Neurogenic Mechanisms Research Articles

Influence of circulatory and hemic hypoxia on cutaneous microcirculation

Objective. To establish the features of cutaneous microhemocirculation in conditions of circulatory and hemic hypoxia. Material and methods. Experiments were carried out on outbred rats, anesthetized by pentobarbital. Blood flow in the skin of the rat ear was recorded by laser Doppler flowmetry (LDF). Stages of the experiment: baseline; acute blood loss (30 % of estimated blood volume); reinfusion (autohemotransfusion in «control» group and infusion of modified gelatin solution in «Gelofusin» group); hemodilution with Gelofusin. The following parameters were analyzed: the mean value of blood flow (M, PU); the maximum (dominant) amplitude of blood flow oscillations (A max ) and the corresponding frequency (F max ) in the frequency band 0.01-0.4 Hz. The coefficient of oxygen delivery to the tissue site under investigation (D t O 2 ) was used to assess the severity of hypoxia. Results. At the posthemorrhagic stage M, blood pressure (BP), hematocrit (Ht), D t O 2 and F max decreased along with an increase in A max . F max shifted from the myogenic frequency band at the baseline into the neurogenic band. A correlation was found between A max and BP (r=-0,38; p max , A max , despite the higher values of BP, Ht and D t O 2 in the «control» group. In comparison with the baseline At the «hemodilution» stage the values of M did not differ from the baseline against the background of lower values of Ht, D t O2 and BP; A max remained elevated, and F max shifted into the myogenic band and did not differ from the baseline. Conclusion. Both blood loss and hemodilution are associated with an increase in the amplitude of fluxmotion. Mechanisms of fluxmotion stimulation are different: increasing the amplitude of fluxmotion in circulatory hypoxia is associated with the neurogenic regulatory mechanisms of microhemocirculation, while in hemic hypoxia it is associated with the myogenic mechanisms. Arterial hypotension is the main factor increasing the amplitude of fluxmotion during blood loss.

AMPK-α1 or AMPK-α2 Deletion in Smooth Muscles Does Not Affect the Hypoxic Ventilatory Response or Systemic Arterial Blood Pressure Regulation During Hypoxia.

The hypoxic ventilatory response (HVR) is markedly attenuated by AMPK-α1 deletion conditional on the expression of Cre-recombinase in tyrosine hydroxylase (TH) expressing cells, precipitating marked increases in apnea frequency and duration. It was concluded that ventilatory dysfunction caused by AMPK deficiency was driven by neurogenic mechanisms. However, TH is transiently expressed in other cell types during development, and it is evident that central respiratory depression can also be triggered by myogenic mechanisms that impact blood supply to the brain. We therefore assessed the effect on the HVR and systemic arterial blood pressure of AMPK deletion in vascular smooth muscles. There was no difference in minute ventilation during normoxia. However, increases in minute ventilation during severe hypoxia (8% O2) were, if affected at all, augmented by AMPK-α1 and AMPK-α2 deletion in smooth muscles; despite the fact that hypoxia (8% O2) evoked falls in arterial SpO2 comparable with controls. Surprisingly, these mice exhibited no difference in systolic, diastolic or mean arterial blood pressure during normoxia or hypoxia. We conclude that neither AMPK-α1 nor AMPK-α2 are required in smooth muscle for the regulation of systemic arterial blood pressure during hypoxia, and that AMPK-α1 deficiency does not impact the HVR by myogenic mechanisms.

Ischemic Versus Non-Ischemic (Neurogenic) Myocardial Contractility Impairment in Acute Coronary Syndromes: Prevalence and Impact on Left Ventricular Systolic Function Recovery.

