Cardioscience最新文献

It is generally believed that nuclear enlargement indicates polyploidy. The purpose of this study was to establish whether nuclear enlargement is also a marker for cellular hypertrophy. Using isolated myocytes, we examined the growth of cardiac myocyte nuclei during cellular hypertrophy in rats with aortocaval fistulas or left ventricular myocardial infarction. A Coulter Channelyzer was used to measure the volume of the myocytes. Isolated myocytes were stained with the DNA-specific fluorochrome 4'-6-di-amidino-2 phenylindole-HCl for measurements of nuclear length and width, and calculation of nuclear volume. One week, 1 month and 5 months after aortocaval fistula surgery, the nuclear volume of right ventricular myocytes increased by 24, 55 and 56% respectively. Increased length, rather than width, accounted for most of the nuclear growth. Nuclear hypertrophy was associated with a progressive increase in cell volume at each time point (34, 88 and 118%). Adaptive growth of left ventricular myocytes followed the same trend, though the extent of cellular and nuclear hypertrophy was reduced. One month after producing a myocardial infarction, there was an increase in nuclear volume (18%) and nuclear length (11%) in right ventricular myocytes, but no changes in the surviving left ventricular myocytes. The cell volume increased in both right and left ventricles (72 and 18%, respectively). Thus, nuclear size increased as myocytes enlarged, though at a slower rate. Since nuclear DNA content does not increase in rats with aortocaval fistulas or myocardial infarction, the increase in nuclear volume was associated with cellular enlargement rather than increased polyploidy.

Although most research on developmental cardiovascular physiology has focused on the bird embryo as a model for emulating developmental processes in mammals, there are increasingly compelling reasons to expand research to a variety of lower vertebrate systems. These reasons include circumventing inherent limitations of the avian embryo and identifying general vertebrate developmental patterns in the cardiovascular system. In this paper, we first review data from hemodynamic studies on amphibians and birds (and what little exists from fish and reptiles), to provide a background against which lower vertebrate development can be examined. We then describe non-mammalian, non-avian paradigms for studying developmental patterns of vertebrate hearts. Developmental spects of cardiovascular performance, especially heart rate, blood pressure and cardiac output and how they change with ontogeny, are described for several amphibians and a few reptiles, identifying, where possible, processes in common with birds and mammals. Finally, we indicate productive areas for future research with lower vertebrate cardiovascular systems, such as establishing "critical windows" for cardiovascular physiology during development, and determining the extent of developmental plasticity at the level of organ system physiology.

The microcirculation of the respiratory organ of water and air breathing vertebrates is similar and can be described as sheet flow. The gross morphologies of the systems, however, are very different and reflect the properties of the medium. The fish heart has a single ventricle that forces blood first through the gills and then through the body. The pressure in the gills is higher than in the systemic circulation, the reverse of the situation seen in mammals. The gill epithelium is thicker than that in the lung and is involved in ionic and acid-base functions carried out in the kidney of mammals. Gills stick together in air. Therefore, fish breathe air using some other structure, such as the gut or mouth, the swimbladder, or the skin. The gills are retained for carbon dioxide excretion and ion and acid-base regulation. This results in a separation of oxygen uptake and carbon dioxide excretion. The gills are often modified in air-breathing fish such that venous blood flows to well developed gills for carbon dioxide and acid excretion, whereas oxygenated blood flow bypasses the gills. This is the beginning of a separation of flows in the heart which is more highly developed in amphibians and reptiles and complete in mammals. The loss of gills requires transfer of ionic and acid base regulation processes to the skin in amphibia and to the kidney in reptiles and mammals, allowing a completely terrestrial existence. The organization of the venous system is influenced by the degree of support offered by the medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Until recently, direct measurements of coronary blood flow in fishes had not been made. This review presents and compares in vivo measurements of coronary flow recorded from the school shark, Galeorhinus australis, and the coho salmon, Oncorhynchus kisutch. In both species, the coronary blood flow was phasic and strongly influenced by the cardiac cycle. Coronary blood flow in the school shark was more severely compromised by the cardiac cycle with a short retrograde flow occurring during systole. In the coho salmon, there was an anterograde coronary blood flow throughout the cardiac cycle. Differences in coronary hemodynamics are discussed in relation to differences in the myoarchitecture of the school shark and coho salmon hearts. The regulation of coronary blood flow through changes in vascular resistance (vasoactivity of the coronary vessels) is also discussed.

The crocodilian heart is completely divided into two atria and two ventricles, resembling the arrangement in birds and mammals. However, in addition to the systemic aorta (right aorta, RAo) which emerges from the left ventricle, there is a second aorta (left aorta, LAo) that leaves the right ventricle beside the common pulmonary artery. The two aortae communicate immediately outside the valves through a small aperture, the foramen of Panizza. During diastole, the blood pressures in the RAo and LAo equalize through the foramen, and the pressure in the LAo therefore remains higher (under most circumstances) than that generated by the right ventricle preventing the LAo valve from opening. Blood flow in the LAo is biphasic, with a reversal of blood flow in systole due to the closure of the foramen of Panizza by the medial cusp of the RAo valve. Under these circumstances net LAo flow is low, and due solely to flow through the foramen. When peak systolic right ventricular pressure rises above that in the LAo, the valve will open, producing a (partial) pulmonary bypass (right-to-left shunt). This may occur during pulmonary vasoconstriction, or when the systemic (and hence the LAo) blood pressure decreases.

