Elevated plasma levels of adrenomedullin in congenital cyanotic heart disease

1999 ◽  
Vol 96 (6) ◽  
pp. 543-547 ◽  
Author(s):  
Muneo YOSHIBAYASHI ◽  
Tetsuro KAMIYA ◽  
Toshio NISHIKIMI ◽  
Yoshihiko SAITO ◽  
Hisayuki MATSUO ◽  
...  
Keyword(s):  
Heart Disease ◽  
Pulmonary Circulation ◽  
Venous Blood ◽  
Compensatory Mechanism ◽  
Cyanotic Heart Disease ◽  
Elevated Plasma ◽  
Arterial Blood ◽  
Pulmonary Uptake ◽  
Pulmonary Arterial ◽  
Congenital Cyanotic Heart Disease

Adrenomedullin is a novel hypotensive peptide originally isolated from human pheochromocytoma. Accumulating evidence suggests the possible involvement of adrenomedullin in the physiology of the pulmonary circulation and the pathophysiology of hypoxaemia. The aim of the present study was to investigate the pathophysiological significance of adrenomedullin in hypoxaemia caused by congenital cyanotic heart disease. Subjects were 16 patients with congenital cyanotic heart disease aged 0.8–10 years (Group C) and 12 age-matched control subjects (patients with coronary artery dilatation after Kawasaki disease; Group N). Plasma adrenomedullin concentrations were measured, using radioimmunoassay, in femoral venous, pulmonary arterial and pulmonary venous blood obtained during cardiac catheterization. Plasma adrenomedullin concentrations in Group C were significantly (3-fold) higher than those in Group N at all sampling sites. In Group C, plasma adrenomedullin concentrations in pulmonary venous blood were significantly lower than those in pulmonary arterial blood. Pulmonary uptake of adrenomedullin in Group C was significantly greater than that in Group N. Patients with congenital cyanotic heart disease showed elevated plasma adrenomedullin concentrations and an increased uptake of adrenomedullin in the pulmonary circulation, which may act to dilate pulmonary vessels and increase pulmonary blood flow to alleviate hypoxaemia. Intrinsically increased adrenomedullin levels may function as a compensatory mechanism for hypoxaemia in congenital cyanotic heart disease.

Influence of pulmonary blood flow on management and outcome

2011 ◽  
Keyword(s):  
Blood Flow ◽  
Heart Disease ◽  
Pulmonary Circulation ◽  
Early Life ◽  
Pulmonary Blood Flow ◽  
Venous Blood ◽  
Cyanotic Heart Disease ◽  
Capillary Membrane ◽  
Pulmonary Vascular Development ◽  
Alveolar Capillary

Introduction 50Pulmonary vascular development in early life 50Cyanotic heart disease and pulmonary blood flow 52Delivery of systemic venous blood to the alveolar capillary membrane to allow release of waste CO2 and uptake of O2 depends on the integrity of the pulmonary circulation. Too little blood flow to the lungs and the patient is hypoxic; too much and the lungs become oedematous....

Elevated plasma levels of adrenomedullin in congenital cyanotic heart disease

1999 ◽  
Vol 96 (6) ◽  
pp. 543 ◽  
Author(s):  
Muneo YOSHIBAYASHI ◽  
Tetsuro KAMIYA ◽  
Toshio NISHIKIMI ◽  
Yoshihiko SAITO ◽  
Hisayuki MATSUO ◽  
...  
Keyword(s):  
Heart Disease ◽  
Plasma Levels ◽  
Cyanotic Heart Disease ◽  
Elevated Plasma ◽  
Congenital Cyanotic Heart Disease

Cyanosis and Clipping: Noninfectious Aneurysm in a Patient with 22q11.2 Deletion Syndrome

