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PubMed1987

Immunohistochemical study of atrial natriuretic polypeptides in the embryonic, fetal and neonatal rat heart.

An immunohistochemical study of atrial natriuretic polypeptides was carried out on embryonic, fetal and neonatal rat hearts, using an antiserum raised against alpha-human atrial natriuretic polypeptide (alpha-hANP). Weakly immunoreactive cells were seen in both atrial and ventricular walls at 11 days post coitum (pc). After this stage, the immunoreactive cells became more intensely stained in both atrial and ventricular walls. The immunoreactivity during the prenatal period was stronger in the superficial cell layer beneath the endocardium, than in the deep cell layer of the atrial wall. The cells in the trabecular meshwork also had an apparent, but weak, immunoreactivity, which showed a greater intensity in the left ventricle than in the right one. It is suggested that these immunoreactive cells in the ventricle may differentiate, in situ, into the cells of the impulse-conducting system during the further development of the heart.

Animals↗
PubMed1984

Distribution of vasoactive intestinal polypeptide-like immunoreactivity in the mammalian heart. Interrelation with neurotensin- and substance P-like immunoreactive nerves.

The distribution of vasoactive intestinal polypeptide (VIP) immunoreactivity has been studied in the mammalian heart and compared with that of neurotensin and substance P by use of light-microscopic peroxidase-antiperoxidase immunohistochemistry. VIP-immunoreactive cell bodies are present in intracardiac ganglia in various locations. VIP-immunoreactive nerve fibers predominate in the atria and the conduction system but are rare in the ventricles and occur in cardiac ganglia, endocardium, and epicardium. VIP-ergic nerves supply the coronary vasculature having a preference for the microvasculature and the nodal cells of the sinuatrial node. The large vessels of the heart and periarterial cardiac glomera also receive a VIP-immunoreactive nerve supply. There is partial co-distribution with neurotensin- and substance P-immunoreactive nerve fibers but no co-location in identical nerve fibers is detectable. The VIP-ergic cardiac innervation, which is probably predominantly intrinsic, may stem from postganglionic parasympathetic neurons and is less substantial than the more homogeneous neurotensin-ergic and substance P-ergic nervous supply which is probably extrinsic. The occurrence of an extrinsic VIP-ergic cardiac innervation cannot be excluded however. The differential histotopography of the multitarget cardiac nerves containing the cardiovascular active peptides VIP, neurotensin and substance P may suggest multiple and complex peptide-peptide and peptide-classical transmitter interactions. These may contribute to the regulation of various cardiac functions.

Animals↗
PubMed1986

Distribution and origin of substance P- and neuropeptide Y-immunoreactive nerves in the guinea-pig heart.

The localization and origin of substance P (SP)-, neuropeptide Y (NPY)-, and noradrenaline/tyrosine hydroxylase (NA/TH)- immunoreactive (IR) nerves in the guinea-pig heart were investigated by means of immunohistochemistry; quantitative analysis was performed by radio-immunoassay (NPY) and high performance liquid chromatography (NA). Both untreated animals and animals subjected to stellatectomy, combined stellatectomy and local capsaicin pretreatment of the vagal nerves or systemic application of capsaicin were studied. A dense network of SP-IR nerves was observed in the right atrium in different locations: (1) around local cardiac ganglion cells, (2) close to blood vessels, (3) within the myocardium, and (4) close to and within peri- and endocardium. A moderately dense SP-innervation, mainly related to blood vessels, was found in the ventricles. Very dense networks of NPY- and TH-IR nerve fibers with an overlapping distributional pattern around blood vessels and in the myocardium were seen in both the atria and the ventricles. In addition, some cell bodies in local cardiac ganglia were NPY-IR. Bilateral stellatectomy resulted in a reduction of SP-IR in the right atrium (55% of control), which was more pronounced after additional capsaicin pretreatment of the vagal nerves (44% of control). In the left ventricle no significant depletion of SP-IR was seen by either stellatectomy or combined stellatectomy and capsaicin treatment of the vagal nerves. It was not possible to establish any defined target areas within the heart for vagal or spinal SP-IR afferents by use of immunohistochemical methods. Systemic capsaicin treatment caused a total loss of SP-IR nerves in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Atrial natriuretic factor in the impulse-conduction system of rat cardiac ventricles.

