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Pressure-volume relations of aorta and arteries are considered using a fiber-fluid continuum analysis. A Windkessel model is revised to investigate the effects of the exponential pressure-volume relation of the present study on the cardiovascular system. It is shown that the elastic properties of the fibers in large blood vessels play an important role in the circulation of blood in health and in disease.
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The linear relationship between the initial acceleration of blood flow and the I-wave as well as the HI-jerk of the acceleration ballistocardiogram is shown by experiments with a physical model of the cardiovascular system.
Magnetic resonance (MR) is a noninvasive technique to obtain tomographic images in any desired plane of the body. MR offers possibilities not only for morphologic imaging, but also for various physiological measurements, e.g. investigation of blood flow and angiography. This paper summarizes the possibilities of the technique in evaluation of congenital and acquired cardiovascular diseases. The conclusion is that MR may become an important clinical tool for examination of the cardiovascular system providing high accuracy and quantitative measurements.
BACKGROUND: Microgravity and simulated microgravity (SM) lead to important changes in orthostatic tolerance (OT), the autonomic nervous system (ANS), and the volume-regulating systems. After one is exposed to microgravity or SM, a period of readaptation to gravity is known to take place, but it is not certain if orthostatic function returns to baseline within the initial recovery and what mechanisms are involved. We hypothesized that after a period of recovery, OT, ANS, and volume-regulating systems would return to pre-SM levels. METHODS: To test this hypothesis, 24 healthy men were placed on a constant diet for 3 to 5 days, after which a tilt-stand test (pre-TST) was performed. The TST was repeated after 14 to 16 days of head-down tilt bed rest (HDTB) (post-TST) and a 3-day period of recovery (rec-TST), at which times measurements of renal, cardioendocrine, and cardiovascular systems were conducted. RESULTS: Presyncope occurred in 46% of subjects pre-TST, in 72% post-TST, and in 23% during rec-TST. OT was significantly better during the recovery period than at baseline (p = .03). There was a significant decrease in urinary sodium and potassium excretion, along with a decrease in plasma renin activity and serum and urine aldosterone compared with baseline. Serum norepinephrine and sympathetic responsiveness remained below baseline values. CONCLUSION: In summary, OT improved compared with baseline after a period of readaptation. Retention of electrolytes (sodium, potassium) could be involved. These findings indicate that recovery after SM is not simply a gradual return to baseline values but is instead a dynamic process reflecting interaction of multiple regulatory systems.
The effects of TCV-116 ((+/-)-1-(cyclohexyloxycarbonyloxy) ethyl 2-ethoxy-1-[[2'-(1 H-tetrazol-5-yl)biphenyl-4-yl] methyl]-1 H-benzimidazole-7-carboxylate, CAS 145040-37-5) on the cardiovascular system and renal function were investigated in rats, guinea pigs, and dogs. TCV-116 at doses of 3 mg/kg (i.d.) and higher markedly increased renal blood flow in anesthetized dogs. TCV-116 at 30 mg/kg (i.d.) had no effect on heart rate, left ventricular systolic pressure, its dp/dtmax, or cardiac output in anesthetized dogs. Furthermore, TCV-116 at 10 and 30 mg/kg (p.o.) had little effect on cardiac output, right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure or respiration in conscious dogs. In isolated guinea pig perfused heart, CV-11974 even at a dose of 0.1 mg/ heart had no effect on cardiac function. In isolated guinea-pig atria, CV-11974, the active metabolite of TCV-116, even at 10(-4) mol/l had no effect on the spontaneous beating rate of the right atria or the contractile force of electrically-paced left atria. No significant effect of TCV-116 on urinary volume or urinary excretion of sodium and potassium was observed in rats (at 30, 100 or 300 mg/kg p.o.). These findings suggest that TCV-116 exerts no any additional pharmacological effects on cardiac and respiratory functions in dogs or on renal function in rats, other than an increase in renal blood flow in anesthetized dogs thought to be due to its inhibitory effect on the renin-angiotensin system.
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Anoïkis is defined as programmed cell death induced by the loss of cell/matrix interactions. Adhesion to structural glycoproteins of the extracellular matrix is necessary for survival of the differentiated adherent cells in the cardiovascular system, including endothelial cells, smooth muscle cells, fibroblasts, and cardiac myocytes. Adhesion is also a key factor for the differentiation of mesenchymal stem cells. In particular, fibronectin is considered a factor of survival and differentiation for many adherent cells. Adhesion generates cell tensional integrity (tensegrity) and repression of apoptotic signals, whereas detachment has the opposite effect. Anoïkis plays a physiological role by regulating cell homeostasis in tissues. However, anoïkis can also be involved in pathological processes, as illustrated by the resistance to anoïkis in cancer and its enhancement in degenerative tissue remodeling. Extracellular mediators of anoïkis include matrix retraction, leading to loss of tensegrity in fibroblasts, pharmacological disengagement of integrins by RGD-like peptides and fragments of fibronectin, and focal adhesion disassembly by fragments of thrombospondin, plasminogen activator-1, and high-molecular-weight kininogen. In addition to binding of the RGD peptide by integrins, the engagement of the heparin binding sites of adhesive glycoproteins with glycosaminoglycans on the cell surface is also involved in the prevention of cell detachment-induced apoptosis. Proteases able to degrade adhesive glycoproteins, such as fibronectin, induce anoïkis of vascular adherent cells. Active proteases can either be secreted directly by inflammatory cells, as elastase and cathepsin G by polymorphonuclear leukocytes, chymase and tryptase by mast cells, and granzymes by lymphocytes, or generated from circulating zymogens by activation in close contact with the cells. This is the case for the pericellular conversion of plasminogen to plasmin, which degrades fibronectin and induces anoïkis of smooth muscle cells. Involvement of proteases has also been proposed in the apoptotic response of cultured adherent cells to serum starvation. Anoïkis is probably involved in pathological remodeling of cardiovascular tissues, including cardiac myocyte detachment in heart failure, deendothelialization and plaque rupture in atherosclerosis, and smooth muscle cell disappearance in aneurysms and varicose veins. The absence of cell adhesion and growth resulting from cleavage of adhesive proteins also represents a major impediment to cellular healing, including the absence of cell recolonization of proteolytically injured tissue and the low efficacy of cell transplantation. However, the exact role of anoïkis in cardiovascular pathologies remains to be further defined.