2021 ◽  
pp. 1-5
Author(s):  
Bhanu Jayanand Sudhir ◽  
Sanjay Honavalli Murali ◽  
Jaypalsinh Gohil ◽  
Rajalakshmi Poyuran ◽  
Manikantan Sethuraman ◽  
...  
Keyword(s):  
Heart Disease ◽  
Cerebral Aneurysms ◽  
Artery Aneurysm ◽  
22Q11.2 Deletion Syndrome ◽  
Neurological Deficits ◽  
Deletion Syndrome ◽  
Anterior Communicating Artery ◽  
Cyanotic Heart Disease ◽  
22Q11.2 Deletion ◽  
Congenital Cyanotic Heart Disease

Noninfectious cerebral aneurysms are rare in patients with congenital cyanotic heart disease. We present a patient with DiGeorge/velocardiofacial syndrome with a complex congenital cyanotic heart disease with a ruptured anterior communicating artery aneurysm. The 10-year-old child was managed by surgical clipping of the aneurysm. Surgical challenges included prominent veins in the Sylvian fissure, difficulty in differentiating arterial and venous bleed, and anesthetic risks. The patient recovered without any neurological deficits. This is the first report of a patient with 22q11.2 deletion syndrome, with a noninfectious cerebral aneurysm.

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.

Selective coronary angiography via antegrade venous route in congenital cyanotic heart disease

1993 ◽  
Vol 28 (2) ◽  
pp. 179-182 ◽  
Author(s):  
Yunus S. Loya ◽  
Robin J. Pinto ◽  
Dhruman M. Desai ◽  
Usha Sundaram ◽  
Ajit R. Bhagwat ◽  
...  
Keyword(s):  
Heart Disease ◽  
Coronary Angiography ◽  
Cyanotic Heart Disease ◽  
Selective Coronary Angiography ◽  
Congenital Cyanotic Heart Disease

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

Histamine-induced pulmonary edema distal to pulmonary arterial occlusion

1985 ◽  
Vol 58 (4) ◽  
pp. 1092-1098 ◽  
Author(s):  
M. D. Walkenstein ◽  
B. T. Peterson ◽  
J. E. Gerber ◽  
R. W. Hyde
Keyword(s):  
Pulmonary Edema ◽  
Pulmonary Circulation ◽  
Arterial Occlusion ◽  
Arterial Blood Flow ◽  
Water Volume ◽  
Lung Water ◽  
Arterial Blood ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
The Right

Histological studies provide evidence that the bronchial veins are a site of leakage in histamine-induced pulmonary edema, but the physiological importance of this finding is not known. To determine if a lung perfused by only the bronchial arteries could develop pulmonary edema, we infused histamine for 2 h in anesthetized sheep with no pulmonary arterial blood flow to the right lung. In control sheep the postmortem extravascular lung water volume (EVLW) in both the right (occluded) and left (perfused) lung was 3.7 +/- 0.4 ml X g dry lung wt-1. Following histamine infusion, EVLW increased to 4.4 +/- 0.7 ml X g dry lung wt-1 in the right (occluded) lung (P less than 0.01) and to 5.3 +/- 1.0 ml X g dry wt-1 in the left (perfused) lung (P less than 0.01). Biopsies from the right (occluded) lungs scored for the presence of edema showed a significantly higher score in the lungs that received histamine (P less than 0.02). Some leakage from the pulmonary circulation of the right lung, perfused via anastomoses from the bronchial circulation, cannot be excluded but should be modest considering the low pressures in the pulmonary circulation following occlusion of the right pulmonary artery. These data show that perfusion via the pulmonary arteries is not a requirement for the production of histamine-induced pulmonary edema.

Determinants of platelet count in pediatric patients with congenital cyanotic heart disease: Role of immature platelet fraction

2017 ◽  
Vol 13 (1) ◽  
pp. 118-123 ◽  
Author(s):  
Randa M. Matter ◽  
Iman A. Ragab ◽  
Alaa M. Roushdy ◽  
Ahmed G. Ahmed ◽  
Hanan H. Aly ◽  
...  
Keyword(s):  
Platelet Count ◽  
Heart Disease ◽  
Pediatric Patients ◽  
Cyanotic Heart Disease ◽  
Immature Platelet Fraction ◽  
Congenital Cyanotic Heart Disease
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