Cold wind stimulation reflex.

The bradycardia induced by cold wind blown on the face and the early cephalic release of insulin induced by feeding have been shown to be caused by a vagal reflex stimulation. An experiment was designed to determine whether cold wind blown on the face would induce both pancreatic and cardiac stimulation. A 4 degrees C wind blown on the face for 4 min produced a rapid and persistent bradycardia, which interestingly persisted for up to 35 min after the test. The effect on respiration rate is more gradual and vanishes immediately after cold wind stimulation. Cold wind produced a slight reduction of insulin secretion, as evidenced by the fall of both plasma insulin and C-peptide, and caused a significant increase in plasma norepinephrine. These results suggest that the cold wind action of the vagus nerve is exerted on the heart and that of the sympathetic on the pancreas, whereas during the cephalic phase of feeding a vagal influence is observed on the pancreas and a sympathetic action on the heart. The mechanisms of the quantitative and qualitative control of these autonomic responses are not known and deserve further investigation.     

Effects of age, sex, and physical fitness on responses to local cooling

The response to local cooling was estimated by the cold hand test (5 degrees C for 2 min) and the cold face test (0 degrees C with 66 km.h-1 wind for 2 min). Heart rate, blood pressure, and skin temperature were measured before, during, and after the tests. The increase in blood pressure (cold hand test) and the fall in Tsk (cold face test) were reduced in trained subjects. Similarly older subjects (53-60 yr of age) responded less to a cold hand test than younger subjects aged 20-40. However, the bradycardia caused by the cold face test was more pronounced in the older subjects. The responses to the cold hand and cold face tests were the same for male and female subjects. During the 2 min after the test, blood pressure and heart rate fell below initial values in the female group but not in the male. It is concluded that, besides adaptation to cold, individual factors such as age, sex, and physical fitness also have a relative importance in the responses to local cooling.     

Effects of the cold pressor test on cardiac autonomic control in normal subjects

The cold pressor test (CPT) triggers in healthy subjects a vascular sympathetic activation and an increase in blood pressure. The heart rate (HR) response to this test is less well defined, with a high inter-individual variability. We used traditional spectral analysis together with the non-linear detrended fluctuation analysis to study the autonomic control of HR during a 3-min CPT. 39 healthy young subjects (23.7+/-3.2 years, height 180.4+/-4.7 cm and weight 73.3+/-6.4 kg) were divided into two groups according to their HR responses to CPT. Twenty subjects have a sustained increase in HR throughout the test with reciprocal autonomic interaction, i.e. increase in sympathetic activity and decrease vagal outflow. In the 19 remainders, HR decreased after an initial increase, with indication of involvement of both sympathetic and vagal outflow. Baseline evaluation of the subjects revealed no difference between the two groups. Nevertheless, a higher sympathetic activity at the skin level during CPT was present in the group with decreased HR. Further studies are needed to explain why healthy subjects react differently to the CPT and if this has potential clinical implications.     

Central and peripheral mechanisms underlying gastric distention inhibitory reflex responses in hypercapnic-acidotic rats

We have observed that in chloralose-anesthetized animals, gastric distension (GD) typically increases blood pressure (BP) under normoxic normocapnic conditions. However, we recently noted repeatable decreases in BP and heart rate (HR) in hypercapnic-acidotic rats in response to GD. The neural pathways, central processing, and autonomic effector mechanisms involved in this cardiovascular reflex response are unknown. We hypothesized that GD-induced decrease in BP and HR reflex responses are mediated during both withdrawal of sympathetic tone and increased parasympathetic activity, involving the rostral (rVLM) and caudal ventrolateral medulla (cVLM) and the nucleus ambiguus (NA). Rats anesthetized with ketamine and xylazine or α-chloralose were ventilated and monitored for HR and BP changes. The extent of cardiovascular inhibition was related to the extent of hypercapnia and acidosis. Repeated GD with both anesthetics induced consistent falls in BP and HR. The hemodynamic inhibitory response was reduced after blockade of the celiac ganglia or the intraabdominal vagal nerves with lidocaine, suggesting that the decreased BP and HR responses were mediated by both sympathetic and parasympathetic afferents. Blockade of the NA decreased the bradycardia response. Microinjection of kainic acid into the cVLM reduced the inhibitory BP response, whereas depolarization blockade of the rVLM decreased both BP and HR inhibitory responses. Blockade of GABA(A) receptors in the rVLM also reduced the BP and HR reflex responses. Atropine methyl bromide completely blocked the reflex bradycardia, and atenolol blocked the negative chronotropic response. Finally, α(1)-adrenergic blockade with prazosin reversed the depressor. Thus, in the setting of hypercapnic-acidosis, a sympathoinhibitory cardiovascular response is mediated, in part, by splanchnic nerves and is processed through the rVLM and cVLM. Additionally, a vagal excitatory reflex, which involves the NA, facilitates the GD-induced decreases in BP and HR responses. Efferent chronotropic responses involve both increased parasympathetic and reduced sympathetic activity, whereas the decrease in BP is mediated by reduced α-adrenergic tone.     

