scholarly journals SAT-212 Management of VHL-Associated Pheochromocytoma in Pregnancy

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Andrew Reed Reikes ◽  
Ruchi Desai
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Adrenal Mass ◽  
Case Series ◽  
Normal Serum ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Intrauterine Pregnancy ◽  
Imaging Characteristics ◽  
In Pregnancy

Abstract Background: The appropriate treatment of pheochromocytoma during pregnancy is crucial because, while its incidence is rare (0.007%), it is associated with increased maternal and fetal mortality1. Clinical Case: A 32 year old Caucasian primigravida female presented with intrauterine pregnancy at 25 weeks for evaluation and management of a 9 mm left adrenal mass. The patient was previously diagnosed at age 10 with Von-Hippel Lindau (VHL) syndrome and genetic testing was positive for a VHL gene mutation (Type 2C VHL). At age 14, she underwent laparoscopic adrenalectomy to excise a right sided pheochromocytoma. At age 20, imaging revealed an enhancing left adrenal mass with imaging characteristics consistent with pheochromocytoma and with catecholaminergic labs that were normal or only mildy increased to 1.5 times upper normal range. Pre-partum the patient had been experiencing periodic episodes of headaches and palpitations. She reported experiencing baseline levels of palpitations and sweating with new onset of pre-syncope and hypotension during her pregnancy. Labs revealed normal serum levels of fractionated free metanephrines. Alpha adrenergic blockade, beta adrenergic blockade, and surgery were considered but deemed unnecessary as the patient was asymptomatic, imaging indicated the left adrenal mass was stable in size, and the patient wished to avoid lifelong adrenal replacement therapy. The patient’s blood pressure and heart rate were monitored closely throughout pregnancy and the use of alpha blockade or beta blockade was not needed. The patient had an uncomplicated induced delivery at 39 weeks. MRI with contrast of abdomen performed 10 months postpartum confirmed the presence of an enhancing 8 mm lesion on the inferior pole of the left adrenal gland with imaging characteristics again consistent with pheochromocytoma. Conclusion: This case demonstrates that a conservative approach of monitoring blood pressure and heart rate can be sufficient and appropriate for management of some patients with pheochromocytoma and VHL during pregnancy. Citation: 1. ENDOCRINOLOGY IN PREGNANCY: Pheochromocytoma in pregnancy: case series and review of literature in: European Journal of Endocrinology Volume 177 Issue 2 (2017).

Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats

1991 ◽  
Vol 261 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Control ◽  
Area Postrema ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Blocking Agent ◽  
Adrenergic Blockade ◽  
Neural Pathways ◽  
Heart Rate Control

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

Effect of beta-blockade on the drift in O2 consumption during prolonged exercise

1988 ◽  
Vol 64 (2) ◽  
pp. 753-758 ◽  
Author(s):  
J. K. Kalis ◽  
B. J. Freund ◽  
M. J. Joyner ◽  
S. M. Jilka ◽  
J. Nittolo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Minute Ventilation ◽  
Cycle Ergometer ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
O2 Consumption ◽  
Double Blind ◽  
Cycle Ergometer Test ◽  
Ergometer Test

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Propranolol on Blood Pressure in Normal and Hypertensive Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 101s-103s
Author(s):  
J. Conway ◽  
K. Darwin ◽  
A. Hilditch ◽  
B. Loveday ◽  
M. Reeves
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Chronic Treatment ◽  
Spontaneous Hypertension ◽  
Beta Blockade ◽  
Experimental Hypertension ◽  
Hypertension Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Propranolol Treatment

1. Propranolol has been given orally in a dose sufficient to achieve beta-blockade throughout the day in normal rats, renal hypertensive animals with and without contralateral nephrectomy, spontaneously hypertensive and deoxycorticosterone (DOCA) hypertensive rats. The drug was given either after hypertension had become fully established or during the phase of rising blood pressure. 2. With this treatment, heart rate was reduced by approximately 100 beats/min in all experimental groups. 3. In established hypertension, treatment with propranolol for 7–9 days was ineffective in lowering blood pressure in any of the models of experimental hypertension. It also had no effect on blood pressure in normal animals. 4. Chronic treatment with propranolol during the phase of rising blood pressure had no effect in renal hypertensive animals. In spontaneous hypertension, the rise in blood pressure was limited to 28 mmHg with propranolol treatment as compared with 58 mmHg in control animals. Likewise, in DOCA hypertension, the rise in pressure was limited to 18 mmHg as compared with 46 mmHg in control animals.

scholarly journals Beta-adrenergic Receptor Blockade Effects on Cardio-pulmonary Exercise Testing

2021 ◽  
Author(s):  
Kevin Forton ◽  
Michel Lamotte ◽  
Alexis Gillet ◽  
Martin Chaumont ◽  
Van De Borne Philippe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Single Dose ◽  
Adrenergic Receptor ◽  
Adrenergic Blockade ◽  
Receptor Blockade ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Chronotropic Response ◽  
Adrenergic Receptor Blockade