BackgroundNeurogenic mechanism is believed to contribute to left ventricular (LV) systolic dysfunction in acute coronary syndromes (ACS); its extreme form is known as takotsubo cardiomyopathy. However, the magnitude of neurogenic contribution to LV dysfunction in all-comer first-time ACS remains unknown.Material/MethodsIn 120 consecutive patients with first-time ACS (age 66.3±12.3years, 40 women) coronary angiograms were individually matched to the echocardiographic left ventricular (LV) segments (17-segment model). Baseline contractility impairment was classified as ischemic (I): confined to the stenotic artery(ies) supply area(s), neurogenic (N): in absence of attributable coronary stenosis, or partially ischemic/partially neurogenic (I&N). Echocardiography was repeated at 6 months to determine LV systolic function recovery.ResultsNeurogenic component (NC) contribution to myocardial contractility impairment was present in 24.2% of ACS patients, with pure N in 6.7% and I&N in 17.5%. Diabetes/pre-diabetes was present in 38.5% vs. 33.5% vs. 0% (I vs. I&N vs. N; p=0.02). Major stressor preceding symptom onset was reported in 3.3% in I, 9.5% in I&N, and 25.0% in N (p=0.03). The number of LV segments with contractility impairment was 2±4 in I, 17±11 in I&N, and 3±16 in N (p<0.05). NC presence was independently associated with better recovery of global LV systolic function (OR 2.99, 95% CI: 1.16–7.76; p=0.024).ConclusionsNovel findings from this study are: (1) NC may contribute to myocardial contractility impairment in 1 in every 4 first-time ACS patients, (2) NC contribution to contractility impairment in ACS is blunted in diabetes or pre-diabetes, and (3) LV systolic function recovery is better in patients with NC.

Evaluation of gray matter perfusion in episodic migraine using voxel-wise comparison of 3D pseudo-continuous arterial spin labeling

BackgroundAlthough previous studies have demonstrated that structural and functional abnormalities in episodic migraine (EM), less is known about altered brain perfusion in the EM. The aim of this study is to investigate altered gray matter perfusion in EM using a 3D volumetric perfusion imaging.MethodsFifteen EM patients and 15 normal controls (NC) underwent structural and 3D pseudo-continuous arterial spin labeling (3D pc-ASL). The structural images were segmented using DARTEL methods and the generated normalized T1 tissue probability maps were used to coregister the cerebral blood flow (CBF) images, which would further be performed with standardization using Fisher Z Transformation. Voxel-wise analysis was applied to CBF map with Z standardization, and the Z value of the abnormal brain region was extracted and performed with correlation with the clinical variables.ResultsThe increased CBF value located in the left Brodmann 38 (BA38) and no significantly decreased CBF value were detected in EM. HAMD scores presented significantly positive correlation with the CBF value of the left BA38.ConclusionThe current study indicated that the pattern of cerebral hyperperfusion may elucidate the neurogenic mechanism in the EM genesis, and 3D pc-ASL technique would non-invasively provide valuable cerebral perfusion information for the further pathophysiological and neuropsychological study in EM.

Dynamic cerebral autoregulation is impaired during submaximal isometric handgrip in patients with heart failure.

The incidence of neurological complications, including stroke and cognitive dysfunction, is elevated in patients with heart failure (HF) with reduced ejection fraction. We hypothesized that the cerebrovascular response to isometric handgrip (iHG) is altered in patients with HF. Adults with HF and healthy volunteers were included. Cerebral blood velocity (CBV; transcranial Doppler, middle cerebral artery) and arterial blood pressure (BP; Finometer) were continuously recorded supine for 6 min, corresponding to 1 min of baseline and 3 min of iHG exercise, at 30% maximum voluntary contraction, followed by 2 min of recovery. The resistance-area product was calculated from the instantaneous BP-CBV relationship. Dynamic cerebral autoregulation (dCA) was assessed with the time-varying autoregulation index estimated from the CBV step response derived by an autoregressive moving-average time-domain model. Forty patients with HF and 23 BP-matched healthy volunteers were studied. Median left ventricular ejection fraction was 38.5% (interquartile range: 0.075%) in the HF group. Compared with control subjects, patients with HF exhibited lower time-varying autoregulation index during iHG, indicating impaired dCA ( P < 0.025). During iHG, there were steep rises in CBV, BP, and heart rate in control subjects but with different temporal patterns in HF, which, together with the temporal evolution of resistance-area product, confirmed the disturbance in dCA in HF. Patients with HF were more likely to have impaired dCA during iHG compared with age-matched control subjects. Our results also suggest an impairment of myogenic, neurogenic, and metabolic control mechanisms in HF. The relationship between impaired dCA and neurological complications in patients with HF during exercise deserves further investigation. NEW & NOTEWORTHY Our findings provide the first direct evidence that cerebral blood flow regulatory mechanisms can be affected in patients with heart failure during isometric handgrip exercise. As a consequence, eventual blood pressure modulations are buffered less efficiently and metabolic demands may not be met during common daily activities. These deficits in cerebral autoregulation are compounded by limitations of the systemic response to isometric exercise, suggesting that patients with heart failure may be at greater risk for cerebral events during exercise.

