Dysphagia in Alzheimer disease: a review.

Pseudobulbar dysphagia is a common feature of Alzheimer disease (AD) especially in the late stages. In the majority of cases the clinician can select the most appropriate therapeutic modalities based on a thorough history and bedside assessment. The role of videofluoroscopy in managing the dysphagia of AD has not been established. It is unclear whether the weight loss associated with advanced AD can entirely be prevented by optimizing the management of dysphagia. Pneumonia is a common cause of morbidity and death in patients with AD. The risk of pneumonia is related not only to dysphagia and aspiration but to mobility, nutritional status and host immune response. Prevention of pneumonia through appropriate management of dysphagia is not supported by empirical evidence. The potential role of enteral feeding in patients with advanced AD is small. An evidence-based approach to enteral feeding in AD patients is outlined.

Participation of prostaglandin E2 in the endothelial protective effect of ischaemic preconditioning in isolated rat heart.

OBJECTIVE: To assess whether the protective effect of ischaemic preconditioning (IPC) on endothelial function in coronary arteries of the rat involves prostaglandins. METHODS: Isolated rat hearts perfused under constant flow conditions were exposed to 30 min of partial ischaemia (flow-rate 1 ml/min) followed by 20 min of reperfusion, after which coronaries were precontracted with U-46619 0.1 microM, and the coronary response to the endothelium-dependent vasodilator, serotonin (5-HT, 10 microM), was compared to that of the endothelium-independent vasodilator, sodium nitroprusside (SNP, 3 microM). Prostaglandin production was blocked with a perfusion of indomethacin 10 microM started 15 min before IPC or a corresponding sham period and stopped just before the 20-min reperfusion period. RESULTS: In untreated hearts, ischaemia diminished selectively 5-HT-induced vasodilatation, compared to sham hearts. The vasodilatation by SNP was unaffected after ischaemia and reperfusion. IPC (5 min of zero-flow ischaemia followed by 10 min reperfusion before the 30-min partial ischaemia) preserved the vasodilatation produced by 5-HT. Enzymeimmunoassays showed an increased production of PGE2 in the IPC group. Treatment of hearts with indomethacin blocked the protective effect of IPC on the vasodilatation produced by 5-HT and decreased the production of PGE2. A 5-min perfusion with 3 nM PGE2 started 15 min before the partial ischaemia, protected the endothelium. This was blocked by 1 microM chelerythrine, but not by 0.3 microM glibenclamide. CONCLUSIONS: These results suggest that IPC affords protection to endothelial function in coronary arteries of the rat partially via the release of PGE2. Under our experimental conditions, the protective effect of PGE2 is mediated by PKC.

[Role of B1 receptors in the endothelial protective effect of ischaemic preconditioning]. / Implication des récepteurs B1 aux kinines dans la protection endothéliale produite par le préconditionnement ischémique.

The aim of this study was to assess whether the cardioprotective effect of ischaemic preconditioning (IPC) on endothelial function in resistance coronary arteries of the rat involves activation of kinin receptors. Isolated rat hearts perfused under constant flow conditions were exposed to 30 min of partial ischaemia (flow rate 1 mL/min) followed by 20 min of reperfusion. Preconditioning was performed with 5 min zero-flow ischaemia and 10 min reperfusion before the 30-min ischaemia. After the 20-min reperfusion period, coronaries were precontracted with U-46619 0.1 microM, and the coronary response to the endothelium-dependent vasodilator, serotonin (5-HT, 10 microM), was compared to that of the endothelium-independent vasodilator, sodium nitroprusside (SNP, 3 microM). Kinin B1 and B2 receptors were blocked with perfusion of either [Lys0, Leu8, des-Arg0]-Bradykinin 30nM (LLDBK) or Hoe 140 10 nM (Hoe) respectively, started 15 min before IPC or a corresponding sham period and stopped just before the 20-min reperfusion period. In untreated hearts, ischemia diminished selectively 5-HT-induced vasodilatation, compared to sham hearts (without ischaemia). The vasodilatation by SNP was unaffected after ischaemia and reperfusion. Preconditioning in untreated hearts preserved the vasodilatation produced by 5-HT. Treatment of hearts with either Hoe or LLDBK had no effect on the vasodilatation produced by both 5-HT and SNP in sham hearts. Pre-treatment with Hoe did not block the protective effect of IPC on the 5-HT vasodilatation. LLDBK halved the protective effect of IPC on endothelium-dependent vasodilatation. In addition, the protective effect of BK on the endothelial function in the isolated rat heart was blocked by LLDBK. These results suggest that IPC and exogenous kinin perfusions afford protection to endothelial function in resistance coronary arteries of the rat partially by activation of B1 kinin receptors. B2 receptors do not play any role in that protection.

