Baroreflex sensitivity and heart-rate variability in insulin-dependent diabetics with polyneuropathy

Lengyel, C; Török, Tamás L.; Vákonyi, Tamás; Kempler, Péter; Rudas, László

doi:10.1016/s0140-6736(05)79485-x

Cited by 25 publications

(20 citation statements)

References 4 publications

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“…The Neurometer test is widely used clinically in the evaluation of sensory function in humans with complex regional pain syndrome or other types of peripheral neuropathic pain, which can result from common diseases such as diabetes mellitus (Masson and Boulton, 1991;Katims, 1997;Lengyel et al, 1998). Our results are supported by previous data from animal models of paclitaxelinduced hypersensitivity (Smith et al, 2004) as well as Neurometer analysis of paclitaxel-treated patients, which also show A␤-fiber hypersensitivity, as determined by stimulating the median nerve with 2000-Hz pulses (Doi et al, 2003).…”

Section: Discussionsupporting

confidence: 84%

“…Transcutaneous nerve stimuli with each of the three sine wave pulses of different frequencies of 5, 250, and 2000 Hz to activate C-, A␦-, and A␤-fibers, respectively (Katims, 1997;Lengyel et al, 1998), were applied to the right hind paw of the mice, and the intensity (microampere) was gradually increased. Thresholds were determined, at which paw withdrawal was observed, from preinjection (control) to 4 weeks after paclitaxel treatment (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Inhibition of Paclitaxel-Induced A-Fiber Hypersensitization by Gabapentin

Matsumoto¹,

Inoue²,

Hald³

et al. 2006

J Pharmacol Exp Ther

128

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Paclitaxel (Taxol) is a widely used chemotherapeutic agent in the treatment of several tumors. However, its use is often associated with the generation of peripheral neuropathic pain expressed as mechanical allodynia and thermal hyperalgesia. The molecular mechanism behind this debilitating side effect is obscure, and efficient drugs for its prevention are required. We sought to clarify the cellular changes in the involved nociceptor types underlying paclitaxel-induced neuropathic pain and to test for an alleviating effect of gabapentin treatment in a murine model of paclitaxel-induced neuropathic pain. We found that a single treatment with paclitaxel (4 mg/kg i.p.) led to a decrease in both thermal and mechanical nociceptive thresholds as well as a reduction in the thresholds for 250-Hz (A␦-fiber) and 2000Hz (A␤-fiber) but not 5-Hz (C-fiber) sine wave electrical stimuliinduced paw withdrawal. The paclitaxel-induced neuropathic pain was completely abrogated by gabapentin (30 mg/kg i.p.) treatment. Furthermore, we found that mRNA and protein levels of the voltage-gated calcium channel ␣ 2 ␦-1 subunit (Ca␣ 2 ␦-1), one of the putative targets for gabapentin, was up-regulated in dorsal root ganglions (DRGs), as well as increased expression of Ca␣ 2 ␦-1 protein in medium/large-sized DRG neurons by immunohistochemistry, following paclitaxel treatment. This suggests that paclitaxel induces A-fiber-specific hypersensitization, which may contribute to the functional mechanical allodynia and hyperalgesia, and that gabapentin could be a potential therapeutic agent for paclitaxel-induced neuropathic pain.

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Section: Discussionsupporting

confidence: 84%

Section: Resultsmentioning

confidence: 99%

Inhibition of Paclitaxel-Induced A-Fiber Hypersensitization by Gabapentin

Matsumoto¹,

Inoue²,

Hald³

et al. 2006

J Pharmacol Exp Ther

128

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“…36 It has been shown more recently, on analysing HRV and baroreflex sensitivity, that cardiovascular adaptation mechanisms in type 1 diabetic patients with longterm diabetes are severely impaired. 37 As an important new finding, a highly significant correlation between CAN and cardiovascular disease has been shown by the EURODIAB IDDM Complications Study. 11 Data indicate that silent myocardial ischaemia in diabetic patients may result either from CAN or from autonomic dysfuntion due to coronary artery disease or both.…”

Section: Clinical Presentationmentioning

confidence: 91%

Review: Autonomic neuropathy: a marker of cardiovascular risk

Kempler

2003

Diabetes & Vascular Disease

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C ardiac autonomic neuropathy (CAN) represents a serious complication as it carries an approximately five-fold risk of mortality in patients with diabetes just as in those with chronic liver diseases. The high mortality rate may be related to silent myocardial infarction, cardiac arrhythmias, cardiovascular and cardiorespiratory instability and to other causes not yet explained. Resting tachycardia due to parasympathetic damage may represent one of the earliest signs. Typical findings referring to autonomic dysfunction may include exercise intolerance, orthostatic hypotension and cardiac dysfunction to rest or exercise. Severe autonomic neuropathy may be responsible for spontaneous respiratory arrest and unexplained sudden death. A relationship between the presence and/or severity of CAN and corrected QT interval prolongation is well documented. Better understanding of the prognostic importance of autonomic neuropathy followed the use of simple non-invasive cardiovascular reflex tests. These most commonly include heart rate variation in response to deep breathing, standing, the Valsalva maneouvre and blood pressure response to standing and sustained handgrip. Near normoglycaemia is now generally accepted as the primary approach to the prevention of diabetic neuropathy, but is not achievable in most patients. Our experience of the use of the antioxidant alpha-lipoic acid in the treatment of cardiac autonomic neuropathy is described. Br J Diabetes Vasc Dis 2003;3:84-90

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“…In most clinical studies, diabetic neuropathy is determined by the presence or absence of certain neurologic symptoms. Recent data suggest that the investigation of cardiovascular abnormalities and the perception of transcutaneous stimuli provide satisfactory parameters for the detection and follow-up ofneuropathy [29][30][31]. In the present study, the assessment of five cardiovascular reflex tests and the determination of the current perception threshold allowed a quantitative characterization of the dysfunction of the vagus nerve and the degree of peripheral neuropathy [32].…”

Section: Discussionmentioning

confidence: 70%

Gallbladder hypomotility in diabetic polyneuropathy

Várkonyi

Lengyel

Madácsy

et al. 2001

Clinical Autonomic Research

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This study was performed to evaluate the gallbladder motility in long-standing diabetes mellitus. The gallbladder function of diabetic patients was measured by means of quantitative hepatobiliary scintigraphy, and the severity of the associated autonomic and sensory polyneuropathy was determined. The presence of a marked gallbladder hypomotility was established, and a positive correlation was observed between the severity of the autonomic disturbance and the contractile disorder. This study underlines the important role of the neuropathy in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

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Baroreflex sensitivity and heart-rate variability in insulin-dependent diabetics with polyneuropathy

Cited by 25 publications

References 4 publications

Inhibition of Paclitaxel-Induced A-Fiber Hypersensitization by Gabapentin

Inhibition of Paclitaxel-Induced A-Fiber Hypersensitization by Gabapentin

Review: Autonomic neuropathy: a marker of cardiovascular risk

Gallbladder hypomotility in diabetic polyneuropathy

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