A complex network of atrial natriuretic factor-producing cells has been delineated by biochemical and morphological techniques in the rat ventricular myocardium. The chordae tendineae spuriae (CTS; false tendons) contain ANF mRNA and the ANF propeptide (Asn 1-Tyr 126) as assessed by Northern blot analysis, high-pressure liquid chromatography and immunohisto- and -cytochemistry, using three different affinity-purified antibodies: monoclonal and polyclonal antibodies against C-terminal ANF (Arg 101-Tyr 126) and polyclonal antibodies against N-terminal ANF (Asp 11-Ala 37). Two types of cells harboring ANF-containing secretory granules constitute the CTS: the majority (Purkinje type I) have ultrastructural similarities with both atrial and classical Purkinje fibers. Purkinje type-II fibers resemble working ventricular cardiocytes. Both cell types harbor a large paranuclear Golgi complex. The subendocardial Purkinje network is also made up of these two cell types. In this location, Purkinje type-I fibers form cable-like structures while Purkinje type-II fibers are either located beneath the former or abut directly on the endocardium. The latter are not separated from adjacent working ventricular cardiocytes by connective tissue septa. Coronary arteries and arterioles, as in birds, are surrounded by a cushion of Purkinje type-II fibers which blend with the surrounding myocardium. These results indicate that, in the rat, the entire intraventricular conduction system is constituted of endocrine cells producing ANF.

Animals↗
PubMed1983

Structural organization of the normal and anoxic heart of Scyllium stellare.

The general and ultrastructural organization of the heart of the elasmobranch, Scyllium stellare, was studied in normal and in anoxic animals. The rich coronary supply was revealed three-dimensionally by the use of corrosion casts, showing a thebesian system of coronary arterioles and capillaries in the thin, outer compact layer as well as in the predominant, inner spongy layer of trabeculae. Only the sinus venosus received a neuronal input of large bundles of granule-containing axons terminating at fenestrated regions of the endocardium and suggesting a neurohormonal function. A simple, tubular sarcoplasmic reticulum with flattened junctional cisternae was present in myocardial cells of 1-5 microns diameter, which contained one or two bundles of myofibrils. The latter were closely apposed to the inner aspect of the plasmalemma. Mitochondria were located centrally in the cells, which were joined by unfolded desmosomes involving Z-band material. Long periods of anoxia were tolerated without loss of heart function, but at the expense of cytoplasmic glycogen. Lipid granules were abundant in all layers and chambers, notably in animals prepared in the summer. The lipid granules displayed a marked increased in electron density when the heart was incubated in a buffered oxalate solution prior to fixation. A glycogen-sparing effect of the lipids during anoxia was observed.

Animals↗
PubMed1996

Electrocardiogram changes during positive pressure breathing in rabbits.

Positive pressure breathing produced by mechanical ventilation with an expiratory threshold load (ETL) may modify electrocardiogram (ECG) complexes independently of any recording artefact due to lung volume changes. Anaesthetized, paralyzed rabbits were treated for about 2 h, then killed. In intact then vagotomized animals two situations were studied successively. Firstly, positive inspiratory pressure breathing, and secondly, positive inspiratory plus expiratory pressure breathing by adding ETL to mechanical ventilation. Arterial blood gases were measured and held constant throughout the challenge. Oesophageal pressure, giving indirect measurement of intrathoracic pressure, arterial blood pressure, blood flows in abdominal aorta and inferior vena cava and standard ECG recordings were made at baseline condition during mechanical ventilation, then at the end of a 10-min period of ETL breathing. The ETL breathing decreased arterial blood pressure significantly and reduced arterial and venous blood flows in the same proportion. No change in the duration of ECG complexes was noticed. However, ETL markedly reduced the amplitude of P- and T-waves, but not that of R-wave, an effect significantly accentuated after vagotomy. The ETL breathing increased the T-vector angle, with no associated change in QRS vector angle. The present animal investigations revealed that positive pressure breathing modifies the ECG independently of the consequences of ETL-induced lung volume changes. We speculate that the changes in P- and T-wave amplitude may have resulted from a reduced transmural pressure gradient between the epicardium and endocardium.

