Arterial baroreceptors control plasma vasopressin responses to graded hypotension in conscious dogs

2000 ◽  
Vol 278 (2) ◽  
pp. R469-R475 ◽  
Author(s):  
Terry N. Thrasher ◽  
Hong-Gen Chen ◽  
Lanny C. Keil
Keyword(s):  
Inferior Vena ◽  
Control Period ◽  
Vena Cava ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Inferior Vena Caval ◽  
Arterial Baroreceptors ◽  
Treatment Conditions ◽  
The Individual

We studied the role of cardiac and arterial baroreceptors in the reflex control of arginine vasopressin (AVP) and renin secretion during graded hypotension in conscious dogs. The dogs were prepared with Silastic cuffs on the thoracic inferior vena cava and catheters in the pericardial space. Each experiment consisted of a control period followed by four periods of inferior vena caval constriction, during which mean arterial pressure (MAP) was reduced in increments of ∼10 mmHg. The hormonal responses were measured in five dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD+CD. The individual slopes relating MAP to plasma AVP and plasma renin activity (PRA) were used to compare the treatment effects using a 2 × 2 factorial analysis. There was a significant ( P < 0.01) effect of SAD on the slope relating plasma AVP to MAP but no effect of CD and no SAD × CD interaction. In contrast, the slope relating PRA and MAP was increased ( P < 0.05) by SAD but was not affected by CD. These results support the hypothesis that stimulation of AVP secretion in response to graded hypotension is primarily driven by unloading arterial baroreceptors in the dog.

Arterial baroreceptors control blood pressure and vasopressin responses to hemorrhage in conscious dogs

1998 ◽  
Vol 275 (6) ◽  
pp. R1843-R1857 ◽  
Author(s):  
Terry N. Thrasher ◽  
Lanny C. Keil
Keyword(s):  
Blood Pressure ◽  
Systolic Pressure ◽  
Absolute Magnitude ◽  
Conscious Dogs ◽  
Arterial Baroreceptors ◽  
Treatment Conditions ◽  
Intact Condition ◽  
The Individual ◽  
The Relationship

The goal of this study was to determine the role of arterial baroreceptors in the reflex control of arginine vasopressin (AVP), renin, and cortisol secretion in response to a 30-ml/kg hemorrhage in conscious dogs. The hormonal responses were measured in six dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD + CD. In the intact condition, mean arterial pressure (MAP) was maintained at control levels until blood loss reached 20 ml/kg and the absolute magnitude of the fall at 30 ml/kg was 35 ± 10 mmHg. Similar responses were obtained during acute CD. In contrast, MAP fell earlier (at 5 ml/kg, P < 0.05) and to much lower levels in both the SAD and SAD + CD conditions. The individual slopes relating systolic pressure to plasma AVP, renin activity (PRA), and cortisol were used to compare the treatment effects using a 2 × 2 factorial analysis. There was a significant ( P < 0.01) effect of SAD on the slope relating AVP to systolic pressure but no effect of CD and no SAD × CD interaction. In contrast, there was no effect of either SAD or CD on the relationship between PRA or plasma cortisol and systolic pressure. These results indicate that maintenance of blood pressure and the normal pattern of AVP secretion during hemorrhage depend on intact arterial baroreceptor reflexes.

Role of right heart receptors in the control of renin, vasopressin, and cortisol secretion in dogs

1992 ◽  
Vol 263 (5) ◽  
pp. R1071-R1077 ◽  
Author(s):  
D. H. Carr ◽  
D. B. Jennings ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Plasma Renin ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Heart ◽  
Hormonal Responses ◽  
The Right ◽  
Maximal Reduction

We have reported that increased left heart pressure inhibits increases in plasma renin activity (PRA), arginine vasopressin (AVP), and cortisol during arterial hypotension. The goal of this study was to determine whether increases in right heart pressure also inhibited hormonal responses to hypotension. Seven dogs were chronically instrumented with inflatable cuffs around the ascending aorta (AA), the pulmonary artery (PA), and the thoracic inferior vena cava (IVC), as well as with catheters in both atria, the abdominal aorta, and vena cava. The IVC, the PA, and the AA cuffs were inflated on different days to cause step reductions in mean arterial pressure (MAP) of 5, 10, 20, and 30% below control MAP. Graded constriction of the AA caused large increases in left atrial pressure and plasma atrial natriuretic peptide (ANP), but had no effect on plasma AVP or cortisol and caused only a small increase in PRA at the maximal reduction of MAP. Constriction of the IVC reduced both atrial pressures and plasma ANP, but stimulated increases in PRA, AVP, and cortisol. Constriction of the PA increased right atrial pressure and plasma ANP and caused increases in plasma AVP and cortisol that were similar to responses during IVC constriction, but the PRA response was only half (P < 0.05). These results indicate that increasing pressure on the right side of the heart can attenuate the PRA response to hypotension, and suggest that the inhibition is mediated by the rise in plasma ANP.