Bronchoconstriction: a component of the 'diving response' in man

We have investigated the possibility that a bronchoconstriction accompanies the vagally-mediated bradycardia induced in man by immersion of the face in cold water. Forced expiratory flows (FEF) at 40% and 25% of vital capacity (VC) have been measured from partial flow-volume curves obtained during forced expirations starting at 70% VC. These were performed immediately after 15 s apnoea with or without face immersion, and compared with control expirations having the same volume history but without the preceding apnoea. Five of the 10 subjects showed evidence of a greater than 10% reduction in FEF, which averaged 17% (Fig. 2). Half the response was attributable to the apnoea alone and the other half, which was abolished by ipratropium, to cold face immersion (Fig. 3). This bronchoconstriction appears to be a new component of the 'diving response' in man, mediated, like the bradycardia, by vagal efferents.     

Reflex regulation of the circulation after stimulation of cardiac receptors by prostaglandins

Prostaglandins (PGs) are potent vasoactive substances that may participate in the control of coronary blood flow, platelet aggregation, and inflammation. An important action of PGs may be the stimulation of c fibers in general and vagal cardiac c fibers in particular. The Bezold-Jarisch reflex after intracoronary injection of Veratrum alkaloids is very similar to the vagal bradycardia elicited by stimulation of cardiac PG synthesis or injection of prostacyclin (PGI2). The characteristic features of this reflex are 1) stimulation of c fibers, 2) inferoposterior wall location of receptors, 3) vagal afferents, 4) vagal efferents to the heart, 5) sympathetic efferents to peripheral blood vessels, and 6) interaction with other reflexes. Vagal cardiac c fibers are activated by intracoronary injections of PGI2 or arachidonic acid, resulting in a vagal reflex bradycardia and hypotension due to withdrawal of peripheral alpha-adrenergic tone to resistance vessels. The cardiac receptors are located predominantly in the inferoposterior wall of the left ventricle. When stimulated by PGs, cardiac receptors may also modify the regulation of arterial pressure by the baroreflexes, altering the inverse relationship between systemic arterial pressure and heart rate. Thus, there is a striking parallelism between the veratridine-induced Bezold-Jarisch reflex and PG-induced cardiac reflexes, although the physiological and clinical significance of these reflexes remains to be determined.     

Cardiovascular Vagosympathetic Activity in Rats with Ventromedial Hypothalamic Obesity

Objective: Rats with ventromedial hypothalamic lesion (VMH) are massively obese with endogenous hyperinsulinemia, insulin resistance, low sympathetic activity, and high parasympathetic activity, which are likely to induce hypertension. The goal was to follow in this model the long‐term hemodynamic changes and to investigate the role of autonomic nervous system and insulin resistance in these changes. Research Metho ds and Procedures: Heart rate and blood pressure were monitored for 12 weeks after operation using a telemetric system in VMH and sham rats. Plasma catecholamines and heart β‐adrenoceptors were measured. Glucose tolerance was studied after an intravenous glucose injection and insulin sensitivity during a euglycemic hyperinsulinemic clamp test. Results: A marked bradycardia and only a mild increase in blood pressure occurred in VMH rats compared with sham animals. Response to autonomic‐acting drugs showed an increase in heart vagal tone and responsiveness to a β‐agonist drug. Plasma catecholamine levels were markedly increased, and the density and affinity of heart β‐adrenoceptors were similar in VMH, sham, and control rats. Muscle glucose use was reduced by 1 week after operation in VMH animals. Discussion: These results show the following in this model of massively obese rats with sympathetic impairment: 1) adrenal medulla secretion is increased, probably as a result of hyperinsulinemia and increased vagal activity; 2) cardiac responsiveness to β‐agonist stimulation is increased; and 3) despite these changes and suspected resistance to the vasodilative effect of insulin, blood pressure does not increase. We conclude that high vagal activity may be protective against hypertension associated with obesity.     