Animals↗
PubMed1986

Cardiotoxicity of a new inotrope/vasodilator drug (SK&F 94120) in the dog.

The cardiotoxicity and haemodynamic changes induced by IV administration of high doses of SK&F 94120, a novel positive inotrope/vasodilator, were studied in the dog. Inotropism was observed at a dose of 0.375 mg/kg. Mean blood pressure was reduced in a dose-related manner, reaching a nadir of 43.7 mm Hg at 24 mg/kg. Heart rate was increased at doses of 1.5 mg/kg and above. ECG examination revealed a shortening of PR interval and an increase in T-wave amplitude. At doses of 15 mg/kg and above, occasional AV dissociation with accrochage were sometimes seen shortly after the start of the infusion. Ventricular extrasystoles were only seen at doses of 120 mg/kg and above. A dose-related increase in severity and incidence of haemorrhages, deposition of haemosiderin and fibroplasia were seen in the left ventricular endocardium and atrioventricular valves at doses of 15 mg/kg and above. Focal myocardial necrosis, predominantly of the left ventricular papillary muscle, and mild periarteritis of medium-sized extramural arteries, mostly in the right atrium, were seen at doses of 45 mg/kg and above. Intimal proliferation of intra- and extramural coronary vessels was observed. A necrotising peri/panarteritis of these arteries was noted at doses of 200 and 400 mg/kg. The cardiotoxicity observed was considered to be due to the exaggerated pharmacologic effects seen at these high dose levels.

Animals↗
PubMed1995

Ultrastructural investigation of nitric oxide synthase-immunoreactive nerves associated with coronary blood vessels of rat and guinea-pig.

Ultrastructural investigation of nitric oxide synthase-immunoreactive nerves closely associated with blood vessels in rat and guinea-pig hearts revealed many labelled nerve fibres in the walls of the main branches of the coronary arteries, and in arterioles, capillaries and post-capillary venules. The number of nitric oxide synthase-containing nerve fibres associated with different vessels, even those of the same calibre, varied. Terminal regions of nitric oxide synthase-immunoreactive fibres were observed in the endocardium and myocardium. Nitric oxide synthase-labelled fibres displayed electron-dense immunoproduct in both varicose and intervaricose regions. Immunoreactive axonal varicosities contained both small and large synaptic vesicles. The characteristics of the nitric oxide synthase-immunoreactive nerve fibres observed in the heart and the possibility that these fibres represent the processes of intracardiac neurones and/or sensory neurones of extrinsic origin are discussed.

Amino Acid Oxidoreductases↗
PubMed1986

Distribution of calcitonin gene-related peptide-like immunoreactivity in the guinea pig heart.

The distribution of calcitonin gene-related peptide like-immunoreactivity (CGRP-IR) within the heart and adjacent blood vessels of the guinea pig was investigated immunohistochemically by use of the peroxidase-antiperoxidase (PAP) technique. Numerous paravascular and perivascular immunoreactive nerve fibers were localized around the aorta, coronary arteries and their branches down to the terminal vasculature. Arterioles in the atria showed greatest density of immunoreactive varicosities of all blood vessels. The epicardium, endocardium and the conductive system also contained numerous CGRP-IR nerve fibers. In the myocardium the number of immunoreactive varicosities was variable. Many were present in both atria, moderate amounts were seen in the right ventricle and parts of the intraventricular septum, and only a few occurred in the left ventricle. CGRP-IR was infrequently found within intracardial ganglionic cells but was abundantly distributed in the surrounding nerve fibers.

