middle cardiac nerve, a branch of the vagus, innervates the ventricles of the avian heart. Of 533 myelinated sensory fibers, the size range was 2 micron. The ratio of myelinated to unmyelinated sensory fibers ranged from 2.17 to 3.48. Sensory endings resembled a network pattern with no distinct receptor-like endings. Frequency of nerve population increased from apex to base of the heart.

Pulmonary circulation--vertebral venous interconnections in the chickens.

Injections of India ink colored blood, latex, and plastic followed by study of corrosion casts and dissections were used to determine the interconnections of the vertebral venous system and pulmonary circulation in the chicken. Multiple, minute connections are found to the intercostal veins, small mesenteric veins and others connected to the vertebral venous system. Thus, blood can flow in quantities between the vertebral venous system and the pulmonary circulation depending upon pressure gradients.