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Local application of hydralazine has been found to alter intraocular pressure in animal eyes. This study was undertaken to determine, in normotensive humans, the effects of topically-applied hydralazine on systemic cardiovascular parameters, blood-aqueous barrier, and aqueous humor flow. Two different concentrations of hydralazine were used: 0.03%, and 0.1%. Twenty healthy normotensive subjects were studied. Blood pressure, pulse rate, and intraocular pressure were measured every hour for six hours after hydralazine or placebo was instilled into the conjunctival sac in a double-masked, randomized fashion. With either hydralazine dose, there was no significant change in systemic blood pressure or pulse. In addition, spectrophotometrically-measured polarization of fluorescence and flare failed to show any significant breakdown of the blood-aqueous barrier. In most individuals, application of hydralazine was followed by a brief, mild to moderate, conjunctival hyperemic response. Compared to placebo at the same time of day, a small increase in intraocular pressure was observed with 0.03% hydralazine (p < .05). At 0.1%, this increase tended to be less. There was no statistically significant difference in aqueous humor flow between hydralazine-treated and placebo-treated eyes at the lower concentration (3.20 +/- 0.63 vs. 3.05 +/- 0.61 microL/min (mean +/- S.D.) or at the higher concentration (3.37 +/- 0.53 vs. 3.28 +/- 0.60 microL/min) of hydralazine. These results suggest that acute topical application of 0.1% hydralazine to the eyes of normal humans does not cause clinically significant cardiovascular effects or significant ocular toxicity.
To delineate the importance of cyclic GMP (cGMP) as a second messenger for signal transduction within the cell, catalytic and regulatory features of the proteins involved in the synthesis and degradation of cGMP, i.e., guanylate cyclases and phosphodiesterases, are described. Characteristic features of cGMP-dependent protein kinases as intracellular receptors for cGMP and the contribution of this enzyme to the physiological functions of cGMP in the cardiovascular system are discussed.
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A pressure system externally applied to the limbs of a patient has been proven effective in assisting circulation in animal and clinical studies. In this study a nonlinear mathematical model of the cardiovascular system is utilized to determine the effectiveness of high-frequency components in the external pressure waveform. The development of the model, the method of analysis, and the results acquired with the model are presented in this report, demonstrating its suitability for the study of external counterpulsation.
The cardiovascular effects of dopexamine and dopamine were compared in the anaesthetized and conscious dog by the use of intravenous infusions over the dose range 3 X 10(-9) - 10(-7)mol kg-1 min-1. In the anaesthetized dog, dopexamine produced a dose-related fall in blood pressure due to peripheral vasodilatation and a small rise in heart rate and contractility. By contrast, dopamine did not significantly reduce blood pressure but produced a larger dose-related increase in contractility. At the highest infusion rate (10(-7)mol kg-1 min-1) blood pressure and heart rate were increased by dopamine. Dopexamine dilated the renal and mesenteric vascular beds with a potency similar to that of dopamine. Femoral vascular responses produced by both agents were inconsistent but the highest infusion rate of dopamine did produce vasoconstriction. With the aid of selective receptor antagonists (haloperidol, propranolol and bulbocapnine) the vasodepressor activity of dopexamine was shown to be mediated by stimulation of DA2-, beta- and DA1-receptors. The cardiac stimulation and renal vasodilatation produced by both compounds were due to stimulation of beta-adrenoceptors and DA1-receptors respectively. In the conscious dog, intravenous infusion of dopexamine caused a dose-related fall in blood pressure, renal vasodilatation and an increase in cardiac contractility and heart rate. Dopamine also increased cardiac contractility, and renal blood flow due to renal vasodilatation but without affecting heart rate. At the highest infusion rate, blood pressure was increased. Dopexamine and dopamine produced a similar incidence of panting and repetitive licking at 3 X 10(-8)mol kg-1 min-1 and emesis at 10(-7)mol kg-1 min-1, due to stimulation of dopamine receptors in the chemoreceptor trigger zone. Dopexamine produces a different cardiovascular profile from dopamine in the anaesthetized and conscious dog. Both compounds reduce renal vascular resistance, but in contrast to dopamine, dopexamine reduces afterload and produces only mild inotropic stimulation. These differences reflect contrasting activity at adrenoceptors.