Animals↗
PubMed1982

Congenital "histiocytoid" cardiomyopathy: evidence suggesting a developmental disorder of the Purkinje cell system of the heart.

The so-called "histiocytoid cardiomyopathy" is an unusual cardiac disorder of infancy and childhood, characterized by the presence of numerous foamy, lipid-containing cells between the endocardium and the striated myocardial cells of the left ventricle and the interventricular septum. The disease usually affects females, the clinical picture being dominated by severe disturbances of conduction. The original designations of the disorder stem from the morphological resemblance of the foamy cells to lipid-laden histiocytes. However, subsequent investigations have shown these cells to contain myofibrils interposed with Z lines. It has, therefore, been suspected that the leading cell population might be related to the myocardium. Using a histochemical method for the demonstration of cholinesterase activity in the foamy cells, we present evidence that "histiocytoid" cardiomyopathy may in fact correspond to a maldevelopment of the Purkinje cell system of the heart.

Cardiomyopathies↗
PubMed1986

Histotopographic evidence that amyloid deposits in sclerocalcific heart valves and other chronic lesions of the cardiovascular system are related to old thrombotic material.

Deposition of amyloid in human sclero-calcific heart valves has been reported recently as a localized age-independent and dystrophic form of amyloidosis. Histochemical studies have shown that the deposits are permanganate resistant, contain tryptophan and P component and are immunologically unrelated to any known type of amyloid fibril protein. In this study histological observations from a series of four selected sclerotic heart valves show amyloid deposition in old thrombotic material covering fusing commissures or appositional collagen on the body of the leaflets. Similar cases from extravalvular sites have been added to the series: a partly hyalinized thrombus of the left atrium, a thrombotic aneurysm of the left ventricle, 2 thrombotic atherosclerotic aneurysms of the aorta and popliteal artery respectively, and an encapsulated haematoma of the scalp. The deposits are Congo red positive with typical green dichroism in polarized light, permanganate resistant and contain tryptophan. Electron microscopy of 3 cases displays small fibrils which are typical of amyloid. No patient showed evidence of systemic amyloidosis. The natural history of sclero-calcific valvulopathies and present observations favour the following pathogenesis: first, recurrent thrombotic deposition on thickened and fibrotic endocardium; second, degradation of a coagulation-related protein with beta potential during the aging of the clot with transformation into amyloid fibrils; finally, inclusion of the amyloid in sclerotic replacement tissue.

Adult↗
PubMedDate not supplied

Local glucose utilization and local blood flow in hearts of awake rats.

Local cardiac glucose utilization and local cardiac blood flow in rat heart were measured in vivo by quantitative autoradiographic techniques with 2-[14C] deoxyglucose and [14C] iodoantipyrine, respectively. [14C]methylmethacrylate standards were calibrated for quantitative autoradiography of dried sections of heart tissue; the calibration values for heart tissue differed from those for brain by 8%, probably because of differences in self-absorption within the tissues. The lumped constant required by the deoxyglucose method was determined in isolated, perfused, working rat hearts and found to be 1.11 +/- 0.36 (mean +/- SD, n = 21). The heart: blood partition coefficient for iodoantipyrine required by the [14C]iodoantipyrine method was measured and found to be 1.25. The results obtained in awake rats showed: 1) overall cardiac glucose utilization varied considerably among animals with a mean of 53 (left ventricle) and 30 (right ventricle) mumol/100 g/min; 2) cardiac blood flow was less variable among animals with a mean of 592 (left ventricle) and 420 (right ventricle) ml/100 g/min; 3) glucose utilization was found to be particularly high in the papillary muscle; 4) systematic gradients of glucose utilization or blood flow in the ventricular wall were not observed; 5) glucose utilization and blood flow were not closely correlated on a local level. It is concluded that autoradiographic methods are suitable for the quantification of local glucose utilization and local blood flow in the rat heart in vivo. These methods could not demonstrate transmural gradients for glucose utilization and blood flow between epi- and endocardium in awake rats.

