Dietary advanced glycation end-product restriction for the attenuation of insulin resistance, oxidative stress and endothelial dysfunction: a systematic review.

The benefits of advanced glycation end-product (AGE)-restricted diets in humans are unclear. This review aimed to determine the effect of dietary AGE restriction on the inflammatory profiles of healthy adults and adults with diabetes or renal failure. Eight computer databases were searched for controlled feeding trials published in English between January 1997 and December 2012. Human trials were included if at least one group received an AGE-restricted dietary intervention. A total of 12 trials reporting on 289 participants were included in the review. Five trials (42%) were of high methodological quality. Meta-analysis of two long-term (16 week) trials provided evidence favoring an AGE-restricted diet for the reduction of 8-isoprostanes (standardized mean difference 0.9; 95% confidence interval (CI): 0.3-1.5) and tumor necrosis factor-α (1.3; 95% CI: 0.6-1.9) in healthy adults. Intermediate-term dietary AGE restriction in adults with chronic renal failure reduced serum VCAM-1 (0.9; 95% CI: 0.1-1.7). Individual trials provided some evidence that long-term dietary AGE restriction reduces HOMA-IR (1.4; 95% CI: 0.3-2.6) and AGE-modified low-density lipoprotein (2.7; 95% CI: 1.6-3.9) in adults with type 2 diabetes. Generalisability is limited, as 75% of studies were of less than 6 weeks duration and more than half were of low methodological quality. Evidence quality ranged from low to very low, limiting the conclusions that can be drawn from this review. There is currently insufficient evidence to recommend dietary AGE restriction for the alleviation of the proinflammatory milieu in healthy individuals and patients with diabetes or renal failure. Additional long-term high-quality RCTs with larger sample sizes measuring patient-important outcomes are required to strengthen the evidence supporting the effects of AGE-restricted diets.

High frequency jet ventilation and gas trapping.

We have compared three types of high frequency jet ventilation (HFJV) with conventional positive pressure ventilation in patients recovering from elective coronary artery bypass surgery. Twelve patients were allocated randomly to receive HFJV at ventilatory frequencies of 60, 100, 150 and 200 bpm from a standard jet ventilator at either the proximal or distal airway (HFJV.p and HFJV.d), or from a valveless high frequency jet ventilator acting as a pneumatic piston (VPP). Trapped gas volume (Vtr), cardiac index (CI) and right ventricular ejection fraction (RVEF) were measured. Vtr was related to the type of HFJV used (P < 0.05) and ventilatory frequency (P < 0.05). CI decreased with increasing rate of HFJV (P < 0.05) and there were significant differences between the three types of HFJV (P < 0.05). RVEF showed a linear relationship with ventilatory frequency (P < 0.05) decreasing most with the VPP. The decrease in RVEF was associated with an increase in right ventricular end-systolic volume (P < 0.05) suggesting that an increase in right ventricular afterload was the cause. The same three types of HFJV were compared using a lung model with variable values of compliance and resistance, to assess the impact of lung mechanics on gas trapping (Vtr, ml). Lung model compliance (C) was set at 50 or 25 ml cm H2O-1 and resistance (R) at 5 or 20 cm H2O litre-1 s, where values of 50 and 5, respectively, are normal. Vtr increased with ventilatory frequency for all types of jet ventilation (P < 0.05), varying with the type of jet ventilation used (P < 0.05).

Comparison of the effects of propofol and isoflurane anaesthesia on right ventricular function and shunt fraction during thoracic surgery.

I.v. anaesthetic agents, including propofol, have not been shown to inhibit hypoxic pulmonary vasoconstriction (HPV). This may encourage the use of propofol in thoracic surgery where one lung ventilation (OLV) is required. We have compared the effects of maintaining anaesthesia with either isoflurane or propofol infusion on right ventricular function and shunt fraction. We studied 10 patients who received isoflurane and 12 who received propofol. When OLV commenced there was a greater reduction in both mean cardiac index (3.2 (SEM 0.2) to 2.4 (0.1) litre min-1 m-2 for propofol, and 3.4 (0.2) to 3.3 (0.4) litre min-1 m-2 for isoflurane) and right ventricular ejection fraction (0.45 (0.03) to 0.37 (0.02) for propofol, and 0.48 (0.02) to 0.42 (0.02) for isoflurane) in patients who received propofol. Furthermore, these reductions were sustained for longer in the propofol group. However, propofol was not associated with a significant increase in shunt fraction during OLV, which increased threefold in patients who received isoflurane.

The renin-angiotensin system and angiotensin converting enzyme (ACE) inhibitors.

Anaesthetists will encounter increasing numbers of patients who are receiving long-term treatment with ACE inhibitors for hypertension, congestive heart failure and prophylactically following myocardial infarction. Our understanding of the physiology and pharmacology of the renin-angiotensin system has dramatically increased in the last decade, and has led to the discovery of endogenous renin-angiotensin systems which may be physiologically more important than the better understood circulating system. There are several reports of adverse interactions between anaesthesia and ACE inhibitors, manifested as hypotension and bradycardia, which may be delayed until the postoperative period. The mechanism behind them is not understood and, as yet, no published studies have attempted to address this issue. It is possible, however, that dehydration associated with the pre-operative fast may play an important role. ACE inhibitors may, in the future, prove to be useful in the subspecialties of cardiac and vascular anaesthesia, where they might be used in an attempt to preserve cardiac function following periods of ischaemia and cardiopulmonary bypass, and to avoid renal damage following aortic cross-clamping. Meanwhile, it would seem prudent to exercise caution when anaesthetising patients taking ACE inhibitors and to be fully prepared to treat the hypotension and bradycardia which may occur.