Cardiovascular reflex-reactions on the blood volume changes before and after pharmacological elimination of the efferent heart innervation]

Reflex changes in the heart frequency, blood pressure and respiratory frequency induced by slow changes of the blood volume are observed in the aesthetized European hamster (Cricetus cricetus L.). Tachycardia, hypertension and hyperpnoe occured during intravenous infusion and bradycardia, hypotension and respiratory inhibition during hemorrhages or local distensions of the junction between the superior vena cava and the right atrium. Various receptor organs of the heart and the great vessels and sympathetic as well as parasympathetic effector mechanisms were involved in the reflex effects. An activation of efferent vagal fibers decreased blood pressure and heart frequency; an excitation of efferent sympathetic fibers increased blood pressure and heart frequency.     

Autonomic control in rats with overactivity of tissue renin-angiotensin or kallikrein-kinin system

The renin-angiotensin system (RAS) plays an important role in the regulation of the cardiovascular system and the kallikrein-kinin system (KKS) appears to counteract most of the RAS effects. In this study the vagal and the sympathetic influences on the heart rate and the baroreflex control of the heart rate were evaluated in transgenics rats with human tissue kallikrein gene expression [TGR(hKLK1)], and transgenics rats with tissue renin overexpression [TGR(mREN2)27]. Heart rate was similar in all groups but mean arterial pressure was higher in mREN2 rats than in kallikrein and control rats (149+/-4 vs. 114+/-3 vs. 113+/-3 mm Hg, respectively). The intrinsic heart rate was lower in mREN2 rats than in kallikrein and control rats (324+/-5 vs. 331+/-3 vs. 343+/-7 bpm). The HR response to atropine was similar but the response to propranolol was higher in kallikrein rats than control group (61+/-7 vs. 60+/-9 vs. 38+/-7 bpm, respectively). The vagal tonus was lower in mREN2 than in SD and hKAL rats (18+/-3 vs. 40+/-6 vs. 35+/-6 bpm) whereas the sympathetic tonus was higher in kallikrein rats (118+/-7 vs. 96+/-1 vs. 81+/-9 bpm in the mREN2 and SD rats), respectively. Baroreflex sensitivity to bradycardic responses was attenuated in mREN2 rats (0.37+/-0.05 vs. 1.34+/-0.08 vs. 1.34+/-0,13 bpm/mm Hg) while the tachycardic responses were unchanged. The bradycardic responses to electrical stimulation of the vagal nerve were depressed in both renin and kallikrein rats (129+/-47 vs. 129+/-22 vs. 193+/-25 bpm in control group in response to 32 Hz). In conclusion: 1.The rats with overexpression of renin showed decreased intrinsic heart rate and impairment of vagal function, characterized by decreased vagal tonus, reduced response of HR to electrical stimulation of vagus nerve, and depressed reflex bradycardia provoked by increases of blood pressure. 2. The rats with overexpression of kallikrein showed an increase of sympathetic activity that regulates the heart rate, characterized by increased HR response to propranolol and increased sympathetic tonus, accompanied by decreased bradycardic responses to electrical vagal stimulation.     

Atrial natriuretic factor alters autonomic interactions in the control of heart rate in conscious rats

Regulation of heart rate was studied in rats receiving either i.v. saline at 64 microL/min or synthetic 28-residue rat atrial natriuretic peptide (ANF) at a dose sufficient to decrease mean arterial blood pressure by 10%. Autonomic influences were deduced from steady-state heart rate responses of each group to propranolol, atropine, or propranolol and atropine combined. A multiplicative model of heart rate control was used to derive quantitatively from the data the modulation of intrinsic heart rate by sympathetic and parasympathetic mechanisms. Animals receiving ANF showed a lower heart rate than control animals. This relative bradycardia was abolished by atropine. Blocking of sympathetic effects with propranolol had no effect on basal heart rate in either group, and atropinization led to significant increases in heart rate in both groups of rats. Mathematical analysis of the results showed that the bradycardia produced by ANF was due predominantly to a reduced intrinsic heart rate and to enhanced vagal inhibition of postganglionic sympathetic activity. Parasympathetic contribution to heart rate in the absence of sympathetic activity was negligible in control rats and small during ANF. We conclude that the major influences of ANF on heart rate control are a decrease of intrinsic heart rate and enhanced parasympathetic inhibition of postganglionic presynaptic sympathetic activity.     

