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Veterinary Resources This is a list of citations and summaries of veterinary research journal articles which are applicable to mitral valve disease and cavalier King Charles spaniels. This list is in chronological order, from to the current date, with the most recent additions added at the bottom of this page. Hyper-linked titles are linked to the actual articles which are available on-line. Angiocardiograms are radiographs made while a radiopaque medium is circulating through the heart and closely associated vessels.
In selective angiocardiography, the contrast medium is injected through a catheter, the tip of which has been positioned into a specific vessel or cardiac chamber to visualize best a suspected abnormality based upon the clinical findings.
The principles in selecting the chamber or vessel for the injection are based primarily upon the knowledge that cardiac valves are normally unidirectional and blood pressures in the left atrium, left ventricle, and aorta normally exceed the pressures in corresponding right heart structures.
In dogs with suspected valvular insufficiencies, injections are made into the vessel or cardiac chamber from which the contrast medium would regurgitate i. Patent ductus arteriosus, as in man, was found predominantly in females.
Breed-specific prevalence rates were significantly greater in purebred dogs than in mongrels, and the breed distributions of patent ductus arteriosus, pulmonic stenosis, subaortic stenosis, persistent right aortic arch, and tetralogy of Fallot were significantly different than would be expected if all breeds were equally susceptible to each type of malformation.
On the basis of these observations, two hypotheses were made: Preliminary genetic studies confirmed the specific hereditary transmission of valvular pulmonic stenosis in beagles, persistent right aortic arch in German shepherds, and conal septal defects including ventricular septal defects and tetralogy of Fallot in keeshonden.
The pattern of inheritance of these defects was not consistent with any simple genetic hypothesis. Patent ductus arteriosus in dogs of poodle ancestry and fibrous subaortic stenosis in Newfoundlands were shown provisionally to be transmitted in a manner consistent with autosomal dominant inheritance. The significance of these findings is considered in relation to present and future understanding of the etiology and pathogenesis of congenital heart disease.
Mason, Eugene Braunwald, James W. Sonnenblick, John Ross, Jr. Constriction of the pulmonary artery or thoracic inferior vena cava was maintained for 2 wk while daily measurements were made of plasma renin activity, plasma aldosterone, plasma volume, hematocrit, serum sodium and potassium concentrations, sodium and water balance, body weight, and arterial, caval, and atrial pressures.
The initial response to constriction was a reduction in blood pressure, a rise in plasma renin activity, plasma aldosterone, and water intake, and nearly complete sodium retention. In the days after moderate constriction plasma volume and body weight increased with development of ascites and edema ; blood pressure, sodium excretion, plasma renin acvitity, and plasma aldosterone returned to normal. In animals in which blood pressure was not restored, plasma renin activity and plasma aldosterone remained elevated throughout the period of constriction.
Single injections of converting enzyme inhibitor reduced blood pressure when plasma renin activity was elevated. Chronic infusion of the inhibitor in dogs with thoracic inferior vena caval constriction prevented the restoration of blood pressure and suppressed the rise in plasma aldosterone; sodium retention and volume expansion were less than in control experiments.
Thus the renin-angiotensin-aldosterone system plays an essential role in the maintenance of blood pressure during the genesis of congestive failure. Initially, the restoration of blood pressure is dependent upon circulating angiotensin II; in the later stages, blood pressure is dependent upon the increase in plasma volume.
Lowell Maughan, Artin A. Shoukas, Kiichi Sagawa, Myron L. The instantaneous isovolumic and ejecting pressure-volume relationship of the right ventricle was studied in 11 cross-circulated, isolated canine hearts to characterize the right ventricular contractile state.
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Accurate measurement of volume was achieved by the use of a water-filled, thin latex balloon in the right ventricle connected to a special volume loading and transducing chamber. Pressure was measured with a miniature pressure transducer mounted within the balloon. Wide variations in loading conditions were achieved by changing the volume of air above the volumetric chamber.
The pressure and volume data were collected from multiple beats under a constant contractile state in the same mode of contraction while the left ventricle was vented to air. Linear regression analysis applied to each of the isochronal pressure-volume data sets at msec intervals from the onset of contraction showed a highly linear correlation between the pressure and the volume.