Animals↗
PubMed1990

Left ventriculotomy of the heart: tissue repair and localization of collagen types I, II, III, IV, V, VI and fibronectin.

The reparative process following left ventriculotomy was investigated immunohistochemically using anti-type I, II, III, IV, V and VI collagen antibodies, and anti-fibronectin antibody. Wound healing began with proliferation of young fibroblasts positive for type I, III and V collagens at the wound margin; vascular granulation tissue then grew into the injured myocardium followed by deposition of fibrous components immunoreactive with type I and III. At 30 days after operation when almost the entire thickness of the myocardium at the wound was replaced by fibrosing granulation tissue, a small cluster of adipocytes appeared around capillaries at the wound margin. The granulation tissue was gradually replaced by the adipose tissue with establishment of a fibrous union at the subendocardium by 90 days. In addition to type I and III collagens, type VI collagen was detected in a fine fibrillary pattern along thick collagen fibre bundles in the fibrous tissue and around the adipocytes. Fibronectin was distributed diffusely in the granulation tissue and gradually decreased with increase of the fibrous components. These results indicate that the ventriculotomy was finally repaired in the form of a fibrous scar, particularly in the endocardium. There was marked infiltration of adipose tissue in the damaged myocardium. Presumably type VI collagen, as well as type I and type III collagens, plays an important role in wound union.

Animals↗
PubMed1988

[Value of 2-D echocardiography in the detection of stress-induced wall-motion abnormalities in coronary heart disease--a comparison with biplane cineventriculography].

To determine the accuracy of echocardiography in assessment of exercise-induced wall motion abnormalities, the results of stress-echocardiography were compared with exercise-cineventriculography. In 56 consecutive patients biplane cineventriculography at rest and immediately after supine bicycle exercise was performed. Cross-sectional echocardiography was obtained using the apical 2- and 4-chamber view for LV imaging under identical exercise conditions. In 6 of the 56 patients 2-D echo, in 8 patients LV-angio, and in 2 patients both methods were of inadequate quality during exercise. Thus, in 40 patients (34 patients had coronary artery disease) local wall motion of 360 wall segments was analysed. 49 segments (14%) of 24 patients showed exercise-induced ischemic wall motion abnormalities during cineventriculography. Only 24 of these 49 asynergics (49%) were also detected by 2-D-echo. Using cross-sectional echocardiography, ischemia related wall motion abnormalities were best detected laterally and septaly, whereas apical asynergies were identified in 3 of 12 segments only. Thus, the clinical value of exercise 2-D echo as a screening method in patients suspected to have coronary artery disease is limited and restricted to patients with excellent visualization of the left ventricular endocardium.

Cineangiography↗
PubMed1992

Papillary fibroelastoma in the left ventricular outflow tract.

We report a case of a papillary fibroelastoma originating from the left ventricular endocardium in the outflow tract which was discovered by echocardiography in an asymptomatic patient. Two echocardiographic features were observed: (1) the tumor surface was smooth, and characteristic papillary formation was not detected; and (2) the outline of the mass was clearly defined as a dense echo, with the central, radiolucent, portion surrounded by a highly refractive linear echo at the level of the maximum diameter of the mass. The excised tumor was covered with a gelatinous substance that masked multiple papillae on the surface, but its echolucent center could not be explained by the pathology of the tumor which was solid centrally. Our case indicates that a papillary fibroelastoma may sometimes show echocardiographic findings similar to those of a myxoma, although other investigators have not noted the smooth surface and the echolucent center makes it indistinguishable from a myxoma. Thus, in some cases, it is difficult to distinguish papillary fibroelastoma from myxoma by echocardiography.

Connective Tissue↗
PubMed1993

Myocardial matrix metalloproteinase(s): localization and activation.

