Hypothermic Circulatory Arrest: Renal Protection by Atrial Natriuretic Peptide

2009 ◽  
Vol 17 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Masahiro Ohno ◽  
Tadashi Omoto ◽  
Masaomi Fukuzumi ◽  
Masaya Oi ◽  
Noboru Ishikawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Circulatory Arrest ◽  
Treated Group ◽  
Hypothermic Circulatory Arrest ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Medullary Blood Flow ◽  
Atrial Natriuretic

Moderate hypothermic circulatory arrest with selective cerebral perfusion has been developed for cerebral protection during thoracic aortic surgery. However, visceral organs, particularly the kidneys, suffer greater tissue damage under moderate hypothermic circulatory arrest, and acute renal failure after hypothermic circulatory arrest is an independent risk factor for early and late mortality. This study investigated whether atrial natriuretic peptide could prevent the reduction in renal perfusion and protect renal function after moderate hypothermic circulatory arrest. Twelve pigs cooled to 30°C during cardiopulmonary bypass were randomly assigned to a peptide-treated group of 6 and a control group of 6. Moderate hypothermic circulatory arrest was induced for 60 min. Systemic arterial mean pressure and renal artery flow did not differ between groups during the study. However, renal medullary blood flow increased significantly in the peptide-treated group after hypothermic circulatory arrest. Myeloperoxidase activity was significantly reduced in the medulla of the peptide-treated group. Renal medullary ischemia after hypothermic circulatory arrest was ameliorated by atrial natriuretic peptide which increased medullary blood flow and reduced sodium reabsorption in the medulla. Atrial natriuretic peptide also reduced the release of an inflammatory marker after ischemia in renal tissue.

Effect of atrial natriuretic peptide on vasa recta blood flow in the rat

1987 ◽  
Vol 252 (6) ◽  
pp. F1112-F1117 ◽  
Author(s):  
B. A. Kiberd ◽  
T. S. Larson ◽  
C. R. Robertson ◽  
R. L. Jamison
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urine Flow ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Renal Medullary Blood Flow ◽  
Experimental Group ◽  
Atrial Natriuretic

To determine whether synthetic atrial natriuretic peptide (ANP) increases renal medullary blood flow and if so whether the increase mediates the diuresis and natriuresis induced by ANP, inner medullary vasa recta blood flow in the exposed left renal papilla of anesthetized Munich Wistar rats weighing between 102 and 161 g was measured by fluorescence videomicroscopy. The rats were maintained in a euvolemic state by the infusion of albumin. Synthetic ANP (Auriculin B) was administered intravenously as 2.5 micrograms/kg body wt prime and as a continuous infusion of 0.2 microgram X min-1 X kg body wt-1 to the experimental group (n = 7). Within 2 min after ANP was given, urine flow and sodium excretion increased (29.4 +/- 3.8 to 50.4 +/- 5.8 microliter X min-1 X kidney wt-1, P less than 0.01, and 3.39 +/- 0.57 to 6.05 +/- 0.95 mueq X min-1 X g kidney wt-1, P less than 0.01, respectively), but vasa recta blood flow in descending (DVR) or ascending (AVR) vasa recta did not change significantly (9.5 +/- 2.3 to 10.0 +/- 2.8 nl/min in DVR and 5.3 +/- 1.0 to 6.1 +/- 1.2 nl/min in AVR). Forty-five minutes after ANP was begun, urine flow and sodium excretion increased further (77.1 +/- 11.1 microliter X min-1 X g kidney wt-1 and 12.0 +/- 2.15 mueq X min-1 X g kidney wt-1, respectively), and by this time vasa recta blood flow had increased significantly to 14.0 +/- 2.6 in DVR, P less than 0.01, and 9.8 +/- 1.2 in AVR, P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Direct effect of α-human atrial natriuretic peptide on human vasculature in vivo and in vitro

