PubMed · 4577357
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K A Grigorovich. 1972. [Errors and failures in nerve surgery].. https://pubmed.ncbi.nlm.nih.gov/4577357/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Heart failure is accompanied by sympathetic over-activity, which contributes to the pathophysiology and to poor prognosis. This paper reviews the mechanisms and potential therapy for sympathetic dysregulation in heart failure (HF). Several points are emphasized: (1) There is increased sympathetic activity to skeletal muscle, kidney, and heart, but not to skin, in HF. This information challenges the concept of generalized sympathetic activation in HF and suggests that the factors responsible for sympathetic activation result in a partitioning of excess sympathetic outflow to some but not all tissues and organs. (2) The sympathetic dysregulation appears to result from impairment in cardiac and arterial baroreceptor restraint on sympathetic activity, but this abnormality in baroreceptor function may result from abnormal humoral and/or ionic influences acting on baroreceptor endings or in the central nervous system and not from intrinsic structural abnormalities in baroreceptors. This distinction has potential therapeutic importance because abnormalities in humoral or ionic mechanisms would more likely lend themselves to therapeutic modulation. (3) Digitalis sensitizes cardiac and arterial baroreceptors and inhibits sympathetic nerve activity in patients with HF. This sympathoinhibitory influence of digitalis is maintained during chronic therapy. These observations support the concept that the therapeutic effects of digitalis include autonomic modulation in addition to positive inotropism. In a broader concept, these observations suggest that sympathetic modulation may represent an important target for drugs for treatment of heart failure.
MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and strokelike episodes) is a distinct disorder characterized clinically by repeated strokelike attacks mostly beginning in childhood. We have paid special attention to the blood vessel abnormality seen in most biopsied muscle, in terms of the strokelike episodes in MELAS. The 3243 mutation in 80% of the typical MELAS patients has also been found in patients differing from the MELAS phenotype. Because we have examined muscle biopsies in 94 MELAS or 3243-positive patients, it is worthwhile to summarize the clinical and pathological findings and to prove the discrepancy between phenotype and genotype. This may be a starting point for further discussion of the pathomechanism and so toward further understanding of the disease itself.
UNLABELLED: We report on two children with hemihypertrophy and ipsilateral hemimegalencephaly. Vascular lesions in one were consistent with a diagnosis of the Klippel-Trénaunay-Weber Syndrome. MRI performed in the first days of life and at 1 month of age revealed the presence of the neuronal anomaly. CONCLUSION: The occurrence of hemimegalencephaly in our patients indicates that hemihypertrophy and vascular dysplasia are pathogenetically related phenomena of a continuous spectrum in which this brain disorder may appear.