Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial PaO2 = 38 mmHg), hypercapnia (PaCO2 = 72 mmHg), or hypoxic hypercapnia (PaO2 = 41; PaCO2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.     

Hemodynamic effects of blood loss during a passive response to a stressor in the conscious rabbit

In the conscious rabbit, exposure to an air jet stressor increases arterial pressure, heart rate, and cardiac output. During hemorrhage, air jet exposure extends the blood loss necessary to produce hypotension. It is possible that this enhanced defense of arterial pressure is a general characteristic of stressors. However, some stressors such as oscillation (OSC), although they increase arterial pressure, do not change heart rate or cardiac output. The cardiovascular changes during OSC resemble those seen during freezing behavior. In the present study, our hypothesis was that, unlike air jet, OSC would not affect defense of arterial blood pressure during blood loss. Male New Zealand White rabbits were chronically prepared with arterial and venous catheters and Doppler flow probes. We removed venous blood until mean arterial pressure decreased to 40 mmHg. We repeated the experiment in each rabbit on separate days in the presence and absence (SHAM) of OSC. Compared with SHAM, OSC increased arterial pressure 14 +/- 1 mmHg, central venous pressure 3.3 +/- 0.4 mmHg, and hindquarter blood flow 34 +/- 4% while decreasing mesenteric conductance 32 +/- 3% and not changing heart rate or cardiac output. During normotensive hemorrhage, OSC enhanced hindquarter and renal vasoconstriction. Contrary to our hypothesis, OSC (23.5 +/- 0.6 ml/kg) increased the blood loss necessary to produce hypotension compared with SHAM (16.8 +/- 0.6 ml/kg). In nine rabbits, OSC prevented hypotension even after a blood loss of 27 ml/kg. Thus a stressful stimulus that resulted in cardiovascular changes similar to those seen during freezing behavior enhanced defense of arterial pressure during hemorrhage.     

A method for calculation of human systolic and diastolic blood pressures using an elastic reservoir theory of the systemic arterial system,and some clinical and physiological applications

Two equations have been developed that describe the interrelationship of the clinically measurable variables of the human systemic arterial system. An approximation method is given for their simultaneous solution for systolic and diastolic pressures in terms of heart rate, cardiac output, total peripheral resistance, and aortic distensibility. In this way, blood pressures were calculated for various clinically important and didactically useful situations. The effects on systolic and diastolic pressures due to changing either cardiac output or peripheral resistance or heart rate or aortic distensibility alone are shown. The effects on pulse pressure of varying cardiac output and peripheral resistance while holding mean arterial pressure constant are demonstrated. Compensatory mechanisms in hypertension and exercise are explored. Opinions and conclusions contained in this report are those of the author. They are not to be construed as necessarily reflecting the views or the endorsement of the Navy Department.     

Myogenic origin of the hypotension induced by rapid changes in posture in awake dogs following autonomic blockade

The "push-pull" effect denotes the reduced tolerance to +G(z) (hypergravity) when +G(z) stress is preceded by exposure to hypogravity, i.e., fractional, zero, or negative G(z). The purpose of this study was to test the hypothesis that an exaggerated, myogenically mediated rise in leg vascular conductance contributes to the push-pull effect, using heart level arterial blood pressure as a measure of G tolerance. The approach was to impose control (30 s of 30 degrees head-up tilt) and push-pull (30 s of 30 degrees head-up tilt immediately preceded by 10 s of -15 degrees head-down tilt) gravitational stress after administration of hexamethonium (5 mg/kg) to inhibit autonomic ganglionic neurotransmission in seven dogs. Cardiac output or thigh level arterial pressure (myogenic stimulus) was maintained constant by computer-controlled ventricular pacing. The animals were sedated with acepromazine and lightly restrained in lateral recumbency on a tilt table. Following the onset of head-up tilt, the magnitude of the fall in heart level arterial pressure from baseline was -11.6 +/- 2.9 and -17.1 +/- 2.2 mmHg for the control and push-pull trials, respectively (P < 0.05), when cardiac output was maintained constant. Over 40% of the exaggerated fall in heart level arterial pressure was attributable to an exaggerated rise in hindlimb vascular conductance (P < 0.05). Maintaining thigh level arterial pressure constant abolished the exaggerated rise in hindlimb blood flow. Thus a push-pull effect largely attributable to a myogenically induced rise in leg vascular conductance occurs when autonomic function is inhibited.     

