Search PubMed⌕ Search

Biomedical subjects

M Lesch

Publications and source records attributed to M Lesch.

143 records · Page 8Linked to original sources
PubMed1967

Enhanced protein synthesis in a cell-free system from hypertrophied skeletal muscle.

Hypertrophy of the rat soleus muscle was induced by tenotomy of the synergistic muscles. Four days after the operation, the weight of the muscle had increased by 30 percent. The hypertrophied muscle had an increased concentration of DNA and RNA, when compared to the contralateral control soleus. Although the amount of myofibrillar protein increased during the 4-day period, the concentration of this component decreased. Microsomes prepared from hypertrophied muscle had an increased RNA concentration. The combined microsomes and pH-5 enzyme from hypertrophied muscle supported a faster rate of protein synthesis in vitro than the same system prepared from an equal weight of contralateral muscle which was used as a control.

Animals↗
PubMedDate not supplied

Progression of heart failure: a role for interstitial fibrosis.

Progressive deterioration of left ventricular (LV) function is a characteristic feature of the heart failure (HF) state. The mechanism or mechanisms responsible for this hemodynamic deterioration are not known but may be related to progressive intrinsic dysfunction, degeneration and loss of viable cardiocytes. In the present study, we tested the hypothesis that accumulation of collagen in the cardiac interstitium (reactive interstitial fibrosis, RIF), known to occur in HF, results in reduced capillary density (CD = capillary/fiber ratio) and increased oxygen diffusion distance (ODD) which can lead to hypoxia and dysfunction of the collagen encircled myocyte. Studies were performed in LV tissue obtained from 10 dogs with chronic HF (LV ejection fraction 26 +/- 1%) produced by multiple sequential intracoronary microembolizations. In each dog, CD and ODD were evaluated in LV regions that manifested severe RIF (volume fraction 16 +/- 2%) and in LV regions of little or no RIF (volume fraction 4 +/- 1%). In regions of severe RIF, CD was significantly decreased compared to regions of no RIF (0.92 +/- 0.02 vs. 1.05 +/- 0.03) (P < 0.003). Similarly, ODD was significantly increased in regions of severe RIF compared to regions of no RIF (15.3 +/- 0.4 vs. 12.2 +/- 0.3 microns) (P < 0.001). These data suggest that in dogs with chronic HF, constituent myocytes of LV regions which manifest severe RIF may be subjected to chronic hypoxia; a condition that can adversely impact the function and viability of the collagen encircled cardiocyte.

Animals↗
PubMedDate not supplied

Postinfarction angina.

In conclusion, the PIA patient is at high risk, with higher early as well as late mortality. The pathophysiology of PIA is complex and may vary from patient to patient. The concepts of ischemia at a distance and ischemia in the infarct zone have led to a better understanding of early PIA. Coronary spasm may play an important role in most PIA patients as in the general population of patients with angina pectoris. Medical therapy is efficacious in many, although it may on rare occasion aggravate myocardial ischemia. Urgent coronary arteriography is generally safe and should be performed as soon as possible for medically refractory PIA. CABG appears to be safe in experienced hands, but its timing must be individualized. The IABP should be reserved for more unstable patients for fear of vascular complications. Randomized controlled trials such as the BARI Trial will further compare PTCA with CABG.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Electrocardiographic changes associated with acute cerebrovascular disease: a clinical review.

Patients with acute vascular disorders of the CNS demonstrate an abundance of both rhythm and morphologic changes in their ECG. Of these a few will demonstrate myocardial dysfunction and or damage. The value of the ECG in evaluating and predicting which patients will have myocardial dysfunction or damage is questionable. One would assume the echocardiogram would be of more help than the ECG in identifying patients with myocardial damage; however, little data are available. The reason for the poor correlation between ECG findings and clinical correlates has not been explained to date, but it is possible to postulate a theory. There are two mechanisms that might mediate ECG changes in these patients, ie, autonomic neural stimulation from the hypothalamus or elevated circulating catecholamines. Hypothalamic stimulation may cause ECG changes without associated myocardial damage whereas elevated catecholamines may result in myocardial damage. This might explain why so many patients have ECG changes and very few have demonstrable myocardial damage in general, or ischemic damage in particular. That cardiac antiischemic therapy does not change mortality may relate to the fact that treatment has been directed towards patients with ECG changes, which in turn do not correlate with myocardial damage. Better patient selection for such therapy might rest upon demonstration of wall motion abnormalities on echocardiogram. The weakness of this strategy is that many patients with stroke have preexisting coronary disease and wall motion abnormalities and thus echo findings may only document remote infarction rather than acute ischemia.