Both the slope and the volume intercept of the regression lines changed with time throughout the cardiac cycle. The maximal slope of the regression line E,,,, averaged 2. Epinephrine infusions of J Appl Physiol ; Rapid shallow breathing evoked by selective stimulation of airway C fibres in dogs. J Physiol Vol pp Myocardial function in small dogs with chronic mitral regurgitation and severe congestive heart failure.
Mitral Valve Disease and the Cavalier King Charles Spaniel -- Veterinary Resources
End-systolic diameters were measured on echocardiograms and end-systolic volume indices were calculated. These data suggested that myocardial failure is not a prominent factor contributing to signs of heart failure in dogs with mitral regurgitation. Because of these data, the routine use of digitalis glycosides to increase cardiac contractility is seriously questioned in dogs with heart failure secondary to chronic mitral regurgitation.
This study suggests that the contractile performance of the left ventricle in most dogs with chronic mitral valve fibrosis and clinical evidence of severe congestive heart failure is either normal or mildly depressed. This suggests that congestive heart failure in these patients is due to severe regurgitation and subsequent volume overload of the left ventricle and atrium.
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Heart failure secondary to mitral regurgitation can be due not only to myocardial failure, but also to severe regurgitation by itself or in combination with myocardial failure. Vet Radiol March ;27 2: Two-dimensional echocardiography was performed on 18 unanesthetized, normal dogs 4.
Measurements of wall thickness, intracavitary dimensions, and cross-sectional area of the left atrium, left ventricle, and aorta were made. Satisfactory data were obtained from 17 dogs, and were used to determine normal values. Normal data were tested for significant correlation to body weight kg by linear regression.
Repeatability was studied in six dogs examined, on three separate occasions, during a 5-day period. Differences between values obtained on different days were evaluated by analysis of variance. Satisfactory qualitative echocardiograms were repeatedly obtained by using consistent sites of transducer placement and by identifying internal cardiac structures.
Almost all linear and area measurements were significantly correlated to body size, while most indices of left ventricular function were independent of body weight. Dimensions obtained from the left and right parasternal position were nearly identical.
Cross-sectional echocardiography allows repeatable assessment of cardiac anatomy, and it should prove useful for identification and quantitation of heart disease in the dog. The pharmacology of ketanserin, the first selective serotonin S2-antagonist. Ketanserin was a potent, orally very effective antagonist of endogenous serotonin 5-HT: Many other in vivo observations, such as antagonism of tryptamine-induced cyanosis in rats ED50 s.
In these experiments, ketanserin was devoid of serotonin! The absence of all these secondary activities is pharmacologically characteristic for ketanserin when compared to known serotonin-antagonists. On the basis of this profile of pure and selective serotonin S2-antagonism, ketanserin was studied in experimental hypertension and in many spontaneous and induced circulatory dysfunctions.
A prolonged antihypertensive effect can be obtained with ketanserin in the absence of distinct compensatory mechanisms. Vascular dysfunction can start at low, sensitizing concentrations of serotonin and be almost completely corrected by ketanserin, despite the involvement of other mediators.
Ketanserin is a very effective antagonist of the mixture of vasoactive substances released by aggregating platelets. In experimental thrombosis, sustained ketanserin treatment prevents the impairment of blood flow and the associated organ deficiency. When deviations from normal hemorrheology are long-standing, as in aged spontaneously hypertensive dogs, acute ketanserin administration is distinctly antihypertensive and reduces hemorrheological abnormalities.
At the conclusion of these extensive studies, serotonin appears to act at peripheral S2-receptors as the primary pathological mediator of vascular congestion. Enhanced recovery of diastolic function after global myocardial ischemia in the intact animal.
Kevin Tveter, John St. The purpose of this study was to determine the effects of enhancing ATP recovery on postlsc function. High energy phosphate levels are depressed following global ischemia and require several days to completely recover. Several precursors have been used to augment adenine nucleotide synthesis including adenosine, inosine, adenine, and ribose.