A computer-assisted noninvasive monitoring system with graphic display of online determination of cardiovascular parameters

During anesthesia the cardiovascular system is usually assessed on the basis of heart rate and arterial pressure, although the most important hemodynamic measurement is that of flow. A method for the non-invasive measurement of cardiac output is based on thoracic electrical bio-impedance. The NCCOM3-R7 is a non-invasive cardiac output monitor that makes use of thoracic electrical bioimpedance, which has been shown to provide results comparable with thermodilution in various hemodynamic states both in animals and humans. A new on-line hemodynamic monitoring system has been developed using the non-invasive NCCOM3-R7 (BoMed) cardiac output monitor, a portable microcomputer (NEC Multispeed) in connection with a software package CDDP-1 (BoMed), a Dinamap automatic arterial pressure monitor (Critikon) and an additional 14" display. Every 16 heart beats the cardiac output monitor transfers 11 cardiodynamic parameters in ASCII-format to the microcomputer, where the data are stored. Using the CDDP-1 program the current cardiodynamic status of the patient is displayed numerically and graphically on the monitor screen. Mean arterial pressure is determined by Dinamap and the data must be entered manually in the menu. The program then calculates systemic vascular resistance and left ventricular work index, the CVP being set to 3 torr and PAOP to 6 torr. In the graphic display the current hemodynamic status is shown and the underlying situation is analyzed in terms of systemic vascular resistance and volume-dependent contractility. The reliability of this on-line monitoring system is demonstrated in a high-risk patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Understanding Guyton's venous return curves

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that "venous recoil" does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.     

Cardiac output during labour.

Serial measurements of cardiac output and mean arterial pressure were performed in 15 women during the first stage of labour and at one and 24 hours after delivery. Cardiac output was measured by Doppler and cross sectional echocardiography at the pulmonary valve. Basal cardiac output (between uterine contractions) increased from a prelabour mean of 6.99 l/min to 7.88 l/min at greater than or equal to 8 cm of cervical dilatation as a result of an increase in stroke volume. Over the same period basal mean arterial pressure also increased. During uterine contractions there was a further increase in cardiac output as a result of increases in both stroke volume and heart rate. The increment in cardiac output during contractions became progressively greater as labour advanced. At greater than or equal to 8 cm of dilatation cardiac output increased from a basal mean of 7.88 l/min to 10.57 l/min during contractions. There were also further increases in mean blood pressure during contractions. One hour after delivery heart rate and cardiac output had returned to prelabour values, though mean arterial pressure and stroke volume remained raised. By 24 hours after delivery all haemodynamic variables had returned to prelabour values. Haemodynamic changes of the magnitude found in this series are of considerable clinical relevance in managing mothers with complicated cardiovascular function.     

Integrative control of the skeletal muscle microcirculation in the maintenance of arterial pressure during exercise.

Skeletal muscle blood flow and vascular conductance are influenced by numerous factors that can be divided into two general categories: central cardiovascular control mechanisms and local vascular control mechanisms. Central cardiovascular control mechanisms are thought to be designed primarily for the maintenance of arterial pressure and central cardiovascular homeostasis, whereas local vascular control mechanisms are thought to be designed primarily for the maintenance of muscle homeostasis. To support the high metabolic rates that can be generated during muscle contraction, skeletal muscle has a tremendous capacity to vasodilate and increase oxygen and nutrient delivery. During whole body dynamic exercise at maximal oxygen consumption (VO2 max), the skeletal muscle receives 85-90% of cardiac output. Yet despite receiving such a large fraction of cardiac output during high-intensity exercise, a vasodilator reserve remains with the potential to produce further elevations in skeletal muscle vascular conductance and blood flow. However, because maximal cardiac output is reached during exercise at VO2 max, further elevations in muscle vascular conductance would produce a fall in arterial pressure. Therefore, limits on muscle perfusion must be imposed during whole body exercise to prevent such drops in pressure. Effective arterial pressure control in response to a potentially hypotensive challenge during high-intensity exercise occurs primarily through reflex-mediated increases in sympathetic nerve activity, which are capable of modulating vasomotor tone of the skeletal muscle resistance vasculature. Thus skeletal muscle vascular conductance and perfusion are primarily mediated by local factors at rest and during exercise, but other centrally mediated control systems are superimposed on the dominant local control mechanisms to provide an integrated regulation of both arterial pressure and skeletal muscle vascular conductance and perfusion during whole body dynamic exercise.     

