scholarly journals Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. I. Cardiovascular responses and blood gases

1985 ◽  
Vol 114 (1) ◽  
pp. 415-426
Author(s):  
G. M. Barnas ◽  
M. Gleeson ◽  
W. Rautenberg
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Treadmill Exercise ◽  
Venous Blood ◽  
Blood Gases ◽  
Cardiovascular Responses ◽  
Mixed Venous Blood ◽  
Ambient Temperatures ◽  
Arterial Blood ◽  
Exercise Period

We measured oxygen consumption (VO2), heart rate (HR), stroke volume (SV), cardiac output (CO) and mean arterial blood pressure (MBPa) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. PO2, PCO2, pH and oxygen content (CO2) of the arterial and mixed venous blood were also measured. VO2 during exercise was not significantly affected by Ta. Spinal cord cooling produced definite increases in VO2, CO and SV during 0.5 ms-1 exercise at 9 degrees C; otherwise, effects of spinal cord cooling were not significant. HR, SV and CO were all linearly related to VO2; these relationships were unaffected by spinal cord cooling or Ta. Blood pressure did not increase during exercise. PaCO2 and P-vCO2 did not increase significantly during exercise. The arterial-venous CO2 difference was increased by exercise only at 34 degrees C. The chickens generally hyperventilated at 34 degrees C Ta compared to the other Ta values. No consistent effect on blood gases or on pH and CO2 of the blood could be attributed to spinal cord cooling.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Changes in blood gases and acid-base balance in the exercising dog

1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie
Keyword(s):  
Venous Blood ◽  
Blood Gases ◽  
Respiratory Alkalosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Mixed Venous Blood ◽  
Acid Base Balance ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood ◽  
Mixed Venous

Effects of varying rates of treadmill work on blood gases and hydrogen ion concentrations of four healthy young dogs were determined by analyses of blood for O2 and CO2 contents, Po2, Pco2, and pH. Changes in these parameters were also observed during 30-min recovery periods from hard work. Arterial and mixed venous blood samples were obtained simultaneously during work through a polyethylene catheter in the right ventricle and an indwelling needle in an exteriorized carotid artery. Mixed venous O2 content, Po2 and O2 saturation fell with increased work, whereas arterial values showed little or no change. Mixed venous CO2 content, Pco2, and hydrogen ion concentration exhibited little change from resting levels in two dogs but increased significantly in two others during exercise. These values always decreased in the arterial blood during exercise, indicating the presence of respiratory alkalosis. On cessation of exercise, hyperventilation increased the degree of respiratory alkalosis, causing it to be reflected on the venous side of the circulation. Submitted on January 8, 1962

A respiratory venous chemoreceptor in the young puppy

1975 ◽  
Vol 38 (5) ◽  
pp. 819-826 ◽  
Author(s):  
K. R. Kollmeyer ◽  
L. I. Kleinman
Keyword(s):  
Minute Ventilation ◽  
Venous Blood ◽  
Blood Gases ◽  
High Ratio ◽  
Mixed Venous Blood ◽  
Extracorporeal Circuit ◽  
Shunt System ◽  
Newborn Animal ◽  
Venous Circulation ◽  
Arterial Blood

An extracorporeal venovenous shunt system utilizing a membrane oxygenator to alter venous blood gases was used to study the regulation of ventilation in 28 newborn and 4 adult dogs. There was no effect of the extracorporeal circuit per se (without the oxygenator in the system) on essential cardiovascular or respiratory function. When the puppies were placed on the extracorporeal circuit with the oxygenator in the system to effect changes in mixed venous blood gas composition there was a significant increase in venous P02 (Pv02), a decrease in venous Pco2 (Pvco2), a rise in venous pH (PHv), and a marked fall in minute ventilation (VE). There were no significant changes in cardiovascular function or arterial blood gases to account for the depression of ventilation. Acute changes in Pvo2 produced appropriate directional changes of VE under conditions where other arterial and venous blood gases were held constant. At a low Pvco2/Paco2 ratio, ventilation was depressed compared to those conditions with a high ratio. At any Pvc02/Paco2 ratio, ventilation could be depressed by raising the Pvo2. In adult animals ventilation could not be altered by changing venous blood gases. These experiments support the existence of a respiratory chemoreceptor sensitive to both PO2 and PCO2 in the prepulmonary or venous circulation of the newborn animal.

