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Biomedical subjects

P Trouve

Publications and source records attributed to P Trouve.

5 recordsLinked to original sources
PubMed2004

[Pubalgia: from diagnosis to return to the sports field].

OBJECTIVES: To review reports of the diagnosis and treatment of groin pain (pubalgia) on the basis of anatomical considerations, epidemiology and pathogenicity. METHODS: We searched the Medline database using the key words groin injury, groin pain, and symphisis syndrome for information on groin pain. RESULTS: Despite the limitations of this study, athletic pubalgia appears to be a real diagnosis, with a long duration of symptoms and a therapeutic challenge. The pathophysiologic processes of this lower abdominal pain resulting from over use is unclear, but muscular imbalance might be involved in the pathogenicity. There is no consensus on the diagnostic criteria and the role of imaging (magnetic resonance imaging). Physicians should eliminate the diagnosis of hip and groin injuries in athletes. Specific rehabilitation should include eliminating the pain-triggering factors, increasing the limited flexibility, and strengthening the abdominal muscles and adductor muscles. The multidisciplinary team's goal is to restore function and prevent recurrence. Successful surgical repair is predictable in well-selected patients. CONCLUSION: Further studies are required for better assessment of incidence, the natural course of groin pain, and optimal clinical evaluation in screening patients. Overall, a large prospective randomized study of athletes with groin pain would help determine optimal treatment.

Abdominal Pain↗
PubMed2000

Na(+)-K(+)-ATPase alpha(2)-isoform expression in guinea pig hearts during transition from compensation to decompensation.

Disturbance in ionic gradient across sarcolemma may lead to arrhythmias. Because Na(+)-K(+)-ATPase regulates intracellular Na(+) and K(+) concentrations, and therefore intracellular Ca(2+) concentration homeostasis, our aim was to determine whether changes in the Na(+)-K(+)-ATPase alpha-isoforms in guinea pigs during transition from compensated (CLVH) to decompensated left ventricular hypertrophy (DLVH) were concomitant with arrhythmias. After 12- and 20-mo aortic stenosis, CLVH and DLVH were characterized by increased mean arterial pressure (30% and 52.7%, respectively). DLVH differed from CLVH by significantly increased end-diastolic pressure (34%), decreased sarco(endo)plasmic reticulum Ca(2+)-ATPase (-75%), and increased Na(+)/Ca(2+) exchanger (25%) mRNA levels and by the occurrence of ventricular arrhythmias. The alpha-isoform (mRNA and protein levels) was significantly lower in DLVH (2.2 +/- 0.2- and 1. 4 +/- 0.15-fold, respectively, vs. control) than in CLVH (3.5 +/- 0. 4- and 2.2 +/- 0.13-fold, respectively) and was present in sarcolemma and T tubules. Changes in the levels of alpha(1)- and alpha(3)-isoform in CLVH and DLVH appear physiologically irrelevant. We suggest that the increased level of alpha(2)-isoform in CLVH may participate in compensation, whereas its relative decrease in DLVH may enhance decompensation and arrhythmias.

Adaptation, Physiological↗
PubMed1998

In vivo left ventricular function and collagen expression in aldosterone/salt-induced hypertension.

Cardiac fibrosis is linked to aldosterone-induced hypertension, but the effects on in vivo left ventricular (LV) function are not established. We studied the relations between in vivo LV function and aldosterone/salt cardiac fibrosis. Adult guinea pigs (GPs) were treated for 3 months with an aldosterone infusion and high-salt diet. This treatment induced arterial hypertension (+35%) and moderate LV hypertrophy (LVH; +60%) without right ventricular (RV) hypertrophy. Echo-Doppler LV assessment demonstrated unaltered cardiac output, stroke volume, or LV relaxation. Type I collagen messenger RNA (mRNA) was significantly increased in both ventricles (LV, +48%; RV, +77%) and accompanied by a significant increase in total collagen deposition (LV, from 0.52% in controls to 4.4% in treated GPs; RV, from 0.82 to 5.5% in treated GPs). Plasma norepinephrine levels increased 2.6-fold (p < 0.01) and correlated with the increase in collagen deposition in both ventricles. Collagen content was not correlated with hypertension or LVH. We conclude that aldosterone administration induces cardiac collagen accumulation and a sympathetic stimulation, which might preserve systolic and diastolic function.

Aldosterone↗