Measurement of bronchial blood flow with radioactive microspheres in awake sheep

Distribution of bronchial blood flow was measured in unanesthetized sheep by the use of two modifications of the microsphere reference sample technique that correct for peripheral shunting of microspheres: 1) A double microsphere method in which simultaneous left and right atrial injections of 15-microns microspheres tagged with different isotopes allowed measurement of both pulmonary blood flow and shunt-corrected bronchial blood flow, and 2) a pulmonary arterial occlusion method in which left atrial injection and transient occlusion of the left pulmonary artery prevented delivery to the lung of microspheres shunted through the peripheral circulation and allowed systemic blood flow to the left lung to be measured. Both methods can be performed in unanesthetized sheep. The pulmonary arterial occlusion method is less costly and requires fewer calculations. The double microsphere method requires less surgical preparation and allows measurement without perturbation of pulmonary hemodynamics. There was no statistically significant difference between bronchial blood flow measured with the two methods. However, total bronchial blood flow measured during pulmonary arterial occlusion (1.52 +/- 0.98% of cardiac output, n = 9) was slightly higher than that measured with the double microsphere method (1.39 +/- 0.88% of cardiac output, n = 9). In another series of experiments in which sequential measurements of bronchial blood flow were made, there was a significant increase of 15% in left lung bronchial blood flow during the first minute of occlusion of the left pulmonary artery. Thus pulmonary arterial occlusion should be performed 5 s after microsphere injection as originally described by Baile et al. (1).(ABSTRACT TRUNCATED AT 250 WORDS)     

A theoretical evaluation of cardiac output as a function of mean arterial pressure in the human cardiovascular system

A correlation function of cardiac output and mean arterial pressure is presented for the human cardiovasular system. The function is developed using an energy transfer balance for a unit volume of blood which flows in the vascular system between the aorta and the vena cava. The energy transfer balance equates the energy utilized in the vascular system to the algebraic sum of the pulse energy, the kinetic energy and the potential energy in the vascular system. Each of these energies is defined in terms of the physiology of the cardiovascular system. Pulse energy is defined in terms of the work done by the heart on the aorta. Kinetic energy is defined in terms of the cardiac output and the potential energy is defined in terms of the diastolic pressure in the aorta. The utilization energy is equivalent to the energy transfer in the work done by the blood on the viscoelastic blood vessels, and to the frictional energy loss due to drag on the blood mass as it flows through the vascular system.The correlation function of cardiac output with mean arterial pressure demonstrates that the cardiac output is a double-valued function of the mean arterial pressure. The function also varies with the ratio of the fourth power of the Shear Modulus of the blood vessels to the third power of Young's Modulus. The function shows that mean arterial pressure minimizes for a cardiac output of approximately 51 per min when one holds the ratio of the elastic moduli constant. Further discussion indicates how clinicians can use the function, developed in this research, to interpret the experimental data obtained from cardiac output studies.     

Leg vasoconstriction during dynamic exercise with reduced cardiac output.

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasmodium berghei: malaria infection causes increased cardiac output in rats, Rattus rattus

