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Biomedical subjects

B Crozatier

Publications and source records attributed to B Crozatier.

63 records · Page 4Linked to original sources
PubMed1977

In situ measurement of papillary muscle dynamics in the dog left ventricle.

In five open-chest dogs, pairs of ultrasonic dimension gauges were implanted in the anterior papillary muscle and in a circumferential subendocardial segment of the anterior left ventricular free wall, and simultaneous recordings were made with intracardiac pressure. The average shortening of the anterior segment in isovolumetric systole was 6% of end-diastolic length (EDL), with a total shortening of 19%. In the papillary muscles, isovolumetric shortening averaged 2%, total shortening was 10%, and shortening velocity was only 0.60 length/s. With acute pressure and volume overload, or inotropic interventions, changes in EDL were relatively less in papillary muscles than in the free wall. During acute occlusion of the anterior descending coronary artery, shortening of anterior segments and papillary muscles was replaced by holosystolic lengthening, and occlussion of the circumflex artery produced augmentation of shortening in both these regions, with lengthening of the posterior papillary muscle. The present study documents shortening of the anterior left ventricular papillary muscle throughout systole that is substantially less than that of the circumferential free wall, and demonstrates severe papillary muscle dysfunction with systolic elongation during regional ischemia.

Animals↗
PubMed1977

Loss of regional ventricular postextrasystolic potentiation after coronary occlusion in dogs.

Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.

Animals↗
PubMed1976

[Anomalous ventricular contractile performance in experimental chronic aortic insufficiency in the dog].

Hemodynamics and right (RV) and left (LV) ventricular performances of anaesthetized, closed-chest animals were studied in normal control dogs (N) and in dogs with aortic insufficiency (AI), the latter intervention being performed 33 months before verification. In dogs with AI, LV was hypertrophied (N = 49.6 +/- 6.3 g; AI = 98.7 +/- 10.1, p less than 0.001); forward stroke volume was slightly decreased (N = 20.0 +/- 2.2 ml; IA = 14.6 +/- 5.4 ml, p = NS);LV and diastolic pressure was increased (N = 9.4 +/- 1.4 mmHg; IA = 16.7 +/- 2.9, p less than 0.05); both RV and LV myocardial performace index (e.g. dP/dt max, peak VCE, Vmax) were normals. Relative pressure/velocity of shortening and wall stress/velocity of shortening relationships, however, were decreased, when measured during L.V. isovolumetric beats. LV stiffness of arrested heart was increased in proportions with hypertrophy extent. Thus, myocardial performance of chronically volume-overloaded heart appears to be depressed before the stage of the circulatory failure.

Animals↗
PubMedDate not supplied

Cardiac ultrastructural abnormalities in Syrian hamsters with spontaneous cardiomyopathy or subjected to cardiac overloads.

Ultrastructural and morphometric abnormalities of Syrian hamster cardiomyopathy were compared to those observed in two different models of cardiac hypertrophy produced by mechanical overload (abdominal aortic stenosis, 60-day duration) or by isoproterenol injection during 15 days in normal Syrian hamsters of the same strain. Aspects of increased protein synthesis were observed in all three groups of animals. This was the only abnormality observed in the aortic stenosis group. Cardiomyopathy was different from the two other types of overload by the existence of large calcium deposits inside of the myocytes, by the presence of thin filaments and amorphous material accumulation suggesting abnormal synthesis and by a significant reduction of myofibrils at the heart-failure phase. Nuclear abnormalities with nuclear constrictions suggesting a division process and an increased number of myocytes with two nuclei were present in both spontaneous cardiomyopathy and isoproterenol-induced cardiopathy. Therefore, Syrian hamster cardiomyopathy appears to be different from cardiopathy induced by hemodynamic overload but, in spite of specific aspects, resembles that induced by isoproterenol injections, strengthening the hypothesis of a pathogenic role of catecholamines in the Syrian hamster cardiomyopathy.

Animals↗
PubMedDate not supplied

Diameters and segment relations during the cardiac cycle in the canine left ventricle.

The relations between left ventricular antero-posterior, septum-free wall diameters and an anterior subendocardial segment were studied by sonomicrometry in seven open-chest anesthetized dogs, during the control state and during left ventricular and right ventricular pressure overload for low and high left ventricular filling pressures. A linear relationship between antero-posterior and septal-free wall shortening was observed during control and during left ventricular pressure overload when left ventricular filling pressure was high. For low end-diastolic ventricular pressure, there was the same relationship during ejection with an isovolumic lengthening of the septal-free wall diameter. This relationship was shifted downwards during pulmonary artery stenosis for both high and low left ventricular filling pressure, which produced a significant decrease in end-diastolic septum-free wall diameter without significant modifications of end-diastolic antero-posterior diameter. The anterior segment exhibited behavior similar to that of the calculated left ventricular circumference. Subendocardial anterior segment measurements in the open-chest dog model can be used as indices of left ventricular circumference.

