Heart denervated

These tracers compete with endogenous noradrenalin for transport into pre-synaptic nerve terminals via the neuronal uptake-1 transport system. Once within the neuron, these tracers are not susceptible to metabolism and serve as markers of sympathetic innervation. Recent studies show decreased retention of ["C]HED in patients after cardiac transplant, consistent with heart denervation (Schwaiger et al., 1991). With time, some sympathetic reinnervation occurred particularly in the antero-septal regions of the heart. This correlates with recovery of the sensation of angina pectoris in these patients (Stark et al.,... 

At rest, the parasympathetic system exerts the predominant effect on the SA node and therefore on heart rate. In a denervated heart, such as a trans-... 

The second factor that exerts control on heart rate is the release of the catecholamines, epinephrine and norepinephrine, from the adrenal medulla. Circulating catecholamines have the same effect on heart rate as direct sympathetic stimulation, which is to increase heart rate. In fact, in the intact heart, the effect of the catecholamines serves to supplement this direct effect. In a denervated heart, circulating catecholamines serve to replace the effect of direct sympathetic stimulation. In this way, patients who have had a heart transplant may still increase their heart rate during exercise. 

A reduction of HED uptake in patients with moderate heart failure is a predictor of poor outcome, a finding consistent with SPECT MIBG studies [137]. HED PET imaging demonstrates reinnervation of the transplanted heart [138] paralleling recovery of primarily fatty acids metabolism after an initial metabolic shift from fatty acids to glucose utilization associated with myocardial denervation [139]. 

J.P. Moak, B. Eldadah, C. Holmes, S. Pechnik, D.S. Goldstein, Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy In humans. Heart Rhythm. 2 (2005) 602-609. 

The role of the sympathetic nervous system in renal injury, end-stage renal disease, and renovascular hypertension are discussed through a literature review accompanying sympathetic nerve mechanisms in hypertension and obesity. Relevant studies of sympathetic nerve activity and 32-adrenoceptor polymorphism might contribute to the onset and maintenance of renal injury in healthy subjects and in patients with chronic heart failure and cardiovascular events in ESRD patients. A better understanding of the relationships of sympathetic nerve activity with renal injury might help clinical implications (treatment) for renal injury in hypertensive patients and hypertension in patients with ESRD. Recently, the role of denervation of renal sympathetic nerve in refractory hypertension has been examined and showed its efficacy in humans. The outcome from the study have not been established, but a number of animal studies show theoretical benefits for those patients in the acute phase. Further studies are needed to clarify the relationships between the sympathetic nerve activity and renal injury. 

Jacob P, Ariza P, Osborn JW. Renal denervation chronically lower arterial pressure independent of dietary sodium intake in normal rats. Am. J. Physiol. Heart Circ. Physiol. 2003 284 H2302-2310. 

The fatty acid composition of muscle lipids may show quantitative alterations in diseased muscle. Thus lecithin isolated from human dystrophic muscle had an increased amount of oleic but diminished linoleic acid (Tl). Changes have been recorded also in the fatty acid composition of lecithin from denervated muscle (PI). Recently it has been reported (K16) that the fatty acid pattern of muscle phosphatides from patients with the autosomal dominant form of myotonia congenita differed markedly from that of the autosomal recessive form and from the normal. Tani and his co-workers (F7) have made a detailed study of the phospholipids of normal and dystrophic mouse tissues. In normal mice phosphatidylcholine and phosphatidylethanolamine from skeletal and heart muscles had a very high content of 20-22-carbon polyunsaturated acids, in comparison with those for other tissues the most abundant was docosahexaenoic acid. In dystrophic mice there was a sharp decrease in the proportion of docosahexaenoic acid in the phosphoglycerides from skeletal and heart muscles, suggesting the likelihood of important alterations in muscle membranes. Somewhat similar studies have been reported by Owens (05), who also observed a fall in the proportion of docosahexaenoic acid, mainly in the phosphatidylcholine -j- choline plasmalogen fraction. 

Adenosine Negative chronotropic effect Hypersensitivity Effect on sinus node of denervated heart Life-threatening asystole (>0.5 min) may occur if used to treat supraventricular arrhythmia or stress testing... 

Acetylcholine Negative chronotropic effect Hypersensitivity Effect on sinus node of denervated heart ... 

A pure alpha agonist will cause reflex bradycardia in a subject with intact cardiac innervation, but no change in hean rate if this innervation is severed, eg, in a heart transplant patient. The other drugs listed have direct beta agonist effects and will increase heart rate in the denervated heart. The answer is (D). 

The transplanted heart is characterized by autonomic denervation, therefore chronotropic incompetence and, often during intermittent episodes of allograft rejection, sinus node dysfunction are not abnormal - especially in the early postoperative period. 

Assay of Adrenaline.—The hormone value of preparations may be estimated (i.) colorimetrically, by comparison of the blue colour it yields with Folin s phosphotungstate reagent (ii.) biologically, from the inhibitory effect on the contraction of a strip of involuntary muscle suspended in saline, the accelerating effect on an isolated heart, the dilating effect on a denervated iris, and the vaso-pressor response in an animal. 

Use cautiously In patients with denervated transplanted hearts. 

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