1988 ◽  
Vol 74 (2) ◽  
pp. 207-211 ◽  
Author(s):  
A. Hughes ◽  
S. Thom ◽  
P. Goldberg ◽  
G. Martin ◽  
P. Sever
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Forearm Blood Flow ◽  
Renin Angiotensin System ◽  
Organ Bath ◽  
Human Atrial Natriuretic Peptide ◽  
Atrial Natriuretic

1. The effect of a α-human atrial natriuretic peptide (1–28) (ANP) on human vasculature was investigated in vivo and in vitro. Possible involvement of vascular dopamine receptors and the renin-angiotensin system in the response to ANP was also studied in vivo. 2. Forearm blood blow was measured by venous occlusion plethysmography. Isolated human blood vessels were studied using conventional organ bath techniques. 3. ANP (0.1–1 μg/min, intra-arterially) produced a dose-dependent increase in forearm blood flow, corresponding to a 163% increase in net forearm blood flow in the study arm. This action of ANP was not antagonized by (R)-sulpiride (100 μg/min, intra-arterially), a selective vascular dopamine receptor antagonist, or 50 mg of oral captopril, an inhibitor of angiotensin-converting enzyme. 4. ANP (1 nmol/l–1 μmol/l) produced concentration-dependent relaxation of isolated human arteries, including brachial artery, but was without effect on isolated human saphenous vein. 5. ANP produces vasodilatation in vivo and relaxes isolated human arterial smooth muscle. This action of ANP may contribute to its reported hypotensive effects in vivo.

Atrial natriuretic peptide increases resistance to venous return in rats

1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

Mechanism for decrease in cardiac output with atrial natriuretic peptide in dogs

1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Blood Volume ◽  
Total Blood ◽  
Atrial Natriuretic

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.

scholarly journals Atrial natriuretic peptide augments coronary collateral blood flow: A study during coronary angioplasty

1998 ◽  
Vol 21 (10) ◽  
pp. 737-742 ◽  
Author(s):  
Zenon S. Kyriakides ◽  
Eftihia Sbarouni ◽  
Aias Antoniadis ◽  
Efstathios K. Iliodromitis ◽  
Dimitrios Mitropoulos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Coronary Angioplasty ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Coronary Collateral Blood Flow ◽  
Atrial Natriuretic

Changes in atrial natriuretic peptide concentration and expression of its receptors after pneumonectomy in the rat

2000 ◽  
Vol 99 (4) ◽  
pp. 343-348 ◽  
Author(s):  
Kohichi TAMURA ◽  
Shinzo TAKAMORI ◽  
Hiroharu MIFUNE ◽  
Akihiro HAYASHI ◽  
Kazuo SHIROUZU
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Mrna Expression ◽  
Pulmonary Oedema ◽  
Natriuretic Peptide ◽  
Cell Function ◽  
Control Group ◽  
Sham Operation ◽  
Endothelial Cell Function ◽  
And Control ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) is a cardiac hormone which affects endothelial cell function through a receptor-mediated process. Pneumonectomy is a common thoracic surgical procedure that can cause pulmonary oedema in the remaining lung. Few reports have investigated the aetiology of this complication. The aim of this study was to determine the changes in ANP concentration and expression of its receptors following pneumonectomy as a possible aetiology for postpneumonectomy pulmonary oedema (PPE). We compared plasma ANP concentrations, cGMP concentrations, and natriuretic peptide receptor (NPR)-A mRNA and NPR-C mRNA expression in rat lung 3 h after pneumonectomy (n = 5) or a sham operation (n = 5). The ANP concentrations in plasma and lung tissue in the pneumonectomy group were significantly higher than in the control group (749.5 versus 202.7 pgċml-1, P < 0.01; 33.1 versus 6.8 ngċg-1 wet tissue, P < 0.01 respectively). The level of ANP mRNA expression in the pneumonectomy group was significantly higher than in the control group (1.44 versus 0.41 relative ANP mRNA expression, P < 0.05). The concentration of cGMP and the level of NPR-A mRNA expression were not significantly different between the pneumonectomy and control groups. The level of NPR-C mRNA expression in the pneumonectomy group was significantly higher than in the control group (4.17 versus 2.19 relative NPR-C mRNA expression, P < 0.01). These findings suggest that changes in pulmonary ANP and NPR-C expression may contribute to the development of PPE in the remaining lung in the acute phase following pneumonectomy.

