Vagal blockade does not prevent adrenocorticotropin, cortisol, and cardiopulmonary responses to thromboxane A2

1998 ◽  
Vol 76 (12) ◽  
pp. 1087-1094 ◽  
Author(s):  
Timothy A Cudd

Previously, we reported that thromboxane A2 (TxA2) mediates heart rate, adrenocorticotropin (ACTH), cortisol, and blood gas responses, although the specific site of action was not identified. In the present study, we interrupted vagal nervous transmission in chronically instrumented conscious sheep and infused the TxA2 mimetic U46619 or saline into the carotid artery or U46619 into the vena cava to determine whether TxA2 acts at vagal afferent nerves. Heart rate increased in all three groups during vagal blockade, and responses were not different between groups. Carotid artery and intravenous infusions of U46619 resulted in an increase in blood pressure, but responses were not different between groups. PaO2 decreased in response to vagal blockade in all groups, and responses were not different among groups. Arterial pH increased and PaCO2 decreased during vagal blockade in response to carotid artery U46619 infusions but not in response to vagal blockade alone or combined with carotid artery saline or intravenous U46619. ACTH, cortisol, and hematocrit increased significantly in response to carotid artery infusions of U46619 during vagal blockade but not in response to carotid artery saline or intravenous U46619 infusions. In summary, carotid artery infusions of TxA2 mimetic result in ACTH, cortisol, PaCO2, pHa, and hematocrit responses that are not prevented by vagal blockade. We conclude that these responses are mediated at a site perfused by the carotid vasculature and not at a site innervated by the vagal nerves, findings consistent with the hypothesis that TxA2 acts on the brain to mediate cardiopulmonary and pituitary-adrenal responses.Key words: thromboxane A2, vagus, U46619, adrenocorticotropin, cortisol, prostaglandins, blood pressure, heart rate.

1960 ◽  
Vol 198 (2) ◽  
pp. 333-335 ◽  
Author(s):  
H. E. D'Amato ◽  
Suzanne Kronheim ◽  
B. G. Covino

Heart rate, blood pressure, cardiac output and cardiac minute work were measured in pentobarbitalized dogs prior to induction of hypothermia, at rectal temperatures of 25°C or 20°C and following rapid rewarming in warm water or slow rewarming by wrapping in heated sheeting. During rapid rewarming from either 25°C or 20°C no consistent failure in recovery of normal cardiovascular function was observed, although 1 out of 10 dogs did suffer cardiovascular collapse during rapid rewarming. Slow rewarming from 25° and 20°C resulted in consistent failure of some or all of these functions to recover to prehypothermic levels. Moreover, 5 out of 15 slowly rewarmed dogs suffered cardiovascular collapse during the rewarming process. In five dogs slowly rewarmed from 20°C saline was infused into the superior vena cava. This procedure resulted in moderate increases in blood pressure but dramatic increases in cardiac output and minute work (200% and 270%, respectively), thereby negating myocardial failure as the primary cause of the occasionally observed cardiovascular failure.


1988 ◽  
Vol 255 (3) ◽  
pp. H503-H513 ◽  
Author(s):  
R. B. Schuessler ◽  
T. E. Canavan ◽  
J. P. Boineau ◽  
J. L. Cox

In open-chest dogs, blood pressure was regulated by titrating doses of phenylephrine and nitroprusside to determine its effect on heart rate and pacemaker location. Changes in blood pressure correlated with changes in heart rate (r = 0.86). Activation time mapping demonstrated multicentric atrial activation, with a site of origin-rate relationship. The fastest pacemakers were located in the most cranial regions and slowest in the most caudal areas. In this chloralose-morphine anesthetized model, autonomic blockade with atropine and propranolol suggests that acute baroreflex-induced changes in heart rate were mediated exclusively by either increased sympathetic or parasympathetic tone and were not associated with inhibition of the opposite system. Division of right and left thoracic cardiac nerves indicated the left sympathetics participated in the baroreflex in 50% of the animals and the left parasympathetics in 90% of the animals. Both the right sympathetics and parasympathetics were active in the baroreflex in all animals. The data demonstrate that physiological heart rate response is regulated through an extensive system of right atrial pacemakers modulated by both left and right efferent cardiac nerves.


1962 ◽  
Vol 202 (4) ◽  
pp. 653-660 ◽  
Author(s):  
William F. Geber

Continuous recordings of the fetal carotid artery blood flow, blood pressure, heart rate; renal, brain, uterine, and cotelydon blood flow; and maternal carotid artery blood pressure and heart rate were made during and after varied types of maternal stimulations and chemical injections in three anatomically different types of placental-uterine-fetal arrangements as exemplified by the sheep, dog, and rabbit. Included in this series was pinching of the ear, eyeball pressure, asphyxia, pure tones, stroking of the viscera, vagal stimulation, and intravenous injection of epinephrine, norepinephrine, acetylcholine, serotonin, and sodium pentobarbital. In all three animal species the fetal physiological responses were, in general, the same for any particular type of maternal stimulus or chemical injection. Fetal carotid artery blood flow together with fetal renal and brain blood flow were the most reliable indicators of fetal response to any particular maternal influence, with fetal blood pressure next and fetal cardiac rate the least reliable. Fetal renal and brain vasculature responded in the same qualitative manner to all maternal influences, whereas fetal carotid artery blood pressure and flow and cardiac rate were variable in their responses. All fetal responses were distinguished by their long duration, especially the renal and brain vascular responses.


