Cardiovascular pathophysiology

In summary, plaque imaging with F-labeled MMPIs remains a clinical challenge and is still in its infancy. The transfer of F-labeled MMPIs developed for oncological questions in the field of cardiovascular pathophysiology is one possible starting point. 

Cassady SL. Cardiovascular pathophysiology. In DeTurk WE, Cahalin LP, eds. Cardiovascular and... 

G. Montrucchio, G. Alloati and G. Camussi, Role of platelet-activating factor in cardiovascular pathophysiology, Physiol. Rev. 80, 1669-1699 (2000). 

To conclude, the presendy available Y1 antagonists have at last made it possible to establish that endogenous NPY can act as a sympathetic vasoconstrictor. The next task is to study the relevance of NPY in cardiovascular pathophysiology in various animal models. With the development of more potent and selective NPY antagonists, these studies should ultimately be extended to include man. 

Fisher MMD Clinical observations on the pathophysiology and treatment of anaphylactic cardiovascular collapse. Anesth Intensive Care 1986 17 17-21. Galli S (ed) Anaphylaxis. Novartis Foundation Symposium 157. Chichester, Wiley, 2004. Gronemeyer W Noradrenalin statt Adrenalin beim anaphylaktischen Schock. Dtsch Med Wochenschr 1980 102 101. 

It is important for the clinician to identify the cause(s) of AHF in order to maximize treatment efficacy and reduce future disease exacerbations. Cardiovascular, metabolic, and lifestyle factors can all precipitate AHF. The most common precipitating factors for acute decompensation and how they contribute pathophysiologically are listed in Table 3-3. 

Atherosclerosis (AS) is a progressive disease characterized by the accumulation of lipids and the development of fibrosis in arterial walls. It is the pathophysiologic process behind cardiovascular disease whose clinical... 

Smith, E.R., Pathophysiology of cardiac electrical disturbances, in Physio-pathology of the Cardiovascular System, Alpert, J.S., Ed., Little, Brown, Boston, 1984, chap. 14. 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

Free Radicals and Oxidative Stress in Pathophysiological Processes 31.1 Cardiovascular Diseases... 

At present, numerous free radical studies related to many pathologies have been carried out. The amount of these studies is really enormous and many of them are too far from the scope of this book. The main topics of this chapter will be confined to the mechanism of free radical formation and oxidative processes under pathophysiological conditions. We will consider the possible role of free radicals in cardiovascular disorders, cancer, anemias, inflammation, diabetes mellitus, rheumatoid arthritis, and some other diseases. Furthermore, the possibilities of antioxidant and chelating therapies will be discussed. 

D Qrleans-Juste P, Labonte J, Bkaily G, et al. Function of the endothehn(B) receptor in cardiovascular physiology and pathophysiology. Pharmacol Ther 2002 95 221-38. 

Hypertension is the most common cardiovascular disease and pathophysiologically hypertension can be classified into two main groups. 

The net result of the action of therapeutic concentrations of a cardiac glycoside is a distinctive increase in cardiac contractility (Figure 13-5, bottom trace). In isolated myocardial preparations, the rate of development of tension and of relaxation are both increased, with little or no change in time to peak tension. This effect occurs in both normal and failing myocardium, but in the intact patient the responses are modified by cardiovascular reflexes and the pathophysiology of heart failure. 

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