Intracerebroventricular injection of hemicholinium-3 lowers blood pressure in conscious spontaneously hypertensive rats but not in normotensive rats

Intracerebroventricular (icv) injection of hemicholinium-3 (HC-3) in doses of 10–20 μg causes a dose-related decrease in the blood pressure of conscious spontaneous hypertensive (SH) rats but not of normotensive rats. HC-3 also reduces heart rate (HR) in both SH and normotensive rats. The bradycardia was blocked by intravenous injection of methylatropine, implicating increased vagal activity as a cause of the response. The decrease in HR also was blocked by icv injection of atropine but not by icv injection of mecamylamine, suggesting that the bradycardia is mediated via central muscarinic receptors. In contrast, the fall in blood pressure in SH rats was not influenced by intravenous administration of methylatropine or by the icv injection of either atropine or mecamylamine.     

Differential baroreflex control of sympathetic drive by angiotensin II in the nucleus tractus solitarii

Microinjection of angiotensin II into the nucleus tractus solitarii attenuates the baroreceptor reflex-mediated bradycardia by inhibiting both vagal and cardiac sympathetic components. However, it is not known whether the baroreflex modulation of other sympathetic outputs (i.e., noncardiac) also are inhibited by exogenous angiotensin II (ANG II) in nucleus tractus solitarii (NTS). In this study, we determined whether there was a difference in the baroreflex sensitivity of sympathetic outflows at the thoracic and lumbar levels of the sympathetic chain following exogenous delivery of ANG II into the NTS. Experiments were performed in two types of in situ arterially perfused decerebrate rat preparations. Sympathetic nerve activity was recorded from the inferior cardiac nerve, the midthoracic sympathetic chain, or the lower thoracic-lumbar sympathetic chain. Increases in perfusion pressure produced a reflex bradycardia and sympathoinhibition. Microinjection of ANG II (500 fmol) into the NTS attenuated the reflex bradycardia (57% attenuation, P < 0.01) and sympathoinhibition of both the inferior cardiac nerve (26% attenuation, P < 0.05) and midthoracic sympathetic chain (37% attenuation, P < 0.05) but not the lower thoracic-lumbar chain (P = 0.56). We conclude that ANG II in the nucleus tractus solitarii selectively inhibits baroreflex responses in specific sympathetic outflows, possibly dependent on the target organ innervated.     

Leucine-enkephalin interrupts sympathetically mediated tachycardia prejunctionally in the canine sinoatrial node

This study examined the role of leucine-enkephalin (LE) in the sympathetic regulation of the cardiac pacemaker. LE was administered by microdialysis into the interstitium of the canine sinoatrial node during either sympathetic nerve stimulation or norepinephrine infusion. In study one, the right cardiac sympathetic nerves were isolated as they exit the stellate ganglion and were stimulated to produce graded (low, 20-30 bpm; high 40-50 bpm) increases in heart rate (HR). LE (1.5 nmoles/min) was added to the dialysis inflow and the sympathetic stimulations were repeated after 5 and 20 min of LE infusion. After 5 min, LE reduced the tachycardia during sympathetic stimulation at both low (18.2 +/- 1.3 bpm to 11.4 +/- 1.4 bpm) and high (45 +/- 1.5 bpm to 22.8 +/- 1.5 bpm) frequency stimulations. The inhibition was maintained during 20 min of continuous LE exposure with no evidence of opioid desensitization. The delta-opioid antagonist, naltrindole (1.1 nmoles/min), restored only 30% of the sympathetic tachycardia. Nodal delta-receptors are vagolytic and vagal stimulations were included in the protocol as positive controls. LE reduced vagal bradycardia by 50% and naltrindole completely restored the vagal bradycardia. In Study 2, additional opioid antagonists were used to determine if alternative opioid receptors might be implicated in the sympatholytic response. Increasing doses of the kappa-antagonist, norbinaltorphimine (norBNI), were combined with LE during sympathetic stimulation. NorBNI completely restored the sympathetic tachycardia with an ED50 of 0.01 nmoles/min. A single dose of the micro -antagonist, CTAP (1.0 nmoles/min), failed to alter the sympatholytic effect of LE. Study 3 was conducted to determine if the sympatholytic effect was prejunctional or postjunctional in character. Norepinephrine was added to the dialysis inflow at a rate (30-45 pmoles/min) sufficient to produce intermediate increases (35.2 +/- 1.8 bpm) in HR. LE was then combined with norepinephrine and responses were recorded at 5-min intervals for 20 min. The tachycardia mediated by added norepinephrine was unaltered by LE or LE plus naltrindole. At the same 5-min intervals, LE reduced vagal bradycardia by more than 50%. This vagolytic effect was again completely reversed by naltrindole. Collectively, these observations support the hypothesis that the local nodal sympatholytic effect of LE was mediated by kappa-opioid receptors that reduced the effective interstitial concentration of norepinephrine and not the result of a postjunctional interaction between LE and norepinephrine.     