Because of the short-term nature of previous experiments, recovery had been incomplete and the effects in the intact animal unknown. The purpose of this study was to determine the effects of ribose infusion in a long-term model of global ischemia and attempt to identify the precursor which limits myocardial ATP regeneration in the intact animal.
Ventricular biopsies were obtained through an indwelling ventricular cannula prior to ischemia, at the end of ischemia, and 4 and 24 hr postischemia and analyzed for adenine nucleotides and creatine phosphate levels.
Radiolabeled microspheres were used to measure myocardial and renal blood flows and no significant difference was found between ribose-treated control groups. Total myocardial adenine nucleotide content and energy charge also recovered in the ribose group but not in the control animals. The ribose infusion, therefore, significantly enhanced the recovery of energy levels in the postischemic myocardium in the intact animals. Effects of the positive inotropic agents milrinone and pimobendan on the development of lethal ischemic arrhythmias in conscious dogs with recent myocardial infarction.
The effects of milrinone and pimobendan upon the initiation of programmed ventricular stimulation-induced ventricular tachycardia VT and the incidence of lethal ischemic ventricular arrhythmias were assessed in conscious dogs with recent anterior myocardial infarctions. Based upon the results of previous studies, the animals which were entered into this investigation were nonresponsive to baseline programmed stimulation and, therefore, considered to be at "low risk" toward the development of subsequent lethal ischemic arrhythmias.
At the time of repeat electrophysiologic testing, 9 of 9 pimobendan-, 9 of 10 milrinone-, and 12 of 12 concurrent vehicle-treated animals remained nonresponsive to programmed ventricular stimulation. Milrinone, but not pimobendan, delayed the onset of acute posterolateral myocardial ischemia in the postinfarction dogs. The predominant electrophysiologic effects of both milrinone and pimobendan were decreases in ventricular refractoriness in both non-infarct NZ and in infarct zones IZ , as well as reductions in electrocardiographic QTc or QT intervals.
These findings suggest that with both positive inotropic agents, including milrinone which may possess protective antithrombotic action, sudden death may be increased via a reduction in ventricular refractoriness in the ischemically injured heart.
In this investigation, both pimobendan and milrinone administration resulted in a significant increase in the incidence of sudden ischemic ventricular fibrillation In the present investigation, both milrinone and pimobendan, administered in equivalently inotropic dosing regimens to "low risk" postinfarction dogs, increased the incidence of sudden primary ventricular fibrillation and of total h mortality occurring in response to the development of posterolateral myocardial ischemia and previous anterior myocardial infarction.
The enhanced susceptibility toward the development of ischemic ventricular arrhythmias in the presence of the inotropic interventions is not predicted by programmed ventricular stimulation testing prior to the ischemic event.
Hence, these findings suggest that with both positive inotropic agents, including milrinone which may possess protective antithrombotic action, sudden death may be increased via a reduction in ventricular refractoriness in the ischemically injured heart. It is possible that such a deleterious electrophysiologic action might occur at lower dosages in the setting of more severe myocardial ischemic injury.
Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure. Patients with heart failure frequently exhibit abnormal skeletal muscle metabolic responses to exercise, as assessed with 31P NMR.
To investigate whether these metabolic abnormalities are due to intrinsic skeletal muscle changes, we performed gastrocnemius muscle biopsies on 22 patients with heart failure and on eight normal subjects.
Biopsies were analyzed for fiber type and area, capillarity, citrate synthase, phospho-fructokinase, lactate dehydrogenase, and beta-hydroxyacyl CoA dehydrogenase activity. All patients with heart failure also underwent 31P NMR studies of their calf muscle during plantarflexion at three workloads.
Compared with normal subjects, patients with heart failure exhibited a shift in fiber distribution with increased percentage of the fast twitch, glycolytic, easily fatigable type IIb fibers, atrophy of type IIa and type IIb fibers, and decreased activity of beta-hydroxyacyl CoA dehydrogenase. Type IIb fibers represent fibers that are fast twitch, have a low aerobic potential, and are easily fatigued. Similarly, no linear relation was found between intracellular pH at peak exercise and any muscle variable.