Endogenous angiotensin II in the regulation of hypoxic pulmonary vasoconstriction in anaesthetized dogs

INTRODUCTION: The role played by several vasoactive mediators that are synthesized and released by the pulmonary vascular endothelium in the regulation of hypoxic pulmonary vasoconstriction (HPV) remains unclear. As a potent vasoconstrictor, angiotensin II could be involved. We tested the hypothesis that angiotensin-converting enzyme inhibition by enalaprilat and type 1 angiotensin II receptor blockade by candesartan would inhibit HPV. METHODS: HPV was evaluated in anaesthetized dogs, with an intact pulmonary circulation, by examining the increase in the Ppa–Ppao gradient (mean pulmonary artery pressure minus occluded pulmonary artery pressure) that occurred in response to hypoxia (inspiratory oxygen fraction of 0.1) at constant pulmonary blood flow. Plasma renin activity and angiotensin II immunoreactivity were measured to determine whether activation or inhibition of the renin–angiotensin system was present. RESULTS: Administration of enalaprilat and candesartan did not affect the Ppa–Ppao gradient at baseline or during hypoxia. Plasma renin activity and angiotensin II immunoreactivity increased during hypoxia, and subsequent measurements were consistent with effective angiotensin-converting enzyme inhibition after administration of enalaprilat, and with angiotensin receptor blockade after administration of candesartan. CONCLUSION: These results suggest that, although the renin–angiotensin system was activated in hypoxia, angiotensin II is not normally involved in mediating acute HPV

Successful management of Influenza A associated fulminant myocarditis: mobile circulatory support in intensive care unit: a case report

A 26-year-old woman was referred to an Emergency Department because of common flu-like syndrome with hemodynamic collapse. In Intensive Care Unit (ICU), she was diagnosed as a probable septic shock. But despite treatment her condition rapidly deteriorated during the subsequent hours. Diagnosis of cardiogenic shock was established. Mechanical circulatory support was inserted into the patient. She was transferred in a Cardio-Vascular Surgical ICU where at the 5th day of mechanical circulatory support, echocardiography showed heart recovery which allowed weaning of mechanical circulatory support and progressive withdrawal of inotropic support. She was discharged at the 26th day. During her hospitalization, presence of Influenza A RNA was shown in myocardial biopsy

Acute Pulmonary Embolism Decreases Adenosine Plasma Levels in Anesthetized Pigs

Adenosine plays a role in pulmonary arterial (PA) resistance due to its vasodilator properties. However, the behavior of adenosine plasma levels (APLs) during pulmonary embolism remains unknown. We investigated the effects of gradual pulmonary embolism on right ventricular (RV) contractility and PA coupling and on APLs in an piglet experimental model of RV failure. PA distal resistance by pressure-flow relationships and pulmonary vascular impedance were measured. RV contractility was determined by the end-systolic pressure-volume relationship (Ees), PA effective elastance by the end-diastolic to end-systolic relationship (Ea), and RV-PA coupling efficiency by the Ees/Ea ratio. APLs were measured before and during gradual pulmonary embolization. PA embolism increased PA resistance and elastance, increased Ea from 1.08 ± 0.15 to 5.62 ± 0.32 mmHg/mL, decreased Ees from 1.82 ± 0.10 to 1.20 ± 0.23 mmHg/mL, and decreased Ees/Ea from 1.69 ± 0.15 to 0.21 ± 0.07. APLs decreased from 2.7 ± 0.26 to 1.3 ± 0.12 μM in the systemic bed and from 4.03 ± 0.63 to 2.51 ± 0.58 μM in the pulmonary bed during embolism procedure. Pulmonary embolism worsens PA hemodynamics and RV-PA coupling. APLs were reduced, both in the systemic and in the pulmonary bed, leading then to pulmonary vasoconstriction

Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness

Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder. Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013–June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia. We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 0.66 ± 1.50 μg/L; DCS: 0.0061 ± 0.0040; controls: 0.0090 ± 0.01; IPE versus DCS or controls: P < 0.01). The combined “BNP-cTnI” levels provided most discrimination: all IPE patients, but none of the DCS patients, had elevated levels of either/both of these markers. We propose that antidiuretic hormone acts together with a myocardial ischemic process to promote IPE. Thus, monitoring of antidiuretic hormone and cardiac biomarkers can help to make a quick and reliable diagnosis of IPE

Assistances circulatoires lourdes (Indications , complications, suivi évolutif sur une cohorte de 33 patients)

AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Rôle prédictif de l'adénosine, de l'albumine modifiée et de la troponine Ic dans la survenue d'un SIRS sévère post chirurgie cardiaque avec CEC

AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Facteurs prédictifs de mortalité, analyse de la morbidité et de la qualité de vie des patients opérés d'une implantation valvulaire aortique percutanée

AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocSudocFranceF

Endocardites en réanimation (données épidémiologiques et facteurs de risque de mortalité)

AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocSudocFranceF

Epargne transfusionnelle et économie financière générées par l'acide tranexamique dans les arthroplasties de hanche et de genou

AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocSudocFranceF

Facteurs prédictifs de mortalité, analyse de la morbidité et de la qualité de vie des patients ayant bénéficié d'une assistance circulatoire extra corporelle mobile pour choc cardiogénique réfractaire

AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocSudocFranceF