Cardiac control

Watkins, L. L., Conner, K. M. Davidson, J. R. (2001). Effect of kava extract on vagal cardiac control in generalized anxiety disorder preliminary findings. /. Psychopharmacol., 15, 283-6. 

Surethane Cardiac Control (Palm Coast, FL) Purified Lycra MDI-PTMEG EDA Similar to Biomer Microcracks... 

Bettermann, H., D. Cysarz, A. Portsteffen, and H.C. KummelL 2001. Bimodal dose-dependent effect on autonomic, cardiac control after oral adrninistration of Atropa belladonna. Auton. Neurosci. 90(1-2) 132-137. 

Control of respiration occurs in many different cerebral structures [Johnson, 1991] and regulates many things (Hornbein, 1981). Respiration must be controled to produce the respiratory rhythm, ensure adequate gas exchange, protect against inhalation of poisonous substances, assist in maintenance of body pH, remove irritations, and minimize energy cost. Respiratory control is more complex than cardiac control for at least three reasons ... 

An autonomic space representation of cardiac control modes using the group mean autonomic component (left panel) d PEP and RSA (right panel) difference scores for the low and high intensity exercise tasks. 

Cacioppo, J. T, Bemtson, G. G., Binkley, P. F., Quigley, K. S., Uchino, B. N., Fieldstone, A. (1994). Autonomic cardiac control II. Noninvasive indices and basal response as revealed by autonomie blockade. Psychophysiology, 31, 586-598. 

Grossman, P., Svebak, S. (1987). Respiratory sinus arrhythmia as an index of parasympathetic cardiac control during active coping. Psychophysiology, 24, 228-235. 

Surethane (Cardiac Control Palm Coast, FL, US) Tecoflex (Thermedics Inc Woburn, MA, US)... 

Surethane Cardiac Control Systems, Inc. Redissolved Lycra thread. Some formulations may have a few percent PDMS blended with it. Limited availability. 

Sintov, A., Scott, W., Dick, M., Levy, R.J., 1988. Cardiac controlled release for arrhythmia therapy lidocaine-polyurethane matrix studies. Journal of Controlled Release 8, 157—165. 

Fetotoxicity Cocaine exposure in utero may have a direct effect on autonomic nervous system regulation, cardiac control mechanisms, and cardiovascular functioning in neonates [33 ]. In 21 prenatally cocaine-exposed infants and 23 non-exposed controls, studied within 120 hours of birth, there was a positive interaction between prenatal cocaine exposure and orthostatic stress. Whereas both exposed and non-exposed infants had increased heart rates and heart rate variability, the responses of the exposed... 

Common side effects of theophylline therapy include headache, dyspepsia, and nausea. More serious side effects such as lethal seizures or cardiac arrythmias can occur if blood levels are too high. Many derivatives of theophylline have been prepared in an effort to discover an analogue without these limitations (60,61). However, the most universal solution has resulted from the development of reHable sustained release formulations. This technology limits the peaks and valleys in semm blood levels that occur with frequent dosing of immediate release formulations. ControUed release addresses the problems inherent in a dmg which is rapidly metabolized but which is toxic at levels ( >20 7g/mL) that are only slightly higher than the therapeutically efficacious ones (10—20 p.g/mL). Furthermore, such once-a-day formulations taken just before bedtime have proven especially beneficial in the control of nocturnal asthma (27,50,62). 

Economic Aspects. The cardiovascular devices market is estimated to be approximately 2.9 biUion annually on a worldwide basis. This market can be further segmented as follows angiography and angioplasty, 644 x 10 arrhythmia control, 1500 x 10 cardiovascular surgery, 700 x 10 cardiac assist (intra-aortic balloon pump), 80 x 10 and artificial hearts, which are experimental. 

Mean arterial pressure and cardiac output, an expression of the amount of blood that the heart pumps each minute, are the key Indicators of the normal functioning of the cardiovascular system. Mean arterial pressure is strictly controlled, but by changing the cardiac output, a person can adapt, e.g., to increased oxygen requirement due to increased workload. Blood flow in vital organs may vary for many reasons, but is usually due to decreased cardiac output. However, there can be very dramatic changes in blood pressure, e.g., blood pressure plummets during an anaphylactic allergic reaction. Also cytotoxic chemicals, such as heavy metals, may decrease the blood pressure. 

Chen et al. state that dendrobine produces moderate hyperglycemia, diminishes cardiac activity in large doses, lowers blood pressure, depresses respiration, inhibits isolated rabbit intestine and contracts isolated guinea-pig uterus. It has a weak analgesic, antipyretic action. Chen and Rose found that the convulsions induced by injection of dendrobine can be controlled by use of sodium isoamylethylbarbiturate they appear to be central in origin due to action on the cord and medulla. 

Adenosine is produced by many tissues, mainly as a byproduct of ATP breakdown. It is released from neurons, glia and other cells, possibly through the operation of the membrane transport system. Its rate of production varies with the functional state of the tissue and it may play a role as an autocrine or paracrine mediator (e.g. controlling blood flow). The uptake of adenosine is blocked by dipyridamole, which has vasodilatory effects. The effects of adenosine are mediated by a group of G protein-coupled receptors (the Gi/o-coupled Ai- and A3 receptors, and the Gs-coupled A2a-/A2B receptors). Ai receptors can mediate vasoconstriction, block of cardiac atrioventricular conduction and reduction of force of contraction, bronchoconstriction, and inhibition of neurotransmitter release. A2 receptors mediate vasodilatation and are involved in the stimulation of nociceptive afferent neurons. A3 receptors mediate the release of mediators from mast cells. Methylxanthines (e.g. caffeine) function as antagonists of Ai and A2 receptors. Adenosine itself is used to terminate supraventricular tachycardia by intravenous bolus injection. 

Apelins and the Apelin Receptor. Figure 3 Scheme illustrating the hypothesised mechanisms of control of human (a) vasculartone and (b) cardiac contractility by apelin peptides ( ). In the vasculature, apelins (released via the small vesicles of the constitutive pathway) may act directly to activate apelin receptors on the underlying smooth muscle to produce vasoconstriction. This response may be modified by apelin peptides feeding back onto apelin receptors on endothelial cells to stimulate the release of dilators, such as nitric oxide. In heart, apelin peptides, released from endocardial endothelial cells, activate apelin receptors on cardiomyocytes to elicit positive inotropic actions. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. 

---