Postoperative ileus following major colorectal surgery.

Postoperative ileus (POI) is characterized by delayed gastrointestinal recovery following surgery. Current knowledge of pathophysiology, clinical interventions and methodological challenges was reviewed to inform modern practice and future research. A systematic search of MEDLINE and Embase databases was performed using search terms related to ileus and colorectal surgery. All RCTs involving an intervention to prevent or reduce POI published between 1990 and 2016 were identified. Grey literature, non-full-text manuscripts, and reanalyses of previous RCTs were excluded. Eligible articles were assessed using the Cochrane tool for assessing risk of bias. Of 5614 studies screened, 86 eligible articles describing 88 RCTs were identified. Current knowledge of pathophysiology acknowledges neurogenic, inflammatory and pharmacological mechanisms, but much of the evidence arises from animal studies. The most common interventions tested were chewing gum (11 trials) and early enteral feeding (11), which are safe but of unclear benefit for actively reducing POI. Others, including thoracic epidural analgesia (8), systemic lidocaine (8) and peripheral μ antagonists (5), show benefit but require further investigation for safety and cost-effectiveness. POI is a common condition with no established definition, aetiology or treatment. According to current literature, minimally invasive surgery, protocol-driven recovery (including early feeding and opioid avoidance strategies) and measures to avoid major inflammatory events (such as anastomotic leak) offer the best chances of reducing POI.

Identification of neural transcription factors required for the differentiation of three neuronal subtypes in the sea urchin embryo

Correct patterning of the nervous system is essential for an organism's survival and complex behavior. Embryologists have used the sea urchin as a model for decades, but our understanding of sea urchin nervous system patterning is incomplete. Previous histochemical studies identified multiple neurotransmitters in the pluteus larvae of several sea urchin species. However, little is known about how, where and when neural subtypes are differentially specified during development. Here, we examine the molecular mechanisms of neuronal subtype specification in 3 distinct neural subtypes in the Lytechinus variegatus larva. We show that these subtypes are specified through Delta/Notch signaling and identify a different transcription factor required for the development of each neural subtype. Our results show achaete-scute and neurogenin are proneural for the serotonergic neurons of the apical organ and cholinergic neurons of the ciliary band, respectively. We also show that orthopedia is not proneural but is necessary for the differentiation of the cholinergic/catecholaminergic postoral neurons. Interestingly, these transcription factors are used similarly during vertebrate neurogenesis. We believe this study is a starting point for building a neural gene regulatory network in the sea urchin and for finding conserved deuterostome neurogenic mechanisms.

Role of peripheral vestibular receptors in the control of blood pressure following hypotension.

Hypotension is one of the potential causes of dizziness. In this review, we summarize the studies published in recent years about the electrophysiological and pharmacological mechanisms of hypotension-induced dizziness and the role of the vestibular system in the control of blood pressure in response to hypotension. It is postulated that ischemic excitation of the peripheral vestibular hair cells as a result of a reduction in blood flow to the inner ear following hypotension leads to excitation of the central vestibular nuclei, which in turn may produce dizziness after hypotension. In addition, excitation of the vestibular nuclei following hypotension elicits the vestibulosympathetic reflex, and the reflex then regulates blood pressure by a dual-control (neurogenic and humoral control) mechanism. In fact, recent studies have shown that peripheral vestibular receptors play a role in the control of blood pressure through neural reflex pathways. This review illustrates the dual-control mechanism of peripheral vestibular receptors in the regulation of blood pressure following hypotension.