Abstract Background: Beta-blockers are increasingly prescribed while the effects of beta-adrenergic receptor blockade on cardio-pulmonary exercise test (CPET) derived parameters remain under-studied. Methods: 21 young healthy adults repeated 3 CPET at an interval of 7 days at the same time of the day. The tests were performed 3 hours after a random, double blind, cross-over single dose intake of placebo, 2.5 mg bisoprolol or 5 mg bisoprolol. Gaz exchange, heart rate and blood pressure were measured at rest and during cyclo-ergometric CPET.Results: Maximal workload and VO2max were unaffected by the treatment, with maximal respiratory exchange ratio > 1.15 in all tests. A beta-blocker dose-dependent effect reduced resting and maximal blood pressure and heart rate and the chronotropic response to exercise, evaluated by the heart rate/VO2 slope (placebo: 2,9 ± 0,4 beat/ml/kg; 2,5 mg bisoprolol: 2,4 ± 0,5 beat/ml/kg; 5 mg bisoprolol: 2,3 ± 0,4 beat/ml/kg, p<0.001). Ventilation efficiency measured by the VE/VCO2 slope and the ventilatory equivalent for CO2 at the ventilatory threshold were not affected by beta1-receptor blockade. Post-exercise chronotropic recovery measured after 1 min was enhanced under beta1-blocker (placebo: 26 ± 7 bpm; 2,5 mg bisoprolol: 32 ± 6 bpm; 5 mg bisoprolol: 33 ± 6 bpm, p<0.01).Conclusion: The present results suggest that a single dose of bisoprolol does not affect metabolism, respiratory response and exercise capacity. However, beta-adrenergic blockade dose-dependently reduced exercise hemodynamic response by lowering the pressure and chronotropic responses.

Plasma atriopeptin during exercise in dogs under beta-blockade

1989 ◽  
Vol 256 (5) ◽  
pp. R1098-R1102
Author(s):  
F. Peronnet ◽  
S. A. Adjoa ◽  
L. Beliveau ◽  
D. Bichet ◽  
R. Nadeau ◽  
...  
Keyword(s):  
Heart Rate ◽  
Plasma Renin Activity ◽  
Treadmill Exercise ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Vasopressin Release ◽  
Angiotensin System ◽  
H 26

The purpose of this study was to describe plasma atriopeptin concentrations at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) performed with or without nonspecific beta-adrenergic blockade (1 mg/kg iv propranolol) in 10 mongrel dogs [19 +/- 2 (SE) kg]. A small (20%) but significant (P less than 0.05) increase in plasma atriopeptin concentration was observed from rest (43 +/- 5 pg/ml) to exercise (52 +/- 6 pg/ml) without beta-blockade. Propranolol significantly reduced heart rate at rest (89 +/- 7 vs. 104 +/- 7 beats/min) and during exercise (96 +/- 10 vs. 176 +/- 11 beats/min), and this was associated with a larger increase in plasma atriopeptin concentration during exercise (rest 46 +/- 6 pg/ml; exercise 171 +/- 22 pg/ml). Exercise under beta-blockade is associated with an increased preload of the heart. These results further support the hypothesis that atriopeptin release during exercise is under the control of atrial stretch. The higher plasma atriopeptin concentration observed during exercise under beta-blockade may contribute to the reduction of the response of plasma renin activity (1.0 +/- 0.1 vs. 3.0 +/- 0.6 ng.ml-1.h-1) and aldosterone concentration (87 +/- 36 vs. 138 +/- 25 pg/ml). Vasopressin concentration was lower at rest and during exercise under propranolol (3.5 +/- 1.3 vs. 4.9 +/- 0.9 and 6.1 +/- 2.2 vs. 9.9 +/- 1.5 pg/ml, respectively), which might reflect a dissociation between activity of the renin-angiotensin system and vasopressin release.

Effects of beta-adrenergic blockade on O2 uptake during submaximal and maximal exercise

1983 ◽  
Vol 54 (4) ◽  
pp. 901-905 ◽  
Author(s):  
P. A. Tesch ◽  
P. Kaiser
Keyword(s):  
Heart Rate ◽  
Maximal Exercise ◽  
Pulmonary Ventilation ◽  
Submaximal Exercise ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
O2 Consumption ◽  
O2 Uptake ◽  
Beta Adrenergic

Changes in cardiorespiratory variables and perceived rate of exertion (RPE) were studied in 13 trained men performing cycling exercise before and after beta-adrenergic blockade. Propranolol (Inderal, 80 mg) was administered orally 2 h prior to standardized maximal and submaximal exercises. Muscle biopsies were obtained from vastus lateralis at rest for subsequent histochemical analyses of muscle fiber type distribution and capillary supply. During submaximal exercise O2 consumption decreased from 2.76 to 2.59 l . min-1 following blockade (P less than 0.01), whereas heart rate decreased from 157 to 113 beats . min-1 (P less than 0.001). Maximal O2 uptake was lowered from 3.79 to 3.26 l . min-1 (P less than 0.001) and maximal heart rate was reduced from 192 to 142 beats . min-1 (P less than 0.001) as a result of the blockade. Pulmonary ventilation was unaltered in both exercise conditions. “Local” RPE was higher (P less than 0.001) than “central” RPE after beta-blockade in both submaximal and maximal exercise. During normal condition this difference did not appear. Changes in both local and central RPE during submaximal exercise were positively correlated to changes in O2 uptake. Individual variations in the metabolic profile of the exercising muscle had no influence on beta-blockade-induced changes in O2 uptake. It is concluded that blockade of beta-adrenergic receptors reduces O2 consumption during submaximal (approximately 73% maximal O2 uptake) and maximal exercise in habitually trained men.

Effects of beta-adrenergic blockade on ventilation and gas exchange during exercise in humans

1983 ◽  
Vol 54 (5) ◽  
pp. 1306-1313 ◽  
Author(s):  
E. S. Petersen ◽  
B. J. Whipp ◽  
J. A. Davis ◽  
D. J. Huntsman ◽  
H. V. Brown ◽  
...  
Keyword(s):  
Heart Rate ◽  
Gas Exchange ◽  
Time Constant ◽  
Minute Ventilation ◽  
Work Rate ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
O2 Uptake ◽  
Beta Adrenergic ◽  
Co2 Partial Pressure

The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.

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