Elevation of atrial natriuretic peptide prohormone. Hemodynamic background of the elevation of N-terminal natriuretic peptide prohormone in children with congenital heart disease

1999 ◽  
Vol 9 (2) ◽  
pp. 141-149 ◽  
Author(s):  
Henrik Holmström ◽  
Christian Hall ◽  
Oddvar Stokke ◽  
Harald Lindberg ◽  
Erik Thaulow
Keyword(s):  
Heart Failure ◽  
Congenital Heart Disease ◽  
Blood Flow ◽  
Heart Disease ◽  
Atrial Natriuretic Peptide ◽  
Likelihood Ratio ◽  
Natriuretic Peptide ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Atrial Natriuretic

AbstractWe postulated previously that variables related to pulmonary flow are independent predictors of levels of atrial natriuretic peptide in children with congenital heart disease. The aim of this study was to test this hypothesis in relation to other hemodynamic and clinical variables.During catheterization we measured the levels of plasma N-terminal atrial natriuretic peptide prohormone in the plasma of 68 children with congenital heart disease. All had undergone complete clinical, echocardiographic and invasive hemodynamic investigations. The influence on the prohormone was analyzed for 10 different variables in a multiple linear regression model. The variability could be explained in large parts (adjusted R2 = 77.2%) by variations in atrial pressures or sizes, together with the degree of excessive pulmonary blood flow and signs of heart failure.A value for atrial natriuretic peptide prohormone above 800 pmol/1 predicted hemodynamic imbalance (defined as elevated pressures in left or right atrium or the pulmonary arteries, and/or Qp/Qs > 1.5) with a specificity of 94%, a sensitivity of 73%, a positive likelihood ratio of 12.2, and a negative likelihood ratio of 0.29.In conclusion, variables related to pulmonary blood flow are influential determinants of the levels of atrial natriureic peptide in children with congenital heart disease. Atrial pressures, and symptoms of heart failure are also of major importance.

Response to dynamic exercise in cardiac transplant recipients: implications for control of the sodium regulatory hormone atrial natriuretic peptide

1990 ◽  
Vol 78 (2) ◽  
pp. 159-163 ◽  
Author(s):  
D. R. J. Singer ◽  
N. R. Banner ◽  
A. Cox ◽  
N. Patel ◽  
M. Burdon ◽  
...  
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Control Group ◽  
Cardiac Transplant ◽  
Cardiac Innervation ◽  
Transplant Recipients ◽  
Plasma Atrial Natriuretic Peptide ◽  
Control Subjects ◽  
Atrial Natriuretic

1. To study the importance of cardiac innervation in the regulation of atrial natriuretic peptide, plasma atrial natriuretic peptide levels were measured during symptom-limited, graded exercise on a cycle ergometer in seven male orthotopic cardiac transplant recipients. 2. Resting plasma atrial natriuretic peptide was significantly higher in the transplant recipients than in two control groups, one matched to the transplant recipients (group 1) and the other to the age of the donor heart (group II). 3. The response to exercise of the cardiac transplant recipients was compared with the response of control group II. Mean maximal work load achieved with exercise was around 40% lower in the cardiac transplant recipients. During exercise, plasma atrial natriuretic peptide levels increased in both the cardiac transplant recipients and the control subjects. The increase in plasma atrial natriuretic peptide with exercise was greater in absolute, but less in percentage, terms in transplant recipients than in the control subjects. 4. The increase in mean arterial pressure with exercise was similar in patients and in control subjects; however, heart rate increased in the patients by only 33% compared with a rise of 151% in the control group. 5. These results provide insight into the control of the sodium regulatory hormone atrial natriuretic peptide. First, factors other than a change in heart rate appear of importance in the regulation of atrial natriuretic peptide. Secondly, these findings suggest that cardiac innervation is not of dominant importance in the modulation of atrial natriuretic peptide secretion.

Sign in / Sign up

Export Citation Format

Share Document