Effects of baroreceptor denervation on endocrine and drinking responses to caval constriction in dogs

1990 ◽  
Vol 259 (3) ◽  
pp. R618-R626 ◽  
Author(s):  
E. W. Quillen ◽  
L. C. Keil ◽  
I. A. Reid
Keyword(s):  
Inferior Vena ◽  
Plasma Renin ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Inferior Vena Caval ◽  
Plasma Angiotensin ◽  
Access To Water ◽  
Plasma Arginine

Plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake (H2OIN) are increased by thoracic inferior vena caval constriction (TIVCC). To assess the role of the cardiac and sinoaortic baroreceptors in these responses, 9 sham-, 10 cardiac-(CD), 6 sinoaortic-(SAD), and 4 combined cardiac and sinoaortic-(CD + SAD) denervated conscious dogs were studied. All animals were studied while normally hydrated 1) with no access to water (H2O-) and 2) while drinking was permitted (H2O+). TIVCC caused similar reductions (P less than 0.001) of mean arterial (-32 +/- 4 mmHg), left atrial pressure (-6.5 +/- 1.1 cmH2O), and right atrial pressure (-4.2 +/- 0.8 cmH2O) in all groups. After TIVCC in sham dogs with H2O-, AVP increased from 3.6 +/- 0.7 to 72.8 +/- 12.6 pg/ml (P less than 0.001). AVP was similar with SAD (57.1 +/- 6.9) but was reduced with CD (30.9 +/- 3.0) and CD + SAD (17.7 +/- 4.0). In all groups, PRA increased from 4.5 +/- 0.7 to 23.8 +/- 3.0 ng.ml-1 x 3 h-1 and plasma angiotensin II (ANG II) increased from 14.0 +/- 2.8 to 59.5 +/- 13.0 pg/ml (P less than 0.001). Plasma adrenocorticotropic hormone (ACTH) increased similarly in all groups (55 +/- 5 to 128 +/- 25 pg/ml). Plasma norepinephrine (NE) levels increased similarly in all groups (298 +/- 61 to 654 +/- 88 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Vasopressin, renin, and cortisol responses to hemorrhage during acute blockade of cardiac nerves in conscious dogs

1993 ◽  
Vol 265 (1) ◽  
pp. R220-R229 ◽  
Author(s):  
C. P. O'Donnell ◽  
L. C. Keil ◽  
T. N. Thrasher
Keyword(s):  
Left Atrial ◽  
Inferior Vena ◽  
Vena Cava ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Cortisol Secretion ◽  
Angiotensin I ◽  
Cortisol Responses ◽  
Cardiac Receptors ◽  
Cardiac Nerves

The effect of acute cardiac nerve blockade (CNB) on the increases in plasma renin activity (PRA), arginine vasopressin (AVP), and cortisol in response to a 30 ml/kg hemorrhage was determined in conscious dogs (n = 9). Procaine was infused into the pericardial space to produce acute reversible CNB, or saline was infused in the control hemorrhage. Blood was removed from the inferior vena cava at a rate of 1 ml.kg-1.min-1. In the control hemorrhage, plasma AVP increased from 1.8 +/- 0.3 to 219 +/- 66 pg/ml, PRA increased from 0.63 +/- 0.20 to 3.08 +/- 0.91 ng angiotensin I (ANG I).ml-1.3 h-1, and cortisol increased from 1.4 +/- 0.2 to 4.0 +/- 0.7 micrograms/dl. When the hemorrhage was repeated during acute CNB, plasma AVP increased from 2.8 +/- 1.6 to 185 +/- 59 pg/ml, PRA increased from 0.44 +/- 0.14 to 2.24 +/- 0.27 ng ANG I.ml-1.3 h-1, and cortisol increased from 1.9 +/- 0.3 to 5.4 +/- 0.6 micrograms/dl, and none of the increases differed significantly from the responses during the control hemorrhage. Left atrial pressure fell significantly after removal of 6 ml/kg of blood, but mean arterial pressure was maintained at control levels until blood loss reached 20 ml/kg during pericardial infusion of either saline or procaine. The declines in MAP at the 30 ml/kg level of hemorrhage in both treatments were similar. These results demonstrate that acutely blocking input from cardiac receptors does not reduce the increases in plasma AVP, cortisol, and PRA in response to a 30 ml/kg hemorrhage. The results of this study do not support the hypothesis that input from cardiac receptors is required for a normal AVP response to hemorrhage and suggest that other receptors, presumably arterial baroreceptors, can stimulate AVP and cortisol secretion in the absence of signals from the heart.