Convulsive seizure and pulmonary edema during hyperbaric oxygen therapy:A case report

Hyperbaric oxygen therapy (HBOT) for carbon monoxide (CO) poisoning is widely performed to prevent delayed neuropsychiatric syndrome. Although HBOT can generally be performed with safety, the appropriate management of HBOT still remains unestablished. A 31-year-old man was transferred to our facility to undergo HBOT in a multiplace chamber with a diagnosis of CO poisoning. The first HBOT session ended uneventfully. During the second HBOT session, the patient suddenly experienced convulsive seizures. The accompanying doctor administered intravenous propofol to stop the convulsion and terminated the HBOT. Soon after the convulsion, the patient developed frothy secretions through the endotracheal-tube with impaired oxygenation. Head computed tomography scan showed no abnormalities, suggesting the seizure was associated with complications of HBOT. A chest X-ray revealed bilateral pulmonary edema, and echocardiography revealed normal cardiac function, indicating that the pulmonary edema resulted from HBOT or neurogenic mechanism secondary to the seizure. The patient's respiratory status improved without recurrence of the seizure and no delayed neurological sequelae was seen afterwards. Here we report unexpected rare adverse events during HBOT. Hyperbaric oxygen therapy for acute indications should be performed in multiplace chambers, with appropriate preparation and medical equipment. J. Med. Invest. 65:286-288, August, 2018.

Effects of Transient Cerebral Ischemia on the Adrenoreactivity of the Pial Vessels in Rats

Ischemia is known to affect endothelium-dependent reactions of cerebral vessels and to change the metabolic and myogenic mechanisms regulating brain blood flow. The role of local neurogenic regulatory mechanisms in changes in the reactions of cerebral vessels after ischemia remains incompletely understood. The aim of the present work was to study the reactions of pial arterial and venous vessels in rats to noradrenaline before and 2, 7, 14, and 21 days after ischemia induced by occlusion of both carotid arteries for 12 min with simultaneous control of hypotension at level of 45 ± 3 mmHg. Ischemia was found to increase the constrictor reaction to noradrenaline of mainly small pial arteries and arterioles and third-degree venules. Increases in the number of constrictor reactions in rats subjected to ischemia, persisting to post-reinfusion day 21, were most marked at post-ischemia day 14. The post-ischemic increase in adrenoreactivity may be linked with an increase in the reactivity and sensitivity of adrenoreceptors of cerebral vessels.

The effect of nerve mobilization exercise in patients with rheumatoid arthritis: a pilot study.

Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation of the joints. The neurogenic inflammatory mechanism plays an important role in the inflammatory process of RA, and pathological changes in neural tissues in RA have also been noted. We aim to investigate treatment of the nervous system to relieve joint pain and inflammation in RA. Nerve mobilization, a nervous system-specific therapeutic exercise, was applied on RA patients to determine the effect of nerve mobilization on joint inflammation. Twelve RA patients were recruited from the community and were randomised into an experimental and a control group. In the experimental group, the subjects were taught a set of nerve mobilization exercises while the subjects in the control group were taught a set of gentle joint mobilization exercises. Both groups were instructed to practice the exercises daily. After a 4-week period, their RA pain scale (RAPS) and pain scores were examined, as well as the C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Subjects in the experimental group showed improvements in RAPS and pain scores after 4 weeks of nerve mobilization exercises, while CRP and ESR values remained unaffected. These preliminary data showed that nerve mobilization exercises might be beneficial in controlling joint pain in RA patients.

Microvascular functions in patients with fibromyalgia syndrome: effects of physical exercise.

This study aims to evaluate the current state of microvascular function and to investigate the effect of supervised aerobic exercise on microvascular control mechanisms and health outcomes in women with fibromyalgia syndrome (FMS). Forty female patients (mean age 51±11 years) with a diagnosis of FMS according to the American College of Rheumatology criteria and 20 healthy female controls (mean age 52±9 years) were included in the study. Microvascular blood flow was measured using a laser Doppler flowmeter (LDF) at the volar skin site of the forearm. Pain severity and FMS were assessed using the visual analog scale (VAS) and Fibromyalgia Impact Questionnaire (FIQ), respectively, both at the beginnig and at the end of the study. Fibromyalgia was evaluated and a spectral analysis of LDF signals was carried out to assess the relative contribution of each control mechanisms. The local thermal hyperemia was used to test the microvascular functions. Moderate-intensity aerobic activity (energy expenditure 3.0 to 6.0 metabolic equivalent) was performed by treadmill walking for 30 min for five days each week for a month. The patients with FMS had lower VAS and FIQ scores at the end of the exercise period. There was a positive correlation between improved myogenic and neurogenic mechanisms and reduced FIQ scores. Cardiac signals were positively correlated with the FIQ scores at the end of the exercise period. Endothelial function was under the influence of pain, and baseline nitric oxide activity was found to be positively correlated with VAS. Our study results suggest that microvascular functions are impaired in FMS patients and moderate exercise training is effective to improve the FIQ/VAS scores and enhance vascular functions.