Thirty-two 4-week-old male Wistar rats were infected with Plasmodium berghei malaria. On Days 12 through 14, blood volume, arterial blood pressure, right ventricular pressure, heart rate, cardiac output, stroke volume, hematocrit, and vascular resistances were determined. All of the cardiovascular parameters measured, with the exception of calculated pulmonary vascular resistance, changed progressively as the peripheral blood parasitemia increased. With a rising parasitemia, cardiac output increased, despite a reduced heart rate. The highest parasitemia of 63% was accompanied by a doubling of the normal cardiac output. The relationship between parasitemia and cardiac output can be described by the equation, cardiac output = (6.14) x % parasitemia + 452 ml/min/kg. The mean arterial blood pressure was lower than controls when parasitemia exceeded 20%, whereas systolic right ventricular pressure was elevated only at the highest parasitemias. When noninfected control rats were compared with those animals having parasitemias greater than 40%, in the infected animals, mean arterial pressure was 28% lower (P less than 0.01) and systolic right ventricular pressure rose by 21% (P less than 0.02). A 50% decline was observed in the total peripheral vascular resistance (P less than 0.01), although the pulmonary resistance was apparently unchanged. With P. berghei infection, there is also a marked anemia, an increase in plasma volume, and a 16% increase in blood volume (% body weight). It is concluded from these results that although the hemodynamic changes previously reported in the literature indicate that infection with malaria may result in focal blockages in microvessels and poor tissue perfusion, the total systemic effect, in the rat, is an increase in cardiac output secondary to a reduced peripheral resistance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of neurogenic and humoral stimuli in venous return in cats

Humoral stimuli (i.v. adrenaline) proved to exert a greater effect on venous return in anesthetized cats than neurogenic those (electrical stimulation of either brain stem or femoral nerve). The part of cardiac output, however, in arterial blood shifts was the same. The latter finding is, probably, due to a discrepancy between changes occurring in the venous return and cardiac output caused by blood detention within the lung circulation as well as by an elevation of the blood pressure.     

Influence of vasoactive intestinal polypeptide (VIP) on splanchnic and central hemodynamics in healthy subjects

The influence of VIP, a potent vasodilator, on central hemodynamics, splanchnic blood flow and glucose metabolism was studied in six healthy subjects. Teflon catheters were inserted into an artery, a femoral vein and a right-sided hepatic vein. A Swan-Ganz catheter was introduced percutaneously and its tip placed in the pulmonary artery. Determinations of cardiac output, systemic, pulmonary arterial and hepatic venous pressures as well as splanchnic blood flow were made in the basal state and at the end of two consecutive 45 min periods of VIP infusion at 5 and 10 ng/kg/min, respectively. Arterial blood samples for analysis of glucose, FFA, insulin and glucagon were drawn at timed intervals. VIP infusion at 5 ng/kg/min resulted in an increase in cardiac output (55%) and heart rate (25%) as well as a reduction in mean systemic arterial pressure (15%) and vascular resistance (45%). With the higher rate of VIP infusion heart rate tended to rise further while cardiac output and arterial pressure remained unchanged. At 15 min after the end of VIP infusion the above variables had returned to basal levels. Splanchnic blood flow and free hepatic venous pressure did not change significantly. Arterial concentrations of glucose, FFA, insulin and glucagon increased during VIP infusion. At 15 min after the end of infusion the glucose levels were still significantly higher than basal (20%). Net splanchnic glucose output did not change in response to VIP infusion. It is concluded that VIP exerts a potent vasodilatory effect resulting in augmented cardiac output and lowered systemic blood pressure and vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive measurement of time-varying three-dimensional relative pressure fields within the human heart

Understanding cardiac blood flow patterns is important in the assessment of cardiovascular function. Three-dimensional flow and relative pressure fields within the human left ventricle are demonstrated by combining velocity measurements with computational fluid mechanics methods. The velocity field throughout the left atrium and ventricle of a normal human heart is measured using time-resolved three-dimensional phase-contrast MRI. Subsequently, the time-resolved three-dimensional relative pressure is calculated from this velocity field using the pressure Poisson equation. Noninvasive simultaneous assessment of cardiac pressure and flow phenomena is an important new tool for studying cardiac fluid dynamics.     

Effect of methylene blue on cardiac output response to exercise in dogs

To determine whether the increase in cardiac output during mild to moderate exercise is related to an increase in the tissue redox potential, we compared the responses of cardiac output, total body oxygen consumption, and arterial blood lactate-to-pyruvate ratio (a measure of NADH/NAD) to treadmill exercise between dogs treated with normal saline and those treated with a hydrogen acceptor, new methylene blue. Normal saline was infused into the left atrium in the first group of dogs at a rate of 0.38 ml/min throughout the treadmill exercise (2.5 mph and 5.0 mph on a 6% incline, each for 20 min). In the second group, methylene blue was administered as a loading dose (4 mg/kg) before exercise, followed by a continuous infusion (0.15 mg X kg-1 X min-1) throughout exercise. A similar infusion of methylene blue was given to a third group of dogs without exercise; it reduced the arterial lactate-to-pyruvate ratio from 6.70 +/- 0.35 to 4.12 +/- 0.27 but had no or little effects on cardiac output, heart rate, arterial pressure, and left ventricular dP/dt and (dP/dt)/P. Treadmill exercise doubled cardiac output and increased total body O2 consumption three- to fourfold in the first two groups but increased arterial blood lactate-to-pyruvate ratio only in group 1 (6.0 +/- 0.54 to 9.97 +/- 0.91). The relationship between cardiac output and total body O2 consumption was unaffected by the simultaneous administration of methylene blue during exercise. Groups 1 and 2 also did not differ in their heart rate, left ventricular dP/dt and (dP/dt)/P, and plasma catecholamine responses to exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circulatory and Metabolic Effects of Oxygen in Myocardial Infarction

The circulatory and metabolic effects of inhalation of oxygen in high concentration were investigated in 50 patients with acute myocardial infarction. The heart rate, arterial blood pressure, cardiac out-put, blood gas tensions, pH, and lactate and pyruvate levels were measured. In general, oxygen inhalation produced a fall in cardiac output and stroke volume and a rise in blood pressure and systemic vascular resistance. In a small number of patients with very low cardiac out-puts there was a rise in output. A substantial rise in arterial oxygen tension was obtained even in patients with low initial values. The raised arterial blood lactate levels which were frequently present were reduced after oxygen. The therapeutic implications of these effects are discussed.     

Cardiovascular and neuroendocrine responses to left lateral position in non-obese young males

Previous results from our laboratory indicate that the heart is distended by the left lateral position (LAT) compared to horizontal supine (SUP). We therefore tested the hypothesis that cardiac output is increased by LAT and that mean arterial pressure is maintained unchanged or even decreased through peripheral vasodilatation induced by cardiopulmonary low-pressure receptor stimulation. Twelve non-obese young males were investigated. The location of the mid-aorta between the aortic valves was used as the hydrostatic reference point for the arterial pressure measurements. It was determined by magnetic resonance (n=6) to be 7.0 +/- 0.2 cm below the sternum in SUP (1/3 of anteroposterior chest diameter below the sternum) and 2.5 +/- 0.2 cm below the midsternal level in LAT. Brachial mean (auscultation) and finger mean arterial pressures (infrared photoplethysmography), cardiac output (foreign gas rebreathing), heart rate, and plasma concentrations (n=6) of vasoactive hormones were unchanged by LAT. In conclusion, cardiac output, mean arterial pressures, and vasoactive hormone releases were unaffected by 30 min of LAT. Furthermore, the hydrostatic reference points for arterial pressure measurements is located one third of the antero-posterior chest diameter below the sternum in SUP and 2.5 cm below the midsternal level in LAT in non-obese young males.     

Left ventricular epicardial admittance measurement for detection of acute LV dilation

There are two implanted heart failure warning systems incorporated into biventricular pacemakers/automatic implantable cardiac defibrillators and tested in clinical trials: right heart pressures, and lung conductance measurements. However, both warning systems postdate measures of the earliest indicator of impending heart failure: left ventricular (LV) volume. There are currently no proposed implanted technologies that can perform LV blood volume measurements in humans. We propose to solve this problem by incorporating an admittance measurement system onto currently deployed biventricular and automatic implantable cardiac defibrillator leads. This study will demonstrate that an admittance measurement system can detect LV blood conductance from the epicardial position, despite the current generating and sensing electrodes being in constant motion with the heart, and with dynamic removal of the myocardial component of the returning voltage signal. Specifically, in 11 pigs, it will be demonstrated that 1) a physiological LV blood conductance signal can be derived; 2) LV dilation in response to dose-response intravenous neosynephrine can be detected by blood conductance in a similar fashion to the standard of endocardial crystals when admittance is used, but not when only traditional conductance is used; 3) the physiological impact of acute left anterior descending coronary artery occlusion and resultant LV dilation can be detected by blood conductance, before the anticipated secondary rise in right ventricular systolic pressure; and 4) a pleural effusion simulated by placing saline outside the pericardium does not serve as a source of artifact for blood conductance measurements.     

Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.