Unloading arterial baroreceptors causes neurogenic hypertension

2002 ◽  
Vol 282 (4) ◽  
pp. R1044-R1053 ◽  
Author(s):  
Terry N. Thrasher
Keyword(s):  
Carotid Sinus ◽  
Control Period ◽  
Plasma Renin ◽  
Systemic Hypertension ◽  
Neurogenic Hypertension ◽  
Arterial Baroreceptors ◽  
Flow Through ◽  
Common Carotid Arteries

We developed a new model to examine the role of arterial baroreceptors in the long-term control of mean arterial pressure (MAP) in dogs. Baroreceptors in the aortic arch and one carotid sinus were denervated, and catheters were implanted in the descending aorta and common carotid arteries. MAP and carotid sinus pressure (CSP) averaged 104 ± 2 and 102 ± 2 mmHg (means ± 1 SE), respectively, during a 5-day control period. Baroreceptor unloading was induced by ligation of the common carotid artery proximal to the innervated sinus ( n = 6 dogs). MAP and CSP averaged 127 ± 7 and 100 ± 3 mmHg, respectively, during the 7-day period of baroreceptor unloading. MAP was significantly elevated ( P < 0.01) compared to control, but CSP was unchanged. Heart rate and plasma renin activity increased significantly in response to baroreceptor unloading. Removal of the ligature to restore normal flow through the carotid resulted in normalization of all variables. Ligation of the carotid below a denervated sinus ( n = 4) caused a significant decrease in CSP but no systemic hypertension. These results indicate that chronic unloading of carotid baroreceptors can produce neurogenic hypertension and provide strong evidence that arterial baroreceptors are involved in the long-term control of blood pressure.

scholarly journals Role of Inferior Vena Cava Filter Retrieval in Patients on Chronic Anticoagulation Therapy

2021 ◽  
Vol 23 (2) ◽  
Author(s):  
Savannah Fletcher ◽  
Adam Plotnik ◽  
Ravi N. Srinivasa ◽  
Jeffrey Forris Beecham Chick ◽  
John M. Moriarty
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena Cava Filter ◽  
Inferior Vena ◽  
Treatment Options ◽  
Anticoagulation Therapy ◽  
Vena Cava ◽  
Vena Cava Filter ◽  
Venous Thromboembolic

Abstract Purpose of review Describe the role of inferior vena cava filter (IVCF) retrieval in patients on chronic anticoagulation given the overlap of these treatment options in the management of patients with venous thromboembolic disease. Recent findings Despite the increase in IVCF retrievals since the Food and Drug Administration safety communications in 2010 and 2014, retrieval rates remain low. Previous studies have shown that longer filter dwell times are associated with greater risk for filter complications and more difficulty with filter retrievals. Recent findings suggest that complications are more frequent in the first 30 days after placement. Summary The decision to retrieve an optional IVCF is individualized and requires diligent follow-up with consistent re-evaluation of the need for the indwelling IVCF, particularly in those on long-term anticoagulation therapy.

Reassessment of the Role of Inferior-Vena-Cava Ligation in Venous Thromboembolism

1965 ◽  
Vol 273 (23) ◽  
pp. 1250-1253 ◽  
Author(s):  
Donald C. Nabseth ◽  
John M. Moran
Keyword(s):  
Venous Thromboembolism ◽  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Vena Cava

Budd-Chiari Syndrome in Childhood Secondary to Inferior Vena Caval Obstruction

PEDIATRICS ◽  
1979 ◽  
Vol 63 (5) ◽  
pp. 808-812
Author(s):  
Arvind Taneja ◽  
S. K. Mitra ◽  
P. D. Moghe ◽  
P. N. Rao ◽  
N. Samanta ◽  
...  
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Hepatic Veins ◽  
Budd Chiari Syndrome ◽  
Venous Outflow ◽  
Massive Ascites ◽  
Inferior Vena Caval ◽  
Uncommon Disease ◽  
Chiari Syndrome ◽  
Hepatic Venous Outflow

Budd-Chiari syndrome is an uncommon disease caused by an obstruction to hepatic venous outflow either at the level of the hepatic veins or in the hepatic part of the inferior vena cava. Clinically, it presents with ascites, abdominal pain, hepatomegaly, edema, and occasionally jaundice. The syndrome was first recognised by Lamboran1 in 1842 and later described by Budd2 in 1846 and Chiari3 in 1899. The syndrome is caused by obstruction to the hepatic veins. In the Fig 1. Photograph showing massive ascites and dilated superficial abdominal veins. majority of cases, the obstruction is ascribed to obliterative thrombophlebitis of unknown cause.4

Initial Treatment of Pulmonary Embolism

2007 ◽  
Vol 6 (3) ◽  
pp. 95-101
Author(s):  
Alastair Proudfoot ◽  
◽  
Helen Yarranton ◽  
Simon Gibbs ◽  
Derek Bell ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Initial Treatment ◽  
Acute Pulmonary Embolism ◽  
Inferior Vena ◽  
Previous Article ◽  
Diagnostic Approach ◽  
Inferior Vena Caval ◽  
Common Presentation ◽  
In Pregnancy

Acute pulmonary embolism (PE) is a common presentation on the acute medical take. In our previous article in Vol 6 issue 1 we discussed the diagnostic approach to this condition. This article concentrates on the treatment of PE, including guidance for treatment of PE in pregnancy and cancer. This article also discusses the role of alternative anticoagulants, thrombolysis, surgery and inferior vena caval filters.

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