Relationship of Preexisting Cardiovascular Comorbidities to Newly Diagnosed Atrial Fibrillation After Ischemic Stroke

There remains uncertainty as whether newly diagnosed atrial fibrillation (AF) after ischemic stroke reflects underlying heart disease and represents an increased risk of cardioembolic stroke, or whether it is triggered by neurogenic mechanisms. We aimed to determine whether cardiovascular comorbidities in patients with new AF after ischemic stroke differ from patients with previous known AF or without AF. This French longitudinal cohort study was based on the database covering hospital care from 2009 to 2012 for the entire population. Of 336 291 patients with ischemic stroke, 240 459 (71.5%) had no AF and 95 832 (28.5%) had previously known AF at baseline. Patients without previous AF had a mean CHA2DS2-VASc score of 4.98±1.63 SD. During a mean follow-up of 7.9±11.5 months, 14 095 (5.9%) of these patients had incident AF, representing an annual incidence of AF after ischemic stroke of 8.9 per 100 person-years (95% confidence interval, 8.8-9.0). New AF patients had higher CHA2DS2-VASc score, more likely comorbidities, and more frequent history of previous transient ischemic attack than patients with previous known AF or without AF. Preexisting cardiovascular comorbidities underlie AF newly diagnosed after stroke. Consequently, these high-risk patients should be closely monitored for incident AF to facilitate an earlier diagnosis of AF and avoid stroke with appropriate thromboprophylaxis.

Migraine homocysteine‐related: Old and new mechanisms

AbstractIn this review, we discussed how homocysteinemia can induce migraine. Vascular and neurogenic mechanisms of migraine‐onset, such as the classical “triggers”, were examined. Favourable effects induced on the syndrome by folate supplementation were also illustrated. However, it was recently shown that hyper‐homocysteinemia can favor migraine by the production of homocysteic acid.This acts as an agonist of the N‐acetyl‐aspartame‐D receptor, and is a potent neurotoxic stimulus causing migraine. Its detrimental effects seem to be antagonized by N‐acetyl‐cysteine, calcium chelators, a naturally‐occurring dipeptide widely distribuited in the muscular and nervous systems. This compound showed positive results in animal models. Elevated homocysteic acid levels secondary to hyper‐homocysteinemia could sensitize the dura mater and cerebral arteries and favor the activation of the trigeminovascular system, predisposing to migraine attacks. However, other experimental and human studies are requested to ratify the negative effect of homocysteic acid on migraine and the positive results obtaining with of its antagonists.

Chronic high-sodium diet intake after weaning lead to neurogenic hypertension in adult Wistar rats

In this study, we investigated some mechanisms involved in sodium-dependent hypertension of rats exposed to chronic salt (NaCl) intake from weaning until adult age. Weaned male Wistar rats were placed under high (0.90% w/w, HS) or regular (0.27% w/w, Cont) sodium diets for 12 weeks. Water consumption, urine output and sodium excretion were higher in HS rats compared to control. Blood pressure (BP) was directly measured by the arterial catheter and found 13.8% higher in HS vs Cont rats. Ganglionic blockade with hexamethonium caused greater fall in the BP of HS rats (33%), and central antagonism of AT1 receptors (losartan) microinjected into the lateral ventricle reduced BP level of HS, but not of Cont group. Heart rate variability analysis revealed sympathetic prevalence on modulation of the systolic interval. HS diet did not affect creatinine clearance. Kidney histological analysis revealed no significant change in renal corpuscle structure. Sodium and potassium concentrations in CSF were found higher in HS rats despite no change in plasma concentration of these ions. Taken together, data suggest that animals exposed to chronic salt intake to a level close to that reported for human’ diet since weaning lead to hypertension, which appears to rely on sodium-driven neurogenic mechanisms.

