Cardiovascular system vasculature

Figure 7.1. Vomiting Mechanisms. The afferent nervous (peripheral and central) and humoral inputs converge to the medullary area. Here the signals are examined and integrated and may lead to emesis (expulsion of gastrointestinal contents). The efferent output involves respiratory muscles, visceral organs, cardiovascular system, visceral and cutaneous vasculature. The endogenous factors are released into...

In the cardiovascular system the effect on the heart rate is prominent. The depressive influence of the nervus vagus on the pacemaking activity in the heart is concentration dependently reduced and thereby the heart rate increases. This can be therapeutically useful in various forms of bardycardia, especially if they are caused by a vagus overstimulation, for example in the carotis-sinus syndrom. There is hardly any effect on the vasculature except a vasodilatation in the thoracic region after very high doses of atropine. 

AM is widely distributed in the body. The highest concentrations are found in the adrenal glands, hypothalamus, and anterior pituitary, but high levels are also present in the kidneys, lungs, cardiovascular system, and gastrointestinal tract. AM in plasma apparently originates in the heart and vasculature. 

A method of treatment and prophylaxis of events, conditions and diseases of the systemic vasculature and immune function to decrease cardiovascular risk and pathogenic infection mentions manganese carbonyl [247]... 

The peripheral vasculature is considered a target organ. Physical examination of the systemic vasculature can detect evidence of atherosclerosis, which may present as bruits (in the aortic, abdominal, and peripheral arteries), distended veins, diminished or absent peripheral arterial pulses, or lower extremity edema. Peripheral arterial disease is a clinical condition that can result from atherosclerosis, which is accelerated in hypertension. Other cardiovascular risk factors (e.g., smoking) can increase the hkelihood of peripheral arterial disease as well as all other forms of target-organ damage. 

Polymeric materials that have been used in the cardiovascular system include polytetrafluorethy-lene, polyethylene terephthalate, polyurethane, polyvinyl chloride, etc. Textiles bas on polytetra-fluorethylene and polyethylene terephthalate are us extensively as fabrics for repair of vasculature and larger-vessel replacement (greater than 6 mm in diameter). Stent-grafts are hybrid stent grafts placed by catheter to treat aortic aneurysms nonsurgically and are fabricated of the same metallic alloys used in stents and textiles similar to those used in vascular grafts. Table 14.1 lists many of the biomaterials currently used in the cardiovascular system. 

Four cardiovascular parameters of interest are stroke volnme, cardiac output (CO), total peripheral resistance of the systemic vasculature (TPR), and blood pressure. Measurements of both systolic blood pressnre (SBP) and diastolic blood pressure (DBP) are typically presented when discnssing blood pressnre. 

The physiological and pharmacological effects of histamine are mediated through four different receptors Hi, Hj, Hj, and Ht, all members of the 7-transmembrane g protein-coupled receptor (GPCR) family with amino terminal glycosylation sites and phosphorylation sites for protein kinases A and C. The receptors are widely expressed on different tissues that are responsive to histamine. For the Hi receptor these tissues include smooth muscle cells of the airways and vasculature, the gastrointestinal tract, cardiovascular system, neutrophils, endothelial cells, T and B cells, hepatocy tes, nerve... 

In addition to studying hemodynamic changes caused by liberated histamine, plasma epinephrine and norepinephrine levels have been investigated following injection of morphine. In a study of a patient who experienced an anaphylactoid response following the intravenous injection of morphine 0.3 mg/kg, plasma catecholamines were increased and this was accompanied by decreases in systemic vascular resistance and arterial blood pressure. In another study, intravenous morphine increased cardiac output, histamine, and epinephrine plasma concentrations and decreased arterial blood pressure and systemic vasculature resistance in adult subjects with no history of drug allergy or clinical evidence of cardiovascular, pulmonary, or metabolic disease. 

Despite the use of menthol in culinary and medicinal preparatitMis [2], relatively little is known about its actions on the human cardiovascular system, particularly in vascular smooth muscle. Studies in blood vessels evaluating the effects of menthol demonstrated different actions, particularly related to the precontractile state of the vasculature prior to menthol administration. 

Baroreflexes involving the sympathetic nervous system are responsible for the rapid moment-to-moment regulation of blood pressure. A fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the aortic arch and carotid sinuses) to send fewer impulses to cardiovascular centers in the spinal cord. This prompts a reflex response of increased sympathetic and decreased parasympathetic output to the heart and vasculature, resulting in vasoconstriction and increased cardiac output. These changes result in a compensatory rise in blood pressure (Figure 19.3, and Figure 3.5, see p. 31). 

The in vivo cardiovascular effects of carmabinoids are complex and may involve modulation of the autonomic outflow in both the central and peripheral nervous systems as well as direct effects on the myocardium and vasculature. However, their peripheral actions appear to play the dominant role, at least upon systemic administration at the doses used by most investigators. Moreover, the effects of endocannabinoids are complicated by their rapid metabolism, which may liberate other vasoactive substances and their precursors (reviewed in Mechoulam et al. 1998 Kunos et al. 2002 Randall et al. 2002 Ralevic et al. 2002). 

The same cardiovascular control system regulates blood distribution and blood pressure by affecting the small arterioles of the peripheral blood vasculature. The entrance to each of these vessels is surrounded by a sphincter muscle (a ring of involuntary muscle that surrounds the arteriolar aperture) with sympathetic, and in some cases, parasympathetic, nerve fibers. The sphincter is usually contracted. When the signal comes for the muscle to relax, the neuron produces nitric oxide at the neuromuscular junction, and this gas relaxes the sphincter. When the sphincter muscle expands, it increases the area through which blood flows and decreases its resistance. With decreased resistance, blood pressure falls. 

Quality of the haemodynamic data is also affected by technical factors. Major factors to consider include the possibility of hydrostatic pressure effects (i.e. blood inside the vasculature or fluid-filled catheter systems that are utilized in recording methods), long-term stability of the pressure sensor (subject to possible drift with time), frequency response of the sensor and associated modem solid-state electronics (see Sarazan 2014 for a complete review of technological requirements and potential errors that can be encountered when measuring cardiovascular pressure in safety pharmacology studies). 

The cardiovascular action of SM to lower systemic blood pressure in the rats has been demonstrated. Langendorff cardiac preparation in guinea pig and four types of vasculature in dog, including coronary, renal, femorid, and mesenteric arteries are performed. SM induces dose-related hypotension without changing heart rate. Atropine, propranolol, and chlorpheniramine plus cimetidine antagonize the hypotensive effect. In the isolated whole-heart preparation, SM injection increases coronary blood flow and causes a positive inotropic action. SM relaxes all arteries at low concentration and contracts all, but the coronary artery, at high concentration (7P). 

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