Fishes show the highest diversity among vertebrates. Defined differences in ventricular myoarchitecture exist in fish. There are two main types of cardiac ventricle in fish: a spongy type and a mixed type. In the spongy ventricle, the muscle trabeculae form a sponge-like network, the spongiosa. In the mixed ventricle, one or more superficial layers of compact tissue (compacta) enclose an inner spongiosa. The spongiosa and compacta are respectively associated with a lacunary and a vascularized supply of blood. Interspecies differences exist in the proportion of compacta and the extent of vascularization. Here the mechanical limits and flexibility of the different types of ventricular organization are examined. The spongy type (found only in teleosts) seems to be particularly suitable for performing volume work. An example is the icefish heart. The main characteristics of this fish are the absence of hemoglobin in the blood and the very large volume of blood. The cardiac ventricle of the icefish is characterized by a cardiomegaly of the spongy type with myocardial pseudohypertrophy. It functions as a specialized volume pump which moves large stroke volumes at a low heart rate, but is not able to produce high pressures. The most active teleosts have mixed heart ventricles with different thicknesses of compacta. The presence of compacta gives these types of heart the potential to act as pressure pumps: they move small volumes at a relatively high rate and high pressure. The tuna heart is an extreme example of the mixed type. It has the highest relative mass and proportion of compacta (40-70%) among fishes.(ABSTRACT TRUNCATED AT 250 WORDS)

In vertebrates vagal preganglionic neurons are found in two principle locations in the brain-stem, the dorsal vagal motor nucleus and areas lateral to the dorsal vagal motor nucleus centered on the nucleus ambiguus. In elasmobranch fish 8% of vagal preganglionic neurons are located outside the dorsal vagal motor nucleus; these are all cardiac vagal motoneurones. This proportion increases from fish through amphibians to mammals in which over 30% of vagal preganglionic neurons are outside the dorsal vagal motor nucleus; in the cat 80% of cardiac vagal motoneurons are in the nucleus ambiguus. Vagal tone is the major determinant of heart rate and its relationships to environmental factors (e.g. temperature, hypoxia). Activity in subpopulations of cardiac vagal motoneurons varies with the respiratory rhythm in fish and mammals due to central interactions between respiratory and cardiac vagal motoneurons. This generates cardio-respiratory synchrony in dogfish and respiratory sinus arrhythmia in mammals. The appropriate central connections are established during development. In the neotenous axolotl all vagal preganglionic neurons are in the dorsal vagal motor nucleus; 15% are lateral to the dorsal vagal motor nucleus following metamorphosis, induced by injection of thyroid hormones; a change which may relate in part to the switch from gill to lung-breathing. Respiratory sinus arrhythmia first appears at around normal term gestation in the premature human neonate, at a time when they would normally be switching from reliance on the placenta to lung-breathing.

Rats treated orally for 21 days with aminocarnitine, an inhibitor of carnitine palmitoyltransferase-2 (CPT-2), do not show hypertrophy of the heart. This contrasts with the effects of carnitine palmitoyltransferase-1 (CPT-1) inhibitors, that, according to the literature, cause hypertrophy. As CPT-1 and CPT-2 are both required for the oxidation of long-chain fatty acids in mitochondria, it can be concluded that inhibition of fatty acid oxidation per se is not responsible for cell growth, but rather the accumulation of a metabolite, probably long-chain acylcoenzyme A. CPT-1 and CPT-2 inhibitors cause different metabolic changes in the heart. Electron microscopy of hearts fixed 1 hour after Langendorff perfusion with the two types of inhibitors reveals some of these changes. Multilamellar vesicles were observed with aminocarnitine (CPT-2 inhibitor) but not with etomoxir (CPT-1 inhibitor). When both inhibitors were present, electron-dense spots adjacent to mitochondria were observed, possibly containing long-chain acylaminocarnitine.

The selective removal of endocardial endothelium of rat left ventricular papillary muscles by 1-second immersion in 0.5% Triton X-100 showed little influence on resting tension and only a small decrease in peak isometric tension (8.3 +/- 1.4 vs 9.6 +/- 2.4 mN/mm2 at Lmax, p > 0.05) with no reduction in maximal rate of tension development (+dT/dtmax; 136 +/- 21 vs 137 +/- 18 mN/mm2/s, p > 0.05). In contrast, there was a marked increase in maximal rate of tension decline (-dT/dtmax) from 71 +/- 14 to 92 +/- 15 mN/mm2/s (p < 0.05), so that the ratio between +dT/dtmax and -dT/dtmax fell from 1.98 +/- 0.27 to 1.51 +/- 0.13 (p < 0.01). Removal of endocardial endothelium led to a significant shortening of isometric twitch contractions. Time to peak tension was abbreviated from 111 +/- 20 to 84 +/- 8 ms (p < 0.05) and the half relaxation time from 92 +/- 9 to 68 +/- 8 ms (p < 0.01). Time to +dT/dtmax was also shortened from 31 +/- 6 to 44 +/- 9 ms (p < 0.05) and time to -dT/dtmax from 90 +/- 12 to 62 +/- 10 ms (p < 0.01). These effects were not influenced by alterations in stimulation frequency or muscle length. The early onset of relaxation and abbreviated duration of relaxation together with an increased rate of decline in tension led to a shorter total twitch which may explain the slightly lower peak tension once the endocardial endothelium was removed. Our findings confirm that endocardial endothelium modulates myocardial contraction, with a predominant influence on relaxation.