Angiotensin‐converting enzyme inhibition increases glucose‐induced insulin secretion in response to acute restraint

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Idiopathic Massive Spontaneous Hemothorax: Adhesion Disruption

Background  Hemothorax has been reported to occur along with spontaneous pneumothorax due to adhesion disruption. Rupture of pleural adhesions spontaneously or after unnoticeable trivial trauma causing massive hemothorax alone is rare. Methods  We present a series of seven cases of idiopathic massive spontaneous hemothorax due to adhesion disruption, of which all required emergency thoracotomy with ligation or cauterization of bleeding adhesions. Results  Six patients had bleeding pleural lung adhesions of which five involved the upper lobes. Another had bleeding from pleuropericardial adhesions. All patients are doing well on follow-up. Conclusions  Disruption of pleural adhesions may cause massive hemothorax, requiring early surgical intervention. After thoracotomy the outcome in these patients is excellent.     

Spectrum of abdominal organ injury in a primary blast type

Introduction  

Abdominal organ injury in a primary blast type is always challenging for diagnosis. Air containing abdominal viscera is most vulnerable to effects of primary blast injury. In any patient exposed to a primary blast wave who presents with an acute abdomen, an abdominal organ injury is to be kept in a clinical suspicion.     

GROWTH HORMONE ATTENUATES MYOCARDIAL FIBROSIS IN RATS WITH CHRONIC PRESSURE OVERLOAD-INDUCED LEFT VENTRICULAR HYPERTROPHY

• 1 The role of growth hormone (GH) in cardiac remodelling and function in chronic and persistent pressure overload‐induced left ventricular hypertrophy has not been defined. The aim of the present study was to assess short‐term GH treatment on left ventricular function and remodelling in rats with chronic pressure overload‐induced hypertrophy.
• 2 Twenty‐six weeks after induction of ascending aortic stenosis (AAS), rats were treated with daily subcutaneous injections of recombinant human GH (1 mg/kg per day; AAS‐GH group) or saline (AAS‐P group) for 14 days. Sham‐operated animals served as controls. Left ventricular function was assessed by echocardiography before and after GH treatment. Myocardial fibrosis was evaluated by histological analysis.
• 3 Before GH treatment, AAS rats presented similar left ventricular function and structure. Treatment of rats with GH after the AAS procedure did not change bodyweight or heart weight, both of which were higher in the AAS groups than in the controls. After GH treatment, posterior wall shortening velocity (PWSV) was lower in the AAS‐P group than in the control group. However, in the AAS‐GH group, PWSV was between that in the control and AAS‐P groups and did not differ significantly from either group. Fractional collagen (% of total area) was significantly higher in the AAS‐P and AAS‐GH groups compared with control (10.34 ± 1.29, 4.44 ± 1.37 and 1.88 ± 0.88%, respectively; P < 0.05) and was higher still in the AAS‐P group compared with the AAS‐GH group.
• 4 The present study has shown that short‐term administration of GH to rats with chronic pressure overload‐induced left ventricular hypertrophy induces cardioprotection by attenuating myocardial fibrosis.