Role of cardiac nerves in determination and modulation of blood pressure oscillation pattern

Effects of autonomic innervation of the heart for blood pressure oscillation (BPO) caused by a side pressure exertion procedure in rabbits were studied by intravenous administrations of atropine or beta-blockers (metoprolol and propranolol). When relatively large doses of these drugs were injected the oscillation disappeared. Atropine injection caused three types of effects on BPO: mostly abolition, diminution and sometimes augmentation. In the diminished cases, the oscillation waves were subjected to a successive decrease in the height and the gradient of ascending limbs. And the extent of bradycardia on the descending limb was less than that of the control. In the augmented cases which accounted for one fifth of all the results, the injection enhanced the BPO in wave height and gradient. Meanwhile, the administration of beta-blockers resulted in disappearance or a decrease in wave height and gradient of the ascending limbs of waves. From these, it is suggested that cardiac sympathetic and vagal discharges accelerate blood pressure rise of the ascending limb, and vagal discharges contribute to active descent of each wave. It is suggested that the BPO is influenced not only by the periodic change of the total peripheral resistance but also by the concomitant changes in tones of cardiac nerves.     

The human heart rate response profiles to five vagal maneuvers

Healthy teens and adults performed four vagotonic maneuvers. A large series of strabismus surgery patients had deliberately quantified tension on extraocular rectus muscles during general anesthesia. The mean bradycardia was greatest for diving response (apneic facial exposure to cold) and Valsalva maneuver and least for pressure on the globe and carotid sinus massage. Bradycardia occurred for every subject for the non-surgical maneuvers, however, extraocular muscle tension frequently caused no change in heart rate or even tachycardia. The inter-subject variance in percent heart rate change was greatest for surgical oculocardiac reflex. Of the rectus muscles, the inferior caused the most bradycardia while the lateral caused the least. The percent oculocardiac reflex was not age dependent. Occasional patients demonstrated profound bradycardia with strabismus surgery. Of these maneuvers, diving response has theoretical advantage in treating paroxysmal atrial tachycardia. The human cardiac vagal efferent was stimulated by several carefully controlled maneuvers resulting in wide inter-maneuver differences in bradycardia magnitude. The greatest intra-maneuver variability occurred with surgical oculocardiac reflex.     

Phenotypical evidence for a gender difference in cardiac norepinephrine transporter function

Norepinephrine transporter (NET) function has a central role in the regulation of synaptic norepinephrine concentrations. Clinical observations in orthostatic intolerance patients suggest a gender difference in NET function. We compared the cardiovascular response to selective NET inhibition with reboxetine between 12 healthy men and 12 age-matched women. Finger blood pressure, brachial blood pressure, and heart rate were measured. The subjects underwent cardiovascular autonomic reflex testing and a graded head-up tilt test. In a separate study, we applied incremental concentrations of tyramine and isoproterenol through subcutaneous microdialysis catheters in eight men and in eight women. NET inhibition elicited a threefold greater increase in supine blood pressure in men than women (P < 0.05). The pressor response was driven by an increased cardiac output. The orthostatic heart rate increase during NET inhibition was greater in men than women (56 +/- 5 beats/min in men, 42 +/- 4 beats/min in women, P < 0.001). In contrast, NET inhibition resulted in a similar suppression in the cold pressor and handgrip response, low-frequency blood pressure oscillations, and venous norepinephrine in the supine position. Men and women were similarly sensitive to the lipolytic effect of isoproterenol and tyramine. We conclude that NET inhibition results in more pronounced changes in cardiac regulation in men than women. Our observations suggest that the NET contribution to cardiac norepinephrine turnover may be decreased in women. The gender difference in NET function may not be expressed in tissues that are less NET dependent than the heart.     

