Irradiation of carotid baroreceptor with low-intensity pulsed ultrasound exerts different metabolic protection in perirenal, epididymal white adipose tissue and interscapular brown adipose tissue of obese rats.

This study was designed to clarify whether the irradiation of carotid baroreceptor (CB) with low-intensity pulsed ultrasound (LIPUS) protects against obesity by rebalancing the autonomic nervous system (ANS). Obesity was induced using a high-fat diet (HFD) for 8 weeks in Sprague-Dawley rats. Irradiation with LIPUS was daily (20 minutes a day) applied to the right CB. In our study, LIPUS significantly ameliorated metabolic disorders in obese rats. LIPUS partly restored norepinephrine (NE) and acetylcholine (ACH) levels in the perirenal white adipose tissue (PWAT), epididymal white adipose tissue (EWAT), interscapular brown adipose tissue (IBAT), and plasma of obese rats. LIPUS partially rectified the dysregulated AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor (PPAR) α/É£ pathway in the PWAT, EWAT, and IBAT of obese rats. PPARγ and PPARγ target genes respond more sensitively to HFD and LIPUS in PWAT and EWAT than in IBAT. NE, ACH, uncoupling protein-1, phosphorylated AMPK, PPARα, and PPARα target genes respond more sensitively to HFD and LIPUS in IBAT than in PWAT and EWAT. Conclusion: LIPUS irradiation of CB exerts different metabolic protection in PWAT, EWAT, and IBAT by rebalancing the ANS and rectifying the AMPK/PPARα/É£ pathway in obese rats.

Dialysate temperature adjustment as an effective treatment for baroreflex failure syndrome in hemodialysis patient.

BACKGROUND: Baroreflex failure syndrome is a rare disorder which causes labile blood pressure, headache, flushing, diaphoresis and emotional lability. It is caused by history of trauma or radiotherapy in the cervical legion, bilateral carotid-body tumor or resection of glossopharyngeal nerve. We experienced a case of hemodialysis patient who had difficulty in controlling blood pressure during dialysis because of his baroreflex failure syndrome and successfully controlled his blood pressure by adjusting dialysate temperature. CASE PRESENTATION: We report a case of a 68-year-old CKD5 patient who had difficulty in hemodialysis treatment because of severe fluctuations in blood pressure with hypertensive attacks and hypotensive episodes which caused him a severe discomfort. His dialysis treatment was started in 2010 and since that time baroreflex failure syndrome has been suspected because of his clinical manifestations and history of radiotherapy in the cervical region for his lingual cancer in 1994. Baroreflex failure syndrome is diagnosed by symptoms and cold stressor test. We performed a cold stressor test on an experimental baroreflex failure syndrome mouse and induced a significant elevation of blood pressure. From this experimental finding of model mouse, we changed the patients dialysate temperature between 34-38° according to his change in blood pressure though 80-240 mmHg. From this attempt, his blood pressure was successfully controlled between 100-180 mmHg and he was able to continue hemodialysis without any discomfort. CONCLUSION: In our case, environmental stimulation such as temperature change modified the patients fluctuating blood pressure. Change of dialysate temperature could be an option for controlling the unstable blood pressure due to baroreflex failure syndrome.

Endomorphin-2 in the medial NTS attenuates the responses to baroreflex activation.

We have previously reported that microinjections of endomorphin-2 (E-2; an endogenous mu-receptor agonist) into the medial subnucleus of the NTS (mNTS) elicit depressor and bradycardic responses via activation of ionotropic glutamate receptors located on secondary mNTS-neurons. Based on this report, it was hypothesized that activation of secondary mNTS neurons by E-2 may result in an exaggeration of baroreflex responses. In order to test this hypothesis, baroreflex responses were studied in adult, urethane-anesthetized, artificially ventilated, male Wistar rats before and after the microinjections of E-2 into the mNTS. Baroreceptors were stimulated by applying pressure increments (80-100 mm Hg) in the carotid sinus and by electrical stimulation (stimulus intensity: 0.5 V, frequencies 5, 10, and 25 pulses/s, pulse duration: 1 ms) of the aortic nerve for 30-s periods. Baroreceptor stimulation elicited depressor and bradycardic responses. Microinjections (100 nl) of E-2 (0.4 mmol/l) into the mNTS attenuated the baroreflex responses. Microinjections of naloxone (an opioid receptor antagonist) into the mNTS (0.5 mmol/l) did not alter baroreflex responses. Based on these results, it was concluded that activation of mu-opioid receptors in the mNTS attenuates baroreflex responses. Possible mechanisms for excitatory effects of E-2 in the mNTS resulting in depressor and bradycardic responses, on one hand, and inhibitory effects resulting in attenuation of baroreflex responses, on the other, are discussed.

Chronic hypoxia abolishes expiratory prolongation following carotid sinus nerve stimulation in the anesthetized rat.

In anesthetized rats, increases in phrenic nerve (PN) amplitude and frequency during brief periods of hypoxia or electrical stimulation of the carotid sinus nerve (CSN) are followed by an increase in expiratory duration. We investigated the effects of chronic exposure to hypoxia on PN responses to CSN stimulation. In Inactin anesthetized (100 mg/kg) Sprague-Dawley rats PN discharge and arterial pressure responses to 10-120 s of CSN stimulation (20 Hz, 0.2 ms duration pulses) were recorded after 7-10 days exposure to hypoxia (10 +/- .5% O2). In normoxic rats, the degree of CSN-evoked expiratory prolongation was dependent upon the duration of CSN stimulation. CSN-evoked increases in PN burst amplitude were not different comparing chronic hypoxic rats to rats maintained at normoxia while CSN-evoked increases in PN burst frequency were greater in chronic hypoxic rats (p<.05). CSN-evoked expiratory prolongation was abolished in chronic hypoxic rats. Following chronic hypoxia, changes occur within the central processing of arterial chemoreceptor inputs so that CSN stimulation evokes an enhanced PN frequency response and no expiratory prolongation.

[Labile hypertension due to iatrogenic denervation of the carotid sinus]. / Labiele hypertensie door iatrogene denervatie van de sinus caroticus.

Two patients, a man and a woman aged 36 and 40 years, respectively, were found to have disturbed blood pressure regulation after medical intervention in the jugular area. The man had undergone radiation therapy of the neck due to regional lymph node involvement of a nasopharyngeal carcinoma. Six years later he developed episodic complaints of headache accompanied by labile hypo- and hypertension. Mental and physical stimuli resulted in excessive sympathetic activation. In the woman, a carotid body tumour was resected bilaterally. There was an immediate onset of hypertension after surgery. In both patients, the clinical syndrome was attributed to afferent baroreflex failure due to carotid sinus denervation.