2018 ◽  
Vol 1 (2) ◽  
pp. 65-69
Author(s):  
Sanjaya Kumar Shrestha ◽  
Anupam Ghimire ◽  
Safiur Rahman Ansari ◽  
Ashok Adhikari

Introduction: Accurate assessment of fluid status in hemodialysis patients presents a significant challenge. Nephrologists have long relied on dry weight estimation based solely on clinical parameters to decide the ultrafiltration volume for patients with end-stage kidney disease on dialysis. However, this method is far from accurate and many patients recurrently suffer from signs and symptoms of fluid overload or circulatory collapse from overaggressive ultrafiltration. Invasive methods such as measurement of central venous pressure cannot be used routinely. We evaluated the usefulness of inferior vena cava (IVC) diameter measured by handheld ultrasound in the estimation of fluid status in patients before and after hemodialysis. Materials and Methods: Clinical assessment included patients’ symptoms, weight, blood pressure, heart rate, and presence of edema before and after dialysis session. Dry weight was assessed based on the above parameters. Each patient underwent measurement of inferior vena cava before and after hemodialysis. The anteroposterior IVC diameter (IVCD) was measured 1.5 cm below the diaphragm in the hepatic segment in supine position during normal inspiration and expiration.Results:  Thirty hemodialysis patients (mean age 51.6±18.03 years) were evaluated in outpatient dialysis unit. Following hemodialysis mean IVCe (IVC diameter in expiration) decreased from 1.40±0.38 to 0.91±0.30 cm (p<0.001). Similarly, mean IVCi (IVC diameter in inspiration) decreased from 0.67±0.34 to 0.35±0.19 cm (p<0.001). Changes in IVCD were significantly correlated with alterations in body weight following dialysis (p<0.0001). The IVC collapsibility index (IVC-CI, per cent of change in IVC diameter in expiration vs. inspiration) increased significantly from 0.53±0.18 to 0.68±0.18 after dialysis (p=0.002). IVC diameter and IVC-CI clearly reflected alterations in fluid status. Regarding the clinical parameters of fluid status, following hemodialysis, mean heart rate increased from 81.17±5.21 beats per minute to 86.50±7.99, (p=0.003), systolic blood pressure increased from 148.67±26.36 mmHg to 155.00±28.50, (p=0.05), and diastolic blood pressure increased from 78.62±12.74 mmHg to 84.83±14.55, (p<0.001).Conclusions:  Our findings support the applicability of IVCD measurement and IVC-CI in the estimation of fluid status in end stage kidney disease patients on hemodialysis. The clinical parameters of fluid status including heart rate, systolic blood pressure, and diastolic blood pressure suggest that significant numbers of patients underwent excess ultrafiltration based on their traditional dry weight calculation. Thus, using IVC parameters before and during hemodialysis might give a better estimation of fluid status of the patient and guide the amount of ultrafiltration to be done. 


1979 ◽  
Vol 47 (2) ◽  
pp. 352-359 ◽  
Author(s):  
R. Winn ◽  
J. R. Hildebrandt ◽  
J. Hildebrandt

Receptor sites for the ventilatory response to isoproterenol were investigated in anesthetized rabbits with bolus injections in the common carotid artery (ia) and in the vena cava (iv). The delay from injection to the increase in ventilation (TVE) was significantly shorter following ia (1.5 s) compared to iv injections (about 5 s). The delay to the increase in heart rate (THR) was significantly shorter after iv (about 4.5 s) than after ia injections (12.5 s). When isoproterenol and NaCN injections were compared, there was no difference in TVE. Following carotid body resection, the VE response to isoproterenol was greatly reduced after iv and ia injections; however, THR was unaffected. In intact animals breathing 100% O2 the VE response to isoproterenol was significantly reduced with no change in TVE or in the heart rate response. We conclude that the ventilatory increase following the injection of isoproterenol is due primarily to direct stimulation of the carotid bodies.


1991 ◽  
Vol 260 (1) ◽  
pp. E154-E161 ◽  
Author(s):  
C. E. Wood ◽  
A. Isa

Both respiratory and metabolic acidemia stimulate the secretion of adrenocorticotropic hormone (ACTH), vasopressin, and renin. The present study was designed to test the blood pressure, heart rate, and endocrine responses of conscious sheep to low-rate infusions of H+. We infused HCl and lactic acid at a rate of 500 mueq/min into the inferior vena cava of seven chronically catheterized adult sheep. Control experiments in six sheep consisted of infusion of HCl at a rate of 100 mueq/min. Only the 500 mueq/min infusion of HCl stimulated reflex responses. This infusion increased mean arterial blood pressure and plasma ACTH concentration but transiently decreased blood pH only after the onset of the reflex responses. Heart rate appeared to increase initially but then decreased. Overall, the apparent changes in heart rate were not statistically significant. None of the infusions significantly altered plasma renin activity or vasopressin concentration. We speculate that heart rate, plasma renin activity, and vasopressin may have been partially inhibited by the increase in blood pressure. However, the lack of effect of lactic acid suggests that the HCl stimulated reflex ACTH and blood pressure responses via a mechanism not related to the concentration of the acid in the infusate or to the total amount of acid infused. It is possible that HCl, but not lactic acid, stimulated release of a humoral agent that stimulated ACTH secretion directly or reflexly. The results do not appear consistent with the stimulation of a venous chemoreceptor sensitive to H+.


