Myocardial protection of the homograft II cold coronary perfusion.
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Biomedical subjects
Publications and source records attributed to B Laroche.
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The response to acute oral administration of 50 mg of Captopril was assessed in 17 normal volunteers and 47 patients with hypertension; 17 had renovascular (RVH) abnormalities and 30 patients had essential hypertension (EH). All patients were maintained on ad libitum sodium intake. The effect of Captopril on mean arterial pressure (MAP) was rapid a maximal within 60 minutes. The converting enzyme inhibitor induced a similar decrease in MAP in normal subjects (-5.1 +/- I mm Hg) and patients with EH (-7.2 +/- I mm Hg). Control plasma renin activity (PRA) was similar in both groups; however, the increase in PRA following Captopril was more marked in normals (8.1 +/- 1.7 ng/ml/h) than in EH (1.7 +/- 0.7 ng/ml/h). In patients with RVH a marked fall in MAP occurred (-25.4 +/- 4 mm Hg). A fall in MAP higher than 20 mm Hg was observed in 65% of patients with RVH and none of the EH group. A negative correlation between log PRA and the change in MAP induced by Captopril was obtained (r = 0.65). Assessment of the response to acute administration of Captopril may be useful for screening patients with RVH.
Because severe cardiac insufficiency follows orthotopic heart transplantation, the authors have evaluated protection of the homograft provided by a cooling and isolating bag during the operative period of ischemia and subsequently its effect on cardiac function. In one group or four dogs hearts were transplanted without using hypothermia. In the second group, seven hearts were excised, immediately cooled by immersion in saline at 4 degrees C and orthotopically homotransplanted. In the third group, six hearts were immersed in saline and then isolated in a cooling bag until transplantation had been completed. Cardiac function in all animals was evaluated at rest, 3, 24 and 48 hours after operation. In group 1, lowering of the temperature was minimal and all animals died immediately after operation. In group 2, the myocardial temperature, which had been lowered to 13 degrees C by immersion, had risen to 25 degrees C after 17 minutes. In group 3, the myocardial temperature was maintained at 13 degrees C up to the time the aortic clamp was removed. Three hours after operation, the cardiac performance of group 3 was much better than that of group 3 was much better than that of group 2 as demonstrated by an increase of cardiac output (39%), stroke volume (44%), mean systolic ejection rate (25%), maximum systolic flow (28%), peak velocity (26%), maximum acceleration (20%), left ventricular power (32%) and left ventricular work (47%). In the following days, cardiac function of groups 2 and 3 improved and the disparity between then decreased. These results demonstrate that the cooling bag, while offering technical advantages, maintains profound hypothermia in the donor heart and substantially improves the performance of the homograft in the immediate postoperative phase.
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One child with a pure perinephric abscess and three with renal abscesses, one of which had perinephric extension, are described. All presented with a long course of subacute infection leading to localizing symptoms or signs in the flank. The diagnosis was confirmed by radiologic examination. All the abscesses were surgically drained at various intervals after diagnosis, while the patients were receiving antibiotic therapy. Salvage of renal function was possible in all cases. A rational approach to the diagnosis and management of such abscesses is emphasized.
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A large number of clinical studies has described procalcitonin (ProCT) as a marker of bacterial infection and a good predictor of disease severity and antibiotherapy efficacy. Nevertheless, the mechanism of ProCT synthesis remains unclear. The aim of this study was to demonstrate potential ProCT production by peripheral blood mononuclear cells as is the case for cytokines involved in sepsis. In a whole blood model, LPS (10 micrograms/ml) stimulation on blood samples from healthy volunteers (n = 14) was tested. Early (TNF-alpha and IL1-beta) and late (IL-6 and IL-8) cytokines were produced in large amounts in contrast to the absence of ProCT. Additional experiments with nitric oxide or detection of intra-cellular ProCT (cell lysis, flow cytometry) had negative results. It was concluded that ProCT is not produced in this model. Data are still needed to investigate the cellular origin of ProCT in order to better define its clinical usefulness.
