Vascular effects cardiovascular

Vascular effects Cocaine causes increases in blood pressure and heart rate, which fall to normal levels between doses (Foltin et al. 1995). Tachyphylaxis develops to the cardiovascular effects, even within a single session. Concurrent use of ethanol, cannabis, and cocaine causes even greater cardiovascular effects than those of each drug alone. Interactions can also occur with antidepressant drugs like desipramine. 

Cardiovascular Effects. Myocardial infarction, severe coronary luminal narrowing, and internal alteration of the carotid artery were found in two patients injected 21 -30 years before with an unreported amount of Thorotrast (Isner et al. 1978). The authors concluded that the vascular effects were the result of chronic alpha irradiation. The patients were injected in the carotid artery, and thorotrastoma (see Other Systemic Effects, below) was found in both patients. 

Cardiovascular effects of Infusion of norepinephrine, epinephrine, Isoproterenol, and dopamine in humans. Infusions were made intravenously during the time indicated by the broken lines. Heart rate is given in beats per minute, blood pressure in millimeters of mercury, and peripheral resistance in arterial blood pressure. (Reprinted with permission from Allwood MJ, Cobbald AF, and Ginsburg J. Peripheral vascular effects of noradrenaline, isopropyl-noradrenaline, and dopamine. Br Med Bull 19 132, 1963. Reproduced by permission of the Medical Department, The British Council. 

This pattern differs from that seen following administration with either a conventional (3- or a-blocker. Acute administration of a (3-blocker produces a decrease in heart rate and cardiac output with little effect on blood pressure, while acute administration of an a-blocker leads to a decrease in peripheral vascular resistance and a reflexively initiated increase in cardiac rate and output. Thus, the pattern of cardiovascular responses observed after labetalol administration combines the features of (3- and a-blockade, that is, a decrease in peripheral vascular resistance (due to a-blockade and direct vascular effects) without an increase in cardiac rate and output (due to (3-blockade). 

Another study of the effects of I on the cardiovascular systemic concluded that, in dogs anesthetized with sodium pentobarbital, the response of blood pressure to intravenous administration of I is a resultant of two separate effects a direct myocardial stimulation that was stopped with dichlorolsoproterenol and a stimulation of vascular smooth muscle that results in a slight increase in renal arterial pressure and a slight decrease in renal arterial flow. Neither atropine nor dichlorolsoproterenol affected these vascular effects. Injections of 1 into a jugular vein or a renal artery had no consistent effect on catecholamine concentrations in plasma taken from a femoral artery or a renal vein. In seven experiments in which I at 21-35 mg/kg was injected into a jugular vein, the mean blood pressure increased from 176/125 + 22/11... 

Serotonin (5-hydroxytryptamine, 5-HT) is synthesised in enterochromaffin cells, largely in the gut, and also extensively taken up into blood platelets from which it is released to have vascular effects. It has complex effects on the cardiovascular system, varying with the vascular bed and its physiological state it generally constricts arterioles and veins and induces blood platelet aggregation it stimulates intestinal and bronchial smooth muscle. Carcinoid tumours secrete serotonin and symptoms may be benefited by serotonin antagonists, e.g. cyproheptadine, methysergide and sometimes by octreotide (see Index). It is a neurotransmitter in the brain. 

Luscher TF, Spieker LE, Noll G, Cosentino F. 2001. Vascular effects of newer cardiovascular drugs focus on nebivolol and ACE-inhibitors. J. Cardio-vasc. Pharmacol. 38(Suppl. 3) S3—11... 

A comprehensive review of histamine receptors in the cardiovascular system has Ijeen published. Histamine lowers blood pressure by causing widespread vasodilatation in most animal species but the effects are complex to analyse. It is clear that both H and H2 receptors are involved, but their distribution and effect varies depending on the species and particular vascular bed under study. Both types of antagonist have to be administered together to fully block many of the vascular effects of... 

Cardiovascular System. Dingwall-Fordyce and Lane [17] found marked increase in cerebrovascular mortality among heavily exposed workers. These exposures were in the first quarter of this century, a time of poor working conditions. A similar increase was not found in the mortality of unemployed males. Other studies have concluded that there was excess mortality associated with only two illnesses, chronic nephritis and hypertension. It is unclear whether vascular effects of lead in man are direct effects on blood vessels or if the effects are secondary to renal effects [73). 

Nontraditional Hormones. Novel hormones identified ia cardiovascular tissue have profound effects on maintenance of blood pressure and blood volume ia mammals. Atrial natriuretic hormone (ANH) is a polypeptide hormone secreted from the atria of the heart. When the cardiac atrium is stretched by increased blood volume, secretion of ANH is stimulated ANH ia turn increases salt and water excretion and reduces blood pressure (6). Endothelin is a polypeptide hormone secreted by endothehal cells throughout the vasculature. Although endothelin is released into the circulation, it acts locally in a paracrine fashion to constrict adjacent vascular smooth muscle and increase blood pressure (7). 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

ANPs play an important role in the maintenance of cardiovascular homeostasis by counterbalancing the renin—angiotensin (RAS) system. ANP, the main circulating form of the natriuretic peptides, effectively relaxes vascular smooth muscle, promotes the excretion of sodium and water, and in the CNS inhibits vasopressin release and antagonizes AT-II induced thirst. 

It has been proposed that the development of the complications of diabetes mellitus may be linked to oxidative stress and therefore might be attenuated by antioxidants such as vitamin E. Furthermore, it is discussed that glucose-induced vascular dysfunction in diabetes can be reduced by vitamin E treatment due to the inactivation of PKC. Cardiovascular complications are among the leading causes of death in diabetics. In addition, a postulated protective effect of vitamin E (antioxidants) on fasting plasma glucose in type 2 diabetic patients is also mentioned but could not be confirmed in a recently published triple-blind, placebo-controlled clinical trial [3]. To our knowledge, up to now no clinical intervention trials have tested directly whether vitamin E can ameliorate the complication of diabetes. 

Cardiovascular Effects. A number of eardiovaseular lesions, such as acute myoeardial degeneration and vascular degeneration, eongestion, and hemorrhage, have been observed in individuals exposed to... 

Anaphylaxis is the most dramatic and potentially catastrophic manifestation of allergic disorders. It can affect virtually any organ including the cardiovascular system. Cardiovascular collapse and hypotensive shock in anaphylaxis have been attributed to peripheral vasodilation, enhanced vascular permeability and plasma leakage, rather than any direct effect on the myocardium. However, there is increasing experimental and clinical evidence that the human heart is a site and target of anaphylaxis. 

Cardiovascular disease (CVD) is characterized by the involvement of the heart and allied vascular system. High cholesterol, associated lipid abnormahties and high blood pressure are recognized as the major risk factors of CVD. There have been several animal experiments and clinical studies using rice bran and rice bran oil, which have demonstrated a hypocholesterolemic effect (Raghuram et al., 1989 Rukmini and Raghuram, 1991 Sugano and Tsuji, 1997). The mechanisms involved are briefly summarized. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

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