10.52011/81 ◽  
2021 ◽  
Vol 22 (3) ◽  
pp. 1-9
Author(s):  
Geyson Deley-Muñoz ◽  
Fabricio González-Andrade

Introduction: There is no single criterion available to assess the hemodynamic state of new-born infants and preterm infants and the different variables in the group of newborns, such as gestational age, birth weight, and periods of birth. Methods: This is an epidemiological, cross-sectional, descriptive observational study with two patient cohorts. Newborn-to-term and preterm neonates assisted at the Neonatal Unit of the Pablo Arturo Suarez Hospital participated during the months between November 2019 to January 2020. Results: Ultrasound measurement of the vena cava (FVC) flow is useful for the management treatment of hemodynamically unstable neonatal patients. The sample was made up of 110 newborns treated in the Pablo Arturo Suarez Hospital's neonatology service from November 2019 to January 2020. Quito, Pichincha, Ecuador. The variables low birth weight and moder-ate prematurity have a statistically significant value for inotropic use. The other variables do not present statistically significant values. Heart rate, urinary output, mean blood pressure, lactic acid, capillary filling, upper vena cava flow, and lower vena cava flow had statistically significant values. FVCI and FVCS comparisons with heart rate, urinary output, mean blood pressure, lactic acid, and capillary filling had statistically significant values, except for capil-lary filling> 3 sec in FCVI. Multivariate analysis of categorical main components (CATPCA) was used to characterize the hemodynamic state and inotropic state, which were significant in the bivariate analysis. Dimension, one of the two-dimensional graphs, discriminates the use or not of inotropics and the categories of hemodynamic parameters TAM <35 mmHg, lactic acid, capillary filling, FVCI, and FVCS. Dimension II discriminates between the categories of urinary expenditure and HR. Conclusion: In term and preterm infants with low weight and adequate birth weight with hemodynamic instability in general, who were evaluated with ultrasonography to measure the flow of the vena cava, the agreement between the clinical criteria and the ultrasound assessment of the flow was 0.4 cm/sec in both methods. This situation means that the measurement of venous cava flows by echo sonography is useful for assessing neonatal patients' hemodynamic status.


1979 ◽  
Vol 236 (5) ◽  
pp. H775-H779
Author(s):  
L. D. Byrd

A device suitable for the continuous measurement of physiological activity in large, conscious monkeys has permitted the direct recording of systemic arterial blood pressure and heart rate in caged baboons. The device comprises a lightweight fiberglass backpack, retained in place on the baboon by a thoracic elastic band and shoulder straps, and a flexible stainless steel tether connecting the pack to an electrocannular slip-ring in the top center of the baboon's cage. A chronically indwelling arterial catheter inserted retrograde into the abdominal aorta via the internal iliac artery and connected to a small pressure transducer on the pack provides direct measurement of blood pressure and heart rate. Body fluids can be sampled or drugs administered via an indwelling catheter in the inferior vena cava. Electrical and fluid connections between the fiberglass pack and recording and infusion equipment located outside the cage pass through the flexible tether and remain protected from the subject. The reliability of the tethering system has been demonstrated in physiological, pharmacological, and behavioral experiments with baboons.


2021 ◽  
Author(s):  
Fiona O'Brien ◽  
Caroline Staunton ◽  
Richard Barrett-Jolley

In humans the skin is a primary thermoregulatory organ, with vasodilation leading to rapid body cooling, whereas in rodents the tail performs an analogous function. TRPV4 is a widely distributed ion channel with both mechanical and thermosensitive properties. Previous studies have shown that TRPV4 can act as vasodilator by local action in blood vessels, and in this study we investigated whether there was a constitutive role for TRPV4 in mouse tail vascular tone and thermoregulation. We measured tail blood flow by pressure plethysmography in lightly sedated mice at a range of ambient temperatures, with and without intraperitoneal administration of the blood brain barrier crossing TRPV4 antagonist GSK2193874. We also measured heart rate and blood pressure with and without GSK2193874. As predicted, we found that tail blood flow increased with temperature. However, unexpectedly we found that the TRPV4 antagonist GSK2193874 increased tail blood flow at all temperatures. There were few detectable differences in heart rate, blood pressure or short-range heart rate variability. Since arterial TRPV4 activation is known to cause vasodilation that would increase tail blood flow, these data suggest that increases in tail blood flow resulting from the TRPV4 antagonist must arise from a site other than the blood vessels themselves, perhaps in central cardiovascular control centres such as the paraventricular nucleus of the hypothalamus.


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