The acute effect of the orally-active converting enzyme inhibitor, captopril, was compared to that of saralasin in 13 patients with various forms of hypertension on ad libitum sodium intake. A significant difference between the effects of the two drugs on mean arterial pressure (MAP) was found (-11 +/- 3 mm Hg with saralasin, -24 +/- 4.5 mm Hg after captopril). This difference was not correlated with control plasma renin activity (PRA). To determine the influence of the endogenous kallikrein-kinin system in the antihypertensive action of captopril, the effect of aprotinin (Apro), an inhibitor of kinin generation, on the MAP level achieved by captopril was assessed in five normal subjects and 15 patients with hypertension on ad libitum sodium intake. In normal subjects, captopril did not alter MAP, nor did Apro have any effect. In six patients with essential hypertension and normal PRA, MAP decreased by 5.5 +/- 2 mm Hg following captopril, and Apro did not modify this level. In nine patients with renovascular hypertension (RVH), MAP fell by 22 +/ 3 mm Hg after captopril administration, and Apro infusion induced a rise in MAP of 13 +/- 1.7 mm Hg. A positive correlation between log control PRA and the effect of aprotinin was obtained ( r = 0.63, p less than 0.005). Apro had no effect in two patients with RVH who experiences a large drop in MAP during salasin. These results suggest that endogenous kinins as well as other substances, the generation of which is inhibited by aprotinin, may participate to the antihypertensive effect of captopril in patients with angiotensin-dependent hypertension. The lack of an aprotinin effect on the MAP level achieved during saralasin infusion suggests that the influence of the kallikrein-kinin system is related to the effect of captopril rather than the fall in arterial pressure resulting from angiotensin blockade.
Suppression of androgen levels in blood of stage D2 prostate cancer patients has been the prominent treatment for advanced prostate cancer. However, the duration of hormone sensitivity of prostate tumor is variable. The type of initial response to hormonal treatment, the length of response and patient's survival are in direct association with disease aggressiveness. Recently, an arithmetic formula expressing disease aggressivity was computed using pretreatment values of prostatic acid phosphatase (P.A.P.), alkaline phosphatase (A.P.), degree of tumor differentiation and number of bone metastases. This aggressiveness score was related to disease response and patients outcome receiving hormonal treatments. The use of an arithmetic formula to express disease aggressivity could result in a subdivision of the disease. The identification of the subgroup of stage D2 patients destined not to benefit from hormonal manipulation could change the strategies employed up until today for the treatment of advanced prostate cancer.
The homotransplanted heart is in severe failure in the immediate post-operative period, secondary to ischemia inherent to the technic of orthotopic transplantation. The present work was carried out to investigate if ventricular fibrillation followed by cold coronary perfusion could protect the homograft during implantation by evaluating the post-operative cardiac performance. In the control group, 7 hearts were excised, immediately immersed in physiological saline at 5 degrees C, and homotransplanted. In a second group of 4 grafts, ventricular fibrillation was induced and the coronary bed was perfused immediately with cold (5 degrees C) extracellular solution for a period of 10 minutes before orthotopic implantation. All animals were prepared at the end of surgery for hemodynamic studies to be carried out 3, 24 and 48 hours post-operatively in the resting state. In group I, the myocardial temperature dropped to 13.5 degrees C in 14.5 minutes. In group II, the hypothermia by perfusion was more rapid and deeper (11 degrees C within 10 minutes). Three hours post-operatively, cardiac function of group II was superior to that of group I as demonstrated by the increase of cardiac index (39%), stroke volume index (41%) mean systolic ejection rate index (44%), maximum systolic flow index (58%), maximum acceleration index (36%), stroke power index (88%), stroke work index (67%). Twenty-four and forty-eight hours post-operatively the cardio-vascular function improved in both groups but remained superior in group II. These results demonstrate that ventricular fibrillation followed by cold coronary perfusion increases protection of the homograft during the initial period of implantation.