Does heart rate differentiate neurotic from normal people in a conditional reflex test?

This study is to compare heart reactivity between normals and anxiety neurotic patients. Five male and five female patients with anxiety neurosis and four male and five female normal persons were submitted to classic delayed conditional reflexes with different probabilities of reinforcement (shock), to a defensive instrumental conditional reflex, and to a neutral nonreinforced stimulus. The basal heart frequency was higher in neurotics and in women than in normals and men. The conditional stimulus (CS) associated with a shock generally produced a bradycardia in normal individuals and in neurotic men, but a tachycardia in neurotic women (effects most pronounced in cases with 100% shock probability). The instrumental CS caused a tachycardia in all of the groups, with highest values in neurotic women. The neutral stimulus produced bradycardia in all persons. The aftereffect of the light stimulus depended on whether a shock was administered and on the CS. The differences between neurotics and normals are explained as caused by the heightened excitatory level of the CNS of the neurotic group, produced by the unspecific activating effect of chronic anxiety, and differences of plastic processes in both groups, resulting in different effects of phasic anxiety on the heart. Complex inhibitory-excitatory interactions of the sympathetic and the vagal system underlying the heart rate changes may be assumed. Possible mechanisms leading to sex differences are discussed.     

Serum DBH in three forms of acute stress

We examined the changes in serum dopamine-β-hydroxylase (DBH) activity in men subjected to three forms of acute stress: cold pressor, sustained hand grip, and insulin-induced hypoglycemia. The responses to all three of these stresses are reported to be mediated by the sympathetic nervous system. In spite of striking increases in blood pressure induced by the cold pressor and sustained hand grip tests and the clinical and chemical evidence of hypoglycemia following insulin there was little alteration in serum DBH activity. A change in serum DBH level is not a good measure of acute alterations in sympathetic nervous system activity in men.     

Association of sex and age with responses to lower-body negative pressure

Responses of 21 women and 29 men (29-56 yr of age) to -50 Torr lower body negative pressure (LBNP) were examined for differences due to sex or age. Responses to LBNP were normal, including fluid shift from thorax to lower body, increased heart rate and peripheral resistance, and decreased stroke volume, cardiac output, and Heather index of ventricular function. Mean arterial blood pressure did not change. Comparison of responses of the women to responses of an age-matched subset of the men (n = 26) indicated the men had larger relative increases in calf circumference and greater increases in peripheral resistance during LBNP than the women, whereas the women experienced greater increases in thoracic impedance and heart rate. Analyses of responses of the 29 men for age-related differences indicated older subjects had greater increases in peripheral resistance and less heart rate elevation in response to LBNP (P less than 0.05 for all differences, except sex-related heart rate difference, where P less than 0.10). Based on these data and the data of other investigators, we hypothesize the age-related circulatory differences in response to LBNP are due to a reduction in vagal response and a switch to predominant sympathetic nervous system influence in older men. We cannot exclude the possibility that diminished responsiveness in the afferent arm of the baroreceptor reflex also plays a role in the attenuated heart rate response of older men to LBNP.     

Role of the autonomic nervous system in the development of cardiovascular changes during nasal apnoea and lung inflation.

The role of the sympathetic system in the development of bradycardia during nasal apnoea and the role of the sympathetic and parasympathetic system in the development of cardiovascular changes during and immediately after lung inflation were determined in anaesthetized rabbits. Transection of the cervical cord (C5-7) completely blocked the hypertensive response to chemical stimulation of the nasal mucosa. The degree of nasal bradycardia was 72% lower than in stimulation of the controls. Propranolol had no effect on the hypertensive reaction, but inhibited nasal bradycardia, which was 68% lower than in the controls. Lung inflation induced tachycardia, which was only non-significantly reduced by bilateral vagotomy. Vagotomy inhibited the bradycardiac response to removal of occlusion of the trachea and the subsequent rise in blood pressure, however. Cervical cord transection likewise did not reduce inflation-induced tachycardia, but it significantly influenced the heart rate during the second phase of prolonged inflation, when the heart is affected by hypoxia. Inflation-induced tachycardia was likewise not influenced by bilateral vagotomy associated with cervical cord transection. Similar cardiac responses also occur in the presence of the simple increase in pericardial pressure produced by left pneumothorax without lung inflation.