Matrix metalloproteinases (MMPs) and neutrophil elastase (NE) may each contribute to fibrillar collagen degradation in various disease states. Little, however, is known about the activation and localization of MMP in the heart. Accordingly, we extracted MMP and examined mechanisms of proMMP activation in whole tissue extracts of the adult rat myocardium. Incubation of extracts with serine proteases (i.e., trypsin or neutrophil elastase) at 37 degrees C resulted in a time-dependent activation of proMMPs. Based on immunoblot and measurements of MMP activity by zymography, the molecular weight of active MMP was deduced to be 52 kDa. The second-order rate constant for activation of proMMP by serine protease was 5.5 +/- 0.2 x 10(5) M-1min-1 and for oxidized glutathione (GSSG) 1.5 +/- 0.1 M-1min-1. Incubation of the extract with both serine protease and GSSG increased the rate of activation 30-fold. Based on reverse zymographic analysis of collagenase inhibition, tissue inhibitors of metalloproteinases were identified. Indirect immunofluorescence localized proMMPs/MMPs to the endothelium and subendothelial space of the endocardium and throughout the interstitial space found between groups of muscle fibers. These results suggest that the mechanism of activation of MMPs by either a serine protease and by oxidizing, thiol-modifying reagents are mechanistically different and the presence of either a serine protease or GSSG synergistically increase the rate of activation of proMMPs. Our results also suggest that MMPs may be regulated by its own endogenous inhibitors. The contribution of this proteolytic enzyme to tissue remodeling and wound healing responses that occur in various diseases states remains to be established.

Animals↗
PubMed1991

Quantitative regional curvature analysis: validation in animals of a method for assessing regional ventricular remodelling in ischemic heart disease.

Recent studies show the impact of left ventricular shape and remodelling on patient prognosis. This mandates the development of quantitative methods for measuring shape. Quantitative regional curvature analysis (QRCA) was developed to quantitate shape on a regional basis so that measurements would not be constrained to assessment of only global shape and would, therefore be applicable to ischemic heart disease. To validate QRCA, eleven dogs were instrumented with coronary occluders and radiopaque markers on the epicardium and endocardium to provide fiducial points for calculation of shape, motion and thickening. These parameters were measured in the anterior and inferior walls, at rest, during left anterior descending occlusion and finally during circumflex occlusion. QRCA showed increased curvature (increased globularity) in each wall when thickening and motion deteriorated during occlusion. The most marked shape changes occurred in the inferior wall whereas the most marked deterioration of function was detected by wall thickening measurements of the anterior wall. Thus, QRCA detects regional ventricular shape disorders coincident with regional dysfunction induced by ischemia. These changes show regional heterogeneity and demonstrate the potential importance of this measurement as opposed to simple, global measures of shape. QRCA is, therefore, suitable for monitoring acute changes of shape that occur during acute ischemia.

Algorithms↗
PubMed1992

Autonomic neuropathy and immunological abnormalities in Chagas' disease.

Chagas' disease (American Trypanosomiasis) is caused by infection with the haemoflagellate parasite Trypanosoma cruzi, which is transmitted from animals to man by the Reduviidae bug. The human disease is characterized by two phases. In the first (acute phase) parasitaemia is high and general symptoms variable. The next, which is lifelong (chronic phase), is characterized by inflammatory lesions in cardiac and skeletal muscle, gastrointestinal, the autonomic nervous system. Parasites are difficult to detect in blood and affected tissues. Lesions within the autonomic nervous system, lead to development of cardiomyopathy, megaoesophagus and megacolon. The discrepancy between the profusion of inflammatory lesions and the absence of parasites suggests the development of autoimmunity probably of a cell-mediated type. Several autoimmune abnormalities have been noted during Trypanosoma cruzi infection. These include suppression of the specific response to autoantibodies directed against antigens located in the endocardium and in nerves, and development of cell-mediated immunity against host antigens (cytotoxic T- and delayed type hypersensitivity T-cells). These autoimmune disorders are thought to be responsible for much of the pathological damage in chronic Chagas' disease.

Animals↗