The effect of chronic exogenous androgen on myocardial function following acute ischemia-reperfusion in hosts with different baseline levels of sex steroids

BACKGROUND: Gender differences exist in the myocardial response to acute ischemia/reperfusion (I/R) injury and may be attributed to the effects of the sex hormones estrogen and testosterone. The role of estrogen in myocardial injury has been extensively studied but little information exists regarding the myocardial involvement of testosterone. Based on the deleterious effects of chronic endogenous and acute testosterone exposure observed in our previous studies, we postulated that chronic exogenous testosterone administration would also exhibit deleterious effects on myocardial function following I/R. METHODS: Langendorff perfused rat hearts were subjected to 25 min ischemia, 40 min reperfusion, and left ventricular developed pressure (LVDP) was recorded. Control and 5alpha-dihydrotestosterone (DHT) treated groups each consisted of normal males, castrated males, ovariectomized (OVX) females, and senescent females. P < 0.05 = significant. RESULTS: Chronic DHT replacement therapy showed no difference in functional ischemic recovery as measured by LVDP after 40 min reperfusion in castrated males (65.1 +/- 8.13% versus 66.3 +/- 4.54%), OVX females (64.5 +/- 10.6% versus 50.2 +/- 5.97%), and senescent females (42.1 +/- 0.04% versus 41 +/- 0.05%). Interestingly, LVDP was greater in DHT treated males than control males after I/R (65.2 +/- 8.20% versus 47.6 +/- 5.19%). Also, DHT treatment resulted in significantly increased recovery of LVDP after only 10 min reperfusion in castrated males, OVX females, and senescent females compared with their untreated counterparts (54.8 +/- 11.9% versus 32.9 +/- 5.75%, 66.7 +/- 11.5% versus 43.1 +/- 8.15%, 53.4 +/- 10.1% versus 32.9 +/- 5.75%, respectively). CONCLUSION: Contrary to the adverse effects we observed in earlier studies with both endogenous and brief exogenous testosterone in myocardium injured by I/R, the present study revealed that chronic exogenous testosterone neither improved nor worsened myocardial functional recovery following 25 min ischemia and 40 min reperfusion.     

Postischemic infusion of 17-beta-estradiol protects myocardial function and viability

BACKGROUND: Females demonstrate improved cardiac recovery after ischemia/reperfusion injury compared with males. Attenuation of myocardial dysfunction with preischemic estradiol suggests that estrogen may be an important mediator of this cardioprotection. However, it remains unclear whether post-injury estradiol may have clinical potential in the treatment of acute myocardial infarction. We hypothesize that postischemic administration of 17beta-estradiol will decrease myocardial ischemia/reperfusion injury and improve left ventricular cardiac function. MATERIALS AND METHODS: Adult male Sprague Dawley rat hearts (n = 20) (Harlan, Indianapolis, IN) were isolated, perfused with Krebs-Henseleit solution via Langendorff model, and subjected to 15 min of equilibration, 25 min of warm ischemia, and 40 min reperfusion. Experimental hearts received postischemic 17beta-estradiol infusion, 1 nm (n = 4), 10 nm (n = 4), 25 nm (n = 4), or 50 nm (n = 4), throughout reperfusion. Control hearts (n = 4) were infused with perfusate vehicle. RESULTS: Postischemic recovery of left ventricular developed pressure was significantly greater with 1 nm (51.6% +/- 7.4%) and 10 nm estradiol (47.7% +/- 8.6%) than with vehicle (37.8% +/- 9.7%) at end reperfusion. There was also greater recovery of the end diastolic pressure with 1 nm (47.8 +/- 4.0 mmHg) and 10 nm estradiol (54.0 +/- 4.0) compared with vehicle (75.3 +/- 7.5). Further, 1 nm and 10 nm estrogen preserved coronary flow after ischemia and decreased coronary effluent lactated dehydrogenase compared with controls. Estrogen at 25 nm and 50 nm did not provide additional benefit in terms of functional recovery. Estrogen at all concentrations increased extracellular signal-regulated protein kinase phosphorylation. CONCLUSIONS: Postischemic infusion of 17beta-estradiol protects myocardial function and viability. The attractive potential for the clinical application of postischemic estrogen therapy warrants further study to elucidate the mechanistic pathways and differences between males and females.     

The effects of endogenous sex hormones and acute hypoxia on vasoconstriction in isolated rat pulmonary artery rings

BACKGROUND: Studies have noted gender differences in various models but have not investigated whether hormone depletion will abolish these differences. Therefore, we measured isometric force displacement in normal males, castrated males, normal females, and ovarectomized females. MATERIALS AND METHODS: Adult male, adult female, castrated male, and ovarectomized female (250-350 g) Sprague Dawley rat pulmonary arteries (n = 7-8/group) were isolated and suspended in physiological organ baths. Force displacement was continuously recorded for 60 min of hypoxia. Data (mean +/- SEM) was analyzed with two-way analysis of variance with post-hoc Bonferroni test or Student's t-test. RESULTS: Maximum vasodilation of normal males was -79.47 +/- 3.34%, while normal adult females exhibited a maximum vasodilation of -88.70 +/- 6.21% (P = 0.8149). In addition, delayed, phase II vasoconstriction of male pulmonary arteries rings was 89.79 +/- 7.25%, while adult females demonstrated a maximum phase II vasoconstriction of 95.90 +/- 14.23% (P = 0.9342). Hormone depletion of males exhibited a maximum vasodilation of -70.45 +/- 5.08% for castrated males as compared to -79.47 +/- 3.34% for normal adult males (P = 0.3805). Castrated males exhibited a maximum phase II vasoconstriction of 86.20 +/- 15.76% compared to 89.79 +/- 7.25% exhibited by normal adult males (P = 0.9516). CONCLUSIONS: Hormone depletion in males and females did not alter pulmonary vasoreactivity in acute hypoxia.     

Complex karyotype including chromosomal translocation (8;14) (q24;q32) in one case with B-cell prolymphocytic leukemia

We report a case of a 64-year-old white female patient, who presented with symptomatic anemia (Hgb: 6.8g/dl), thrombocytopenia (platelets: 94,000/mcl) and leukocytosis (WBC: 156,000/mcl). Peripheral blood smear revealed markedly increased white blood cell count with predominance of atypical lymphoid cells of intermediate size, moderately dense chromatin, and prominent large single nucleoli. Bone marrow aspirate smear showed predominance (78%) of atypical lymphoid cells morphologically identical to those seen in the peripheral blood. The bone marrow core biopsy was hypercellular and packed with prominent infiltrate of prolymphocytes. Immunophenotypic analysis revealed a population of monoclonal cells (75% of all -erythroid cells) characterized by CD45+, CD19+, CD20+, CD5+, HLA-DR+, CD10-, CD23+/-, CD38+ and FMC7-. The abnormal cells were restricted to kappa light chain immunoglobulin with low intensity. Cytogenetic study showed an abnormal clone of eight cells with the following karyotype: 45,X,-X,add(8)(p11.2),t(8;14)(q24;q32),add(20)ql3[8]/46,XX[12]. The relative rarity of B-PLL and the heterogeneity of clinical and laboratory parameters make it difficult to define the natural history and prognosis in all cases. The optimal treatment for B-PLL is still unknown and to date there are no reports of chromosomal abnormalities as a prognostic factor. The patient was treated with six cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP). Complete remission was achieved according to the criteria defined by National Cancer Institute Working Group for CLL.     

我国道路交通事故伤概况

以公安部交通管理局公布的数据为基础，报告我国近４０多年来，道路交通事故及其所致的伤亡不断上升，分别增加了约３０倍至５０余倍；万车死亡率有明显下降趋势，由１９５１年的１３７．６４人降至１９９３年的２７．２７人，但仍远高于发达国家（＜５人），１０万人死亡率有增高的趋势，由１９５１年的０．１５人增至１９９３年的５．２９人，但低于发达国家（＞７．７人），这显然与我国人均汽车拥有量较少有关。通过分析道路交通