Altered Hippocampal Neurogenesis during the First 7 Days after a Fluid Percussion Traumatic Brain Injury

Traumatic brain injury (TBI) is a devastating disorder causing negative outcomes in millions of people each year. Despite the alarming number of brain injuries and the long-term detrimental outcomes that can be associated with TBI, treatment options are lacking. Extensive investigation is underway, in hopes of identifying effective treatment strategies. Among the most state-of-the-art strategies is cell replacement therapy. TBI is a seemingly good candidate for cell replacement studies because there is often loss of neurons. However, translation of this therapy has not yet been successful. It is possible that a better understanding of endogenous neurogenic mechanisms after TBI could lead to more efficacious study designs using exogenous cell replacement strategies. Therefore, this study was designed to examine the number and migration of immature neurons at 1 and 7 d after a fluid percussion TBI. The results show that the number of immature neurons increases from 7 d after a fluid percussion injury (FPI), and there is ectopic migration of doublecortin (DCX+) immature neurons into the hilar region of the dentate gyrus. These results add important data to the current understanding of the endogenous neurogenic niche after TBI. Follow-up studies are needed to better understand the functional significance of elevated neurogenesis and aberrant migration into the hilus.

SUDDEN DEATH SYNDROME AND OTHER INDICATORS OF INFANT DEATH IN STAVROPOL REGION

The «Sudden Infant Death Syndrome» stands for unexpected nonviolent death of apparently healthy chest age child when there is no history or pathomorphological features which can be adequate explanations for death reasons. In Russian Federation, the death rate from this syndrome in the range of 0.06 to 2.8 per 1000 live births. In Stavropol region, average figures are equal to 0,36 per 1000 live births in the period of 2005–2014. The maximum recorded rate was 0.53 per 1,000 in 2012, while the minimum was observed in 2007 (0.23 per 1,000). Rates of incidence sudden infant death syndrome are similar to the rates of incidence associated with infectious diseases, and as a result of injury or poisoning. Currently paid attention to neurogenic mechanisms of sudden infant death syndrome, as a consequence in combination cranio-spinal birth injury with delayed fatal in infancy, in the period of residual effects.