Respiratory and cardiovascular adjustments during exercise of increasing intensity and during recovery in thoroughbred racehorses

1993 ◽  
Vol 179 (1) ◽  
pp. 159-180 ◽  
Author(s):  
P. J. Butler ◽  
A. J. Woakes ◽  
K. Smale ◽  
C. A. Roberts ◽  
C. J. Hillidge ◽  
...  
Keyword(s):  
Dead Space ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Haemoglobin Concentration ◽  
Blood Gases ◽  
Stride Frequency ◽  
Mixed Venous Blood ◽  
Systematic Effect ◽  
Arterial Blood ◽  
Thoroughbred Racehorses

A new design of flowmeter is described and used in a comprehensive study of the respiratory and cardiovascular adjustments that occur during a standardised exercise test in Thoroughbred horses. The flowmeter system and associated lightweight, fibreglass mask (total mass, 0.7 kg) have a maximum dead space of 500 ml and negligible resistance to airflow. They have no systematic effect on blood gases and, together with a rapidly responding mass spectrometer, enable an accurate computation of gas exchange to be performed together with breath-by-breath determination of other respiratory variables. At the highest level of exercise (12 ms-1 on a 3 degrees incline), the rate of oxygen uptake (VO2) and carbon dioxide production (VCO2) increased to 29.4 times and 36.8 times their resting values, respectively. Respiratory minute volume (VE) increased to 27.0 times its resting value, with respiratory frequency (fR) making the major contribution at the walk and trot. However, with increasing cantering speeds, fR changed little as it was locked in a 1:1 fashion to stride frequency, and tidal volume (VT) then made the major contribution to the increase in VE. The ratio of ventilatory dead space (VD) to VT in resting horses was lower than that previously reported in the literature and this could be the result of the different respiratory recording systems that were used. There was a close relationship between VT and stride length at increasing cantering speeds. Despite the fact that alveolar ventilation (VA) was well matched to VO2, there was a significant reduction in arterial PO2 (PaO2) when the horses cantered at 8 ms-1 and this eventually fell to 34% below the resting value. The present data tend to support the idea that VA/Vb (where Vb is cardiac output) inequalities are important in causing this hypoxaemia. However, the reduction in PaO2 was more than compensated for by an increase in haemoglobin concentration, [Hb], so the concentration of oxygen in the arterial blood (CaO2) was significantly above the resting value at all levels of exercise. Both lactate concentration and PaCO2 increased during exercise, causing substantial reductions in pH of both arterial and mixed venous blood. This would have inevitably shifted the oxygen equilibrium curve of the Hb to the right, desaturating the arterial blood and thus exacerbating the effect of the hypoxaemia, as would the almost 4 degrees C rise in blood temperature. The tight respiratory/locomotor linkage might prevent the acidosis and hyperthermia having the stimulatory effects on VE that they have in humans at high work loads.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Blood pressure and blood flow variation during postural change from sitting to standing: model development and validation

2005 ◽  
Vol 99 (4) ◽  
pp. 1523-1537 ◽  
Author(s):  
Mette S. Olufsen ◽  
Johnny T. Ottesen ◽  
Hien T. Tran ◽  
Laura M. Ellwein ◽  
Lewis A. Lipsitz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Flow ◽  
Young Subject ◽  
Venous Blood ◽  
Cardiovascular Responses ◽  
Physiological Data ◽  
Postural Change ◽  
Metabolic Demand ◽  
Arterial Blood

Short-term cardiovascular responses to postural change from sitting to standing involve complex interactions between the autonomic nervous system, which regulates blood pressure, and cerebral autoregulation, which maintains cerebral perfusion. We present a mathematical model that can predict dynamic changes in beat-to-beat arterial blood pressure and middle cerebral artery blood flow velocity during postural change from sitting to standing. Our cardiovascular model utilizes 11 compartments to describe blood pressure, blood flow, compliance, and resistance in the heart and systemic circulation. To include dynamics due to the pulsatile nature of blood pressure and blood flow, resistances in the large systemic arteries are modeled using nonlinear functions of pressure. A physiologically based submodel is used to describe effects of gravity on venous blood pooling during postural change. Two types of control mechanisms are included: 1) autonomic regulation mediated by sympathetic and parasympathetic responses, which affect heart rate, cardiac contractility, resistance, and compliance, and 2) autoregulation mediated by responses to local changes in myogenic tone, metabolic demand, and CO2 concentration, which affect cerebrovascular resistance. Finally, we formulate an inverse least-squares problem to estimate parameters and demonstrate that our mathematical model is in agreement with physiological data from a young subject during postural change from sitting to standing.

