Pulmonary Impedance and Right Ventricular-Vascular Coupling in Endotoxin Shock

in Cardiovascular Research (1998), 38(2), 375-82

OBJECTIVE: We tested the hypothesis that right heart failure during endotoxin shock may result from altered ventriculovascular coupling responsible for impeding power transfer to the pulmonary circulation ... [more ▼]

OBJECTIVE: We tested the hypothesis that right heart failure during endotoxin shock may result from altered ventriculovascular coupling responsible for impeding power transfer to the pulmonary circulation. METHODS: The changes in vascular pulmonary input impedance and right ventricular contractility produced by low-dose endotoxin infusion were studied in 6 intact anesthetized dogs. RESULTS: Endotoxin insult resulted in pulmonary hypertension (from 22 +/- 2 to 33 +/- 3 mmHg) associated with significant decreases in stroke volume (from 26.9 +/- 4 to 20.2 +/- 3 ml) and right ventricular ejection fraction (from 41 +/- 3 to 32 +/- 2%). The first minimum of input impedance spectrum and zero phase were shifted towards higher frequencies. Input resistance and characteristic resistance were dramatically increased. The latter change contributed to a significant increase in the pulsatile component of total right ventricular power output from 13 to 21%, indicating a reduction in the hydraulic right ventricle power output delivered into the main pulmonary artery. Overall changes in input pulmonary impedance were indicative of increased afterload facing the right ventricle leading to depressed performance. In contrast, right ventricular systolic elastance was simultaneously increased from 0.56 to 0.93 mmHg/ml indicating an increase in right heart contractility. CONCLUSION: These data suggest that pulmonary hypertension in the setting of experimental endotoxin shock is accompanied by deleterious changes in the pulmonary impedance spectrum, which are responsible for a mismatch of increased contractile state of the right ventricle to the varying hydraulic load ultimately leading to ventricular-vascular uncoupling. [less ▲]

Comparison between Three- and Four-Element Windkessel Models to Characterize Vascular Properties of Pulmonary Circulation

in Archives of Physiology & Biochemistry (1997), 105(7), 625-32

In 11 anaesthetised pigs the accuracy of the three-element (WK3) and the four-element (WK4) Windkessel models to describe hemodynamic properties of the pulmonary circulation was compared during six ... [more ▼]

In 11 anaesthetised pigs the accuracy of the three-element (WK3) and the four-element (WK4) Windkessel models to describe hemodynamic properties of the pulmonary circulation was compared during six different experimental conditions increasing pulmonary arterial pressure: increase in left atrial pressure, increase in alveolar pressure, increase in pulmonary blood flow, endotoxin shock, mechanical obstruction of left pulmonary artery or histamine infusion. Our results showed that WK4 fitted better the data than did WK3 because values of 1-R2 decreased from 6 percent (WK3) to 1.4 percent (WK4) when WK4 was used (P < 0.0005). 1-R2 was an adequate marker of the accuracy of the linear regression used to solve equations of both models. Compliance values estimated by WK4 were decreased by 5% comparatively to WK3 (P = 0.008). However, this difference can be considered as not physiologically relevant. Values of characteristic resistance corresponding to R1 + (L/R2C) in WK4 and to R1 in WK3 were not different (P = 0.22). The relative changes in R1, R2, and C observed due to the different experimental conditions were comparable regardless of the model. In conclusion, the conversion of WK3 in WK4 by adding an inductance, whose physiological meaning is not clear, resulted in an increased statistical accuracy of the model, but did not seem to have relevant influence on parameters or their evolution during experimental conditions. [less ▲]

Accident vasculaire cérébral et thrombus aortique chez un patient déficient en protéine S

in Archives des Maladies du Coeur et des Vaisseaux (1997), 90(1), 99-102

The authors report the case of a 50 year old man admitted to hospital with a right hemiplegia and aphasia of sudden onset in whom embolic fragments were found in the left mid and anterior cerebral artery ... [more ▼]

The authors report the case of a 50 year old man admitted to hospital with a right hemiplegia and aphasia of sudden onset in whom embolic fragments were found in the left mid and anterior cerebral artery territories at left carotid angiography : transoesophageal echocardiography demonstrated a protrusive plaque of atherosclerosis in the ascending aorta and a pediculated thrombosis in the descending aorta. Biological investigations revealed a protein S level of 3% (normal : 70-140%). This case illustrates the acute development of a thromboembolic phenomenon originating from the aortic arch in a patient with a coagulation defect. [less ▲]

Consequences of cold and warm ischemia on pulmonary mitochondrial respiratory function.

in Transplantation Proceedings (1997), 29

IN RECENT years, pulmonary transplantation has become the treatment of choice for several end-stage lung diseases, but remains limited by the scarcity of suitable donors and the lack of reliable prolonged ... [more ▼]

IN RECENT years, pulmonary transplantation has become the treatment of choice for several end-stage lung diseases, but remains limited by the scarcity of suitable donors and the lack of reliable prolonged method of lung preservation.1 Transplantation of lung 6 hours postharvest leads to an increased incidence of primary graft dysfunction, due in part to ischemic damage of pulmonary cell structure and metabolism, and to acute reperfusion injury. However, very little is known about the real mechanisms of pulmonary cell injuries before, during, and after lung transplantation. During ischemia, the cytosolic and mitochondrial adenine nucleotide content falls,2,3 phospholipids are degraded, membrane permeabilities are increased, and the cytosolic levels of Na+, Ca2+ and phosphate are raised.4 Thus, cold and warm ischemia may induce cell dysfunctions and irreversible injuries responsible for necrosis. As mitochondia are believed to be the site of the determinants of irreversibility,5 the study of permanent oxidative phosphorylation damage after ischemia should be of great interest. The aim of this present study was to investigate the consequences of warm and cold ischemia on the oxidative phosphorylation of isolated lung mitochondria [less ▲]

Le cas clinique du mois. Physiopathologie, symptômes, complications et traitement de l'acidocétose alcoolique : a propos d'un cas mortel

in Revue Médicale de Liège (1996), 51(4), 266-9