MP85-03 THE THERAPEUTIC EFFECT OF TRPV4 ACTIVATION IN THE BLADDER ON UNDERACTIVE BLADDER IN RATS WITH PELVIC NERVE CRUSH

You have accessJournal of UrologyUrodynamics/Lower Urinary Tract Dysfunction/Female Pelvic Medicine: Neurogenic Voiding Dysfunction I1 Apr 2017MP85-03 THE THERAPEUTIC EFFECT OF TRPV4 ACTIVATION IN THE BLADDER ON UNDERACTIVE BLADDER IN RATS WITH PELVIC NERVE CRUSH Ei-ichiro Takaoka, Shun Takai, Takahisa Suzuki, Nobutaka Shimizu, Joonbeom Kwon, Hiroki Okada, Hiroyuki Nishiyama, Naoki Yoshimura, and Christopher J. Chermansky Ei-ichiro TakaokaEi-ichiro Takaoka More articles by this author , Shun TakaiShun Takai More articles by this author , Takahisa SuzukiTakahisa Suzuki More articles by this author , Nobutaka ShimizuNobutaka Shimizu More articles by this author , Joonbeom KwonJoonbeom Kwon More articles by this author , Hiroki OkadaHiroki Okada More articles by this author , Hiroyuki NishiyamaHiroyuki Nishiyama More articles by this author , Naoki YoshimuraNaoki Yoshimura More articles by this author , and Christopher J. ChermanskyChristopher J. Chermansky More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2017.02.2665AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Incomplete bladder emptying due to detrusor underactivity (DU) is a significant urological problem underlying underactive bladder (UAB). Also, TRPV4 has been reported to be one of the mechanosensitive channels expressed in the bladder. In this study, we sought to produce a consistent rat model of UAB with the modification of our previous model of pelvic nerve crush (PNC) (2016 AUA) and evaluated the therapeutic effect of intravesical application of a TRPV4 agonist on the UAB condition. METHODS In female Sprague-Dawley rats, the visceral branches of bilateral pelvic nerves were identified near the internal iliac vessels and bilateral PNC was made by two times of nerve compression of either side with each 20-seconds duration using sharp forceps. After 10 days, awake cystometrograms (CMG) were recorded in sham control and PNC rats. Then, in both groups, a TRPV4 agonist (GSK1016790A) was continuously administered into the bladder and the CMG parameters were compared before and after intravesical drug administration. RESULTS The bladder weight was significantly increased in PNC rats vs. control rats. In CMG, PNC rats showed significant increases in voided volume, post-void residual urine volume, and residual urine rate compared to control rats. PNC rats also revealed the significant increases in intercontraction intervals (ICI), a number of non-voiding contractions, and threshold pressure while the amplitude during voiding was significantly decreased (table). In the TRPV4 administration study, intravesical application of 1.5µM of GSK 1016790A significantly decreased ICI, voided volume, and post-void residual urine volume in PNC rats while it did not significantly affect any CMG parameters in control rats. CONCLUSIONS Rats with pelvic nerve injury induced by the modified PNC method, which showed the characteristics of DU, seem to be an appropriate model for evaluation of peripheral neurogenic mechanisms of UAB. Also TRPV4 that reduced the bladder capacity and residual urine volume could be a potential target for the treatment of UAB. © 2017FiguresReferencesRelatedDetailsCited byKaplan S (2017) Re: Qualitative Exploration of the Patient Experience of Underactive BladderJournal of Urology, VOL. 199, NO. 3, (588-589), Online publication date: 1-Mar-2018. Volume 197Issue 4SApril 2017Page: e1148-e1149 Advertisement Copyright & Permissions© 2017MetricsAuthor Information Ei-ichiro Takaoka More articles by this author Shun Takai More articles by this author Takahisa Suzuki More articles by this author Nobutaka Shimizu More articles by this author Joonbeom Kwon More articles by this author Hiroki Okada More articles by this author Hiroyuki Nishiyama More articles by this author Naoki Yoshimura More articles by this author Christopher J. Chermansky More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Comparative study between microvascular tone regulation and rheological properties of blood in patients with type 2 diabetes mellitus.

The aim of the study is to investigate the changes of the skin blood flow responses to cold stress in patients with diabetes mellitus type 2 through wavelet analysis of the peripheral skin temperature oscillations and to estimate their relationship with the blood viscosity values. The amplitudes of the skin temperature pulsations (ASTP) were monitored by "Microtest" device ("FM-Diagnostics", Russia); the whole blood viscosity and the shear stresses were measured by Contraves LS30 viscometer (Switzerland) at a steady flow in 9 healthy subjects and in 30 patients with type 2 diabetes mellitus. Power law and Herschel-Bulkley (HB) equations were applied to describe the blood rheology. Both models include consistency (k) and flow index (m), and the HB also gives the yield stress (τ0). The Spearman rank correlations between these parameters and the ASTP in the frequency ranges, corresponding to the myogenic, neurogenic and endothelial mechanisms of the microcirculation tone regulation were calculated. The ASTP values decreased when the blood viscosity increased. The correlation analysis revealed good ASTP-m (r > 0.5) and ASTP-k (r < -0.5) relationships in the endothelial range, while the ASTP-τ0 correlation was weaker (r≈-0.4). These correlations became lower for the ASTP during the cold stress. The results prompt manifestation of endothelial dysfunction in patients with type 2 diabetes.

Therapeutic management of postoperative ileus

Postoperative ileus is one of the most common complications in patients after abdominal surgery and is a major determinant of recovery after surgery. It leads to increased postoperative morbidity, prolonged hospital stay, and increased costs. The pathogenesis of postoperative ileus is multifactorial, including pharmacological, neurogenic, and inflammatory mechanisms. In this review, we discuss the current therapeutic strategies for postoperative ileus.