Cardiovascular responses to bladder distension in patients with spinal transection

1975 ◽  
Vol 228 (4) ◽  
pp. 1288-1292 ◽  
Author(s):  
RD Wurster ◽  
WC Randall
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Bladder Pressure ◽  
Bladder Distension ◽  
Arterial Blood

Arterial blood pressure, heart rate, and cutaneous volume pulses were recorded during controlled elevation of urinary bladder pressure in a group of seven patients with spinal cord transsection above vertebral level T5 and in another group of four patients below T5. Profound elevations in systolic blood pressure and pulse pressure were induced by bladder distension when the lesion was situated above T5. Lesser elevations occurred in patients with lesions below T5. Marked vasoconstriction characterized skin areas innervated by the "isolated" spinal cord, while passive dilatation occurred in areas supplied by the proximal cord. Only three of seven patients with lesions above T5 level had decreased heart rate during marked elevations in arterial blood pressure. The marked elevations in pulse pressure in patients with lesions above T5 could not be explained solelyby increased vasoconstriction and decreased heart rate, but involves also inotropic cardiac responses. These inotropic responses are mediated by cardiac sympathetic nerves which leave the spinal cord above the T5 level.

scholarly journals Direct comparison of cervical and high thoracic spinal cord injury reveals distinct autonomic and cardiovascular consequences

2020 ◽  
Vol 128 (3) ◽  
pp. 554-564
Author(s):  
Heidi L. Lujan ◽  
Stephen E. DiCarlo
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Peak Level ◽  
Cardiovascular Responses ◽  
Spinal Cord Transection ◽  
Thoracic Spinal Cord ◽  
Hormonal Responses ◽  
Arterial Blood ◽  
Stellate Ganglia ◽  
Thoracic Spinal

A wide range of spinal cord levels (cervical 8–thoracic 6) project to the stellate ganglia (which provides >90% of sympathetic supply to the heart), with a peak at the thoracic 2 (T2) level. We hypothesize that despite the proximity of the lesions, high thoracic spinal cord injuries (i.e., T2–3 SCI) do not closely mimic the hemodynamic responses recorded with cervical SCI (i.e., C6–7 SCI). To test this hypothesis, rats were instrumented with an intra-arterial telemetry device (Data Sciences International PA-C40) for recording arterial pressure, heart rate, and locomotor activity as well as a catheter within the intraperitoneal space. After recovery, rats were subjected to complete C6–7 spinal cord transection ( n = 8), sham transection ( n = 4), or T2–3 spinal cord transection ( n = 7). After the spinal cord transection or sham transection, arterial pressure, heart rate, and activity counts were recorded in conscious animals, in a thermoneutral environment, for 20 s every minute, 24 h/day for 12 consecutive weeks. After 12 wk, chronic reflex- and stress-induced cardiovascular and hormonal responses were compared in all groups. C6–7 rats had hypotension, bradycardia, and reduced physical activity. In contrast, T2–3 rats were tachycardic. C6–7 rats compared with T2–3 and spinal intact rats also had reduced cardiac sympathetic tonus, reduced reflex- and stress induced cardiovascular responses, and reduced sympathetic support of blood pressure as well as enhanced reliance on angiotensin to maintain arterial blood pressure. Thus injuries above and below the peak level (T2) of spinal cord projections to the stellate ganglia have remarkably different outcomes. NEW & NOTEWORTHY Twelve consecutive weeks of resting hemodynamic data as well as chronic reflex- and stress-induced cardiovascular, autonomic, and hormonal responses were compared in spinal intact and C6–7 and T2–3 spinal cord-transected rats. C6–7 rats compared with T2–3 and spinal intact rats had reduced cardiac sympathetic tonus, reduced reflex- and stress-induced cardiovascular responses, and reduced sympathetic support of blood pressure as well as enhanced reliance on angiotensin to maintain arterial blood pressure. Thus injuries above and below the peak level (T2) of spinal cord projections to the stellate ganglia have remarkably different outcomes.

Carbon Dioxide Equilibration in Canine Lungs during Rebreathing and Acute Alkalosis

1979 ◽  
Vol 57 (5) ◽  
pp. 385-388 ◽  
Author(s):  
R. D. Latimer ◽  
G. Laszlo
Keyword(s):  
Whole Blood ◽  
Base Excess ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Significant Difference ◽  
Venous Pco2 ◽  
Pulmonary Arterial ◽  
Gas Pressures

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

Sign in / Sign up

Export Citation Format

Share Document