Acute Disease↗
PubMedDate not supplied

The role of antiplatelet therapy in acute coronary syndromes and for secondary prevention following a myocardial infarction.

Acute Coronary Syndromes: Therapy with aspirin is recommended for all patients with acute myocardial ischemic syndromes unless contraindications for its use is present. None of the studies thus far have conclusively established evidence for a selective dose of aspirin. Until conclusive evidence exists, aspirin in doses of 81 mg (children's tablet) to 325 mg (adult tablet) are recommended. Ticlopidine may prove to be an attractive alternate choice in those who cannot take aspirin. According to the ACC/AHA task force recommendations, patients with acute myocardial infarction receiving thrombolytic therapy should receive both heparin and aspirin. Aspirin is to be administered in a dose of 160 mg daily. Heparin can be discontinued after 2 days if the patient's clinical course remains uncomplicated. Aspirin should be continued indefinitely. An alternative strategy in those who cannot take aspirin is to switch to warfarin before hospital discharge with a view toward long-term anticoagulant therapy. Secondary Prevention: Aspirin in a dose of 325 mg daily is recommended for all survivors of an acute myocardial infarction. No benefit derives from the addition of dipyridamole. The role of sulfinpyrazone remains undefined. Warfarin is an effective antithrombotic alternative to aspirin for secondary prevention after a myocardial infarction. However, aspirin is cheaper to administer and follow up when compared with warfarin. From available information, aspirin appears to be an adequate antithrombotic agent in patients who have near-normal left-ventricular function, the elderly, patients with coexisting cerebrovascular or peripheral vascular disease, and those with contraindications for anticoagulants. Warfarin should be preferred in high-risk patients with anterior or apical myocardial infarction, left-ventricular dysfunction with or without a mural thrombus, and those with associated atrial fibrillation. A randomized study assessing aspirin versus warfarin for secondary prevention after myocardial infarction is being initiated to determine the relative efficacy and safety of these drugs in secondary prevention after myocardial infarction.

Angina, Unstable↗
PubMedDate not supplied

Coronary artery aneurysm: a review.

Coronary artery aneurysm is defined as coronary dilatation which exceeds the diameter of normal adjacent segments or the diameter of the patient's largest coronary vessel by 1.5 times. This is an uncommon disease which has been diagnosed with increasing frequency since the advent of coronary angiography. The incidence varies from 1.5% to 5% with male dominance and a predilection for the right coronary artery. Atherosclerosis accounts for 50% of coronary aneurysms in adults. Reported complications include thrombosis and distal embolization, rupture and vasospasm. The natural history and prognosis remains obscure. Controversies persist regarding the use of surgical or medical management. The authors recommend surgery based on the severity of associated coronary stenosis rather than the mere presence of aneurysm. Medical therapy is indicated for the majority of patients and consists of antiplatelet and anticoagulant medication.

Adult↗
PubMedDate not supplied

The concept of abnormal hemispheric organization in addiction research.

In addition to the established areas of endogenous psychoses, the concept of abnormal hemispheric organization in the field of psychiatry is also generating ever greater interest in the area of research into addiction. On the basis of the demonstrably higher rate of developmental risk factors (pre-, peri-, postnatal), in particular the marker left-handedness (LH) has been interpreted as an indication of induced hemispheric 'malcontrol' in endogenous psychoses. In various studies, elevated rates of LH have also been shown in alcoholics. Alcoholism could be related to biological factors associated with anomalous cerebral dominance. In a joint study carried out by the Anton Proksch Institut in Vienna (Austria), and the University of Erlangen-Nuremberg (Germany) involving a total of 250 alcohol-dependent inpatients, the hypothesis of deviant laterality in the presence of an elevated frequency of developmental risk factors has been confirmed exclusively in male alcoholics. A comparison of subtypes has also revealed that Type IV in the Lesch typology, and Type II in the Cloninger classification, are more vulnerable subtypes. These results clearly show that there are differences to be found within the overall group of alcoholics, and underscore the need for subtyping and gender-specific studies.

Alcoholism↗