Animals↗
PubMedDate not supplied

Pulsus alternans in regionally hypoxic ventricles of open-chest dogs: regional mechanical alternation of potentiation and attenuation of the inotropic state.

Sustained mechanical alternation appeared after a spontaneous premature ventricular contraction in 6 open-chest dogs during the perfusion of the left circumflex coronary artery by Krebs-Henseleit solution equilibrated with 5% CO2 and 95% N2. The animals were instrumented with a catheter in the left ventricle and ultrasonic crystals in hypoxic and control segments. Left ventricular systolic pressure was significantly higher in the strong than in the weak beats with no significant difference of end-diastolic lengths in hypoxic and control segments. In hypoxic segments, systolic shortening was significantly larger in strong beats (11.9 +/- 1.9%) as compared with weak beats (5.1 +/- 1.6%) and with control beats preceding the premature ventricular contraction (9.7 +/- 1.6%) but the postextrasystolic beat was larger (17.9 +/- 1.3%). There was no significant change of systolic shortening in control segments during mechanical alternation which appears thus as a regional phenomenon which cannot be explained by the Starling mechanism: instead, alternation is attributed to a change of excitation-contraction coupling after a premature contraction with alternation of potentiation and attenuation of the inotropic state.

Animals↗
PubMedDate not supplied

Adenine nucleotide content and regional function during ischemia and reperfusion in canine ventricular myocardium.

We have compared in open-chest dogs the evolution of adenine nucleotides and creatine phosphate to that of regional mechanical function during ischemia and reperfusion. Reperfusion restored normal value of creatine phosphate whereas adenine nucleotide level remained depressed. The percentage of systolic shortening, which after occlusion has a zero or negative value, increased to about 20% of control, after reperfusion similarly the pressure-length loop areas decreased to 14.9% of control during ischemia and increased to 39.3% of control during the early phase of the reperfusion period. No individual correlation was found between the ATP content and segmental function during ischemia or reperfusion, suggesting that a low level of ATP did not prevent some restoration of mechanical function. However, the ATP content measured at the end of the ischemic period was correlated with mechanical function measured 75 min after reperfusion, and thus ATP depletion could appear as an indicator of the severity of ischemic damage.

Adenine Nucleotides↗
PubMedDate not supplied

Preserved vasodilator effect of bradykinin in dogs with heart failure.

BACKGROUND: In heart failure (HF), vasoconstrictor systems are activated and endothelium-derived vasodilation is blunted. Bradykinin, a potent vasodilator, may play an important role in this setting. However, it is not known whether its vasodilator effect is modified in HF. METHODS AND RESULTS: Fourteen chronically instrumented dogs were studied in the control state and in pacing-induced HF (250 bpm for 3 weeks). The dose-dependent decrease in mean aortic pressure (MAP) induced by acetylcholine was significantly blunted in HF. In contrast, in both control and HF, bradykinin infusion caused similar dose-dependent decreases in MAP and increases in cardiac output (CO). This vasodilator effect of exogenous bradykinin was potentiated similarly in both states by enalaprilat, which blocks both angiotensin conversion and bradykinin degradation. For evaluating the role of endogenous bradykinin, the effects of enalaprilat were compared with those of ciprokiren, a pure renin inhibitor. In control, ciprokiren did not produce any effect. Enalaprilat, however, produced a significant decrease in MAP and a significant increase in CO, which were attributed to the inhibition of bradykinin degradation, because these effects were absent after pretreatment with Hoe 140 (a bradykinin B2 receptor antagonist). In contrast, in HF, vasodilator effects of ciprokiren were observed, but enalaprilat produced larger changes in MAP and CO, and after Hoe 140, the hemodynamic effects of enalaprilat were significantly decreased, showing the effects of endogenous bradykinin, which were similar to those measured in control. CONCLUSIONS: In this model of HF with a blunted endothelium-derived vasodilation, the vasodilator effects of exogenous and endogenous bradykinin are preserved. These results suggest that bradykinin may play an important role in HF, in which vasoconstriction is present and endothelium-dependent vasodilation is blunted.

Acetylcholine↗