Weight loss, dysphagia, and outcome in advanced dementia.

There has been much debate on the value and risks of long-term enteral feeding in patients with advanced dementia. A retrospective study was carried out on 47 patients with a primary diagnosis of dementia who died over a two-year period. All were inpatients in a nursing home or skilled nursing facility. Marked weight loss and dysphagia occurring in a specific pattern were found to be associated with death from pneumonia. These clinical features probably imply failure of basic homeostatic mechanisms. Patients showing this clinical pattern may be less likely to show benefits from long-term enteral feeding.

Role of kinins in the endothelial protective effect of ischaemic preconditioning.

1. The aim of this study was to assess whether the protective effect of ischaemic preconditioning on endothelial function in coronary arteries of the rat involves kinins. 2. Isolated hearts of the rat were exposed to a 30-min low-flow ischaemia (flow rate of 1 ml min[-1]) followed by 20-min reperfusion, after which coronaries were precontracted with 0.1 microM U-46619, and the response to the endothelium-dependent vasodilator, 5-hydroxytryptamine (5-HT, 10 microM), compared to that of the endothelium-independent vasodilator, sodium nitroprusside (SNP, 3 microM). 3. In untreated hearts, ischaemia-reperfusion diminished selectively 5-HT-induced vasodilatation, compared with time-matched sham hearts. The vasodilatation to SNP was unaffected after ischaemia-reperfusion. Preconditioning (5 min of zero-flow ischaemia followed by 10 min reperfusion) in untreated hearts preserved the vasodilatation produced by 5-HT. 4. Blockade of B1 and B2 receptors with either 3 nM [Lys[0], Leu8, des-Arg9]-bradykinin (LLDBK) or 10 nM Hoe 140 (icatibant), respectively, (started 15 min before ischaemic preconditioning or a corresponding sham period and stopped just before the 20-min reperfusion period) had no effect on the vasodilatation produced by either 5-HT or SNP in sham hearts. Pretreatment with Hoe 140 did not block the protective effect of ischaemic preconditioning on the 5-HT vasodilatation. In contrast, LLDBK halved the protective effect of ischaemic preconditioning on endothelium-dependent vasodilatation. 5. Perfusion with either bradykinin or des-Arg9-bradykinin (1 nM) 30 min before and lasting throughout the ischaemia protected the endothelium. 6. In conclusion, ischaemic preconditioning affords protection to the endothelial function in coronary resistance arteries of the rat partly by activation of B1 receptors. Although exogenous BK perfusion can protect the endothelium, B2 receptors do not play an important role in this protection in the rat isolated heart.

New assumptions concerning IPAs and cost of dental care.

OBJECTIVES: Previous studies suggest that fee-for-service (FFS) patients receive more treatment and at a greater cost than capitation patients. In this study treatment plans of dentists who are members of an independent practice association (IPA), a preferred provider organization (PPO), or who are paid their usual fee for service are compared. METHODS: A carefully selected and trained professional actor, with actual dental disease and recent radiographs, was sent to the offices of general practice dentists for an examination and treatment plan. To one group of dentists (n = 21) the patient said he was a member of a PPO plan served by that dentist, to a second group (n = 15) he said he was a member of an IPA plan served by that dentist, and to the third group (n = 19) he said he would pay by the traditional FFS method. RESULTS: IPA dentists recommended more restorations (mean = 9.60) than those in the PPO program (mean = 5.95) or those paid by the traditional FFS method (mean = 5.58). The anticipated mean cost to the patient was higher for the IPA dentists ($1,815.20) compared to the other two types (PPO = $1,186.24, FFS = $1,470.42). CONCLUSIONS: The IPA models studied in this investigation permitted dentists to charge copayments for most treatments beyond basic services. This type of IPA might be similar to a fee-for-service model that provides practitioners with an incentive to do more rather than less treatment.