Добірка наукової літератури з теми "Afferent limb failure"

Efferent renal sympathetic nerve activity (ERSNA) is increased in the rat with low-cardiac-output congestive heart failure (CHF; myocardial infarction). Arterial and cardiopulmonary baroreflex control of ERSNA in CHF and control rats was examined. Cardiac index and arterial pressure were lower and total peripheral resistance index, left ventricular end-diastolic pressure, and heart-to-body weight ratio were higher in CHF than in control rats. Increases in left ventricular end diastolic pressure produced by intravenous volume loading failed to increase cardiac index in CHF rats as it did in control rats. Single-unit analysis of aortic baroreceptor nerve activity showed that CHF rats had higher pressure threshold, lower frequency at pressure threshold, and lower gain than control rats. Arterial baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. Single-unit analysis of vagal nerve activity showed that CHF rats had higher pressure threshold, lower frequency at saturation, and lower gain than control rats. Cardiopulmonary baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. In the CHF rat, arterial and cardiopulmonary baroreflex control of ERSNA is markedly attenuated because of abnormalities in the periphery at the level of the aortic and cardiopulmonary receptors, respectively, and not in the central nervous system.

Cardiac failure is characterized by increased renal sympathetic nerve activity that is associated with an impairment of both arterial and cardiac baroreceptor reflex function. These reflex dysfunctions are in the afferent limb at the level of the peripheral baroreceptors. This study sought to define the relative quantitative magnitude of the defects in arterial and cardiac baroreceptor function in cardiac failure. Renal sympathetic nerve activity was measured in anesthetized normal control rats and rats with cardiac failure (left coronary ligation) during sequential random order sinoaortic denervation and vagotomy to interrupt afferent input from the arterial and cardiac baroreceptors, respectively. Increases in renal sympathetic nerve activity after individual or combined sinoaortic denervation and vagotomy were less (P < 0.05 for both) in cardiac failure than in normal control rats in both order sequences (42 +/- 5 vs. 87 +/- 8%; 44 +/- 5 vs. 108 +/- 7%). In cardiac failure rats, vagotomy produced lesser increases (P < 0.05 for both) in renal sympathetic nerve activity than sinoaortic denervation in both order sequences (10 +/- 4 vs. 32 +/- 5%; 13 +/- 2 vs. 30 +/- 5%). The relative magnitude of impaired cardiac baroreceptor reflex function that is associated with the increased renal sympathetic nerve activity of cardiac failure is greater than that of impaired arterial baroreceptor reflex function.

Injury of the afferent limb of the baroreflex from neck radiation causes radiation-induced afferent baroreflex failure (R-ABF). Identification and management of R-ABF is challenging. We aimed to investigate the pattern of autonomic dysfunction on standardized autonomic testing in patients with probable R-ABF. We retrospectively analyzed all autonomic reflex screens performed at Mayo Clinic in Rochester, MN, between 2000 and 2020 in patients with probable R-ABF. Additional tests reviewed included ambulatory blood pressure monitoring, plasma norepinephrine, and thermoregulatory sweat test. We identified 90 patients with probable R-ABF. Median total composite autonomic severity score (range, 0–10) was 7 (interquartile range, 6–7). Cardiovascular adrenergic impairment was seen in 85 patients (94.4%), increased blood pressure recovery time after Valsalva maneuver in 71 patients (78.9%; median 17.4 seconds), and orthostatic hypotension in 68 patients (75.6%). Cardiovagal impairment was demonstrated by abnormal heart rate responses to deep breathing (79.5%), Valsalva ratio (87.2%), and vagal baroreflex sensitivity (57.9%). Plasma norepinephrine was elevated and rose appropriately upon standing (722–1207 pg/mL). Ambulatory blood pressure monitoring revealed hypertension, postural hypotension, hypertensive surges, tachycardia, and absence of nocturnal dipping. Blood pressure lability correlated with impaired vagal baroreflex function. Postganglionic sympathetic sudomotor function was normal in most cases; the most frequent thermoregulatory sweat test finding was focal neck anhidrosis (78.9%). Standardized autonomic testing in R-ABF demonstrates cardiovascular adrenergic impairment with orthostatic hypotension, blood pressure lability, and elevated plasma norepinephrine. Cardiovagal impairment is common, while sudomotor deficits are limited to direct radiation effects.

Cardiovascular diseases are a leading cause of death in end-stage renal disease (ESRD) largely as a result of the progressively increasing age of ESRD patients and the broad constellation of uremia-associated factors that can adversely affect cardiac function. Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. In addition to impairing the coronary microcirculation, hypertension may contribute to the development of atherosclerotic coronary artery disease, particularly in the presence of the many lipid abnormalities observed in ESRD. These patients have reduced high-density lipoprotein cholesterol and increased plasma triglyceride concentrations, and there is a defect in cholesterol transport. Other abnormalities that may contribute to atherosclerotic coronary artery disease in ESRD are reduced high-density lipoprotein cholesterol synthesis and reduced activity of the reverse cholesterol pathway. Treatment with fibric acids, nicotinic acids, and lovastatin may be useful in lowering cholesterol and triglyceride concentrations in some of these patients. The incidence of coronary artery disease in ESRD populations is difficult to determine. About 25 to 30% of ESRD patients with angina have no evidence of significant coronary artery disease, and an undetermined number have silent coronary disease. The presence of resting electrocardiographic abnormalities caused by hypertension or conduction defects makes it difficult to accurately diagnosis coronary artery disease in ESRD populations by noninvasive methods, including exercise testing and thallium scintigraphy with or without the use of dipyridamole. Hypotension is a frequent complication of the dialytic process. Many factors have been implicated, including autonomic neuropathy. There is no consensus on the function of the efferent limb of the sympathetic nervous system. The afferent limb (arterial baroreflex function) is felt to be impaired. Further, there may be defects in the ability of the cardiovascular system to respond to sympathetic nerve activity. Most studies of autonomic function have used indirect measurements. Studies are underway that use techniques to assess sympathetic function directly. Such experiments with microneuropathy suggest greater skeletal sympathetic muscle discharge in uremic patients than in normal patients.

Heart failure (HF) patients demonstrate impaired pulmonary, circulatory, and nervous system responses to exercise. While HF demonstrates prolonged [time constant (τ)] pulmonary O2 uptake (V̇o2) on-kinetics, contributing to exercise intolerance, it is unknown whether abnormal V̇o2 kinetics couple with ventilatory and circulatory dysfunction secondary to impaired group III/IV afferents in HF. Because lower lumbar intrathecal fentanyl inhibits locomotor muscle afferents, resulting in improved exercise ventilation and hemodynamics, we tested these hypotheses: HF will demonstrate 1) rapid V̇o2 on-kinetics and 2) attenuated steady-state V̇o2 amplitude and O2 deficit (O2def) during exercise with fentanyl versus placebo. On separate visits (randomized), breath-by-breath V̇o2 was measured in HF (ejection fraction: 27 ± 6%, New York Heart Association class I–III) and age- and sex-matched controls (both n = 9, ages: 60 ± 6 vs. 63 ± 8 yr, P = 0.37) during cycling transitions at 65% peak workload (78 ± 24 vs. 115 ± 39 W, P < 0.01) with intrathecal fentanyl or placebo. Regardless of group or condition, optimal phase II (primary component) curve fits reflected a phase I period equal to 35 s (limb-to-lung timing) via single-exponential functions. Condition did not affect steady-state V̇o2, the phase II τ of V̇o2, or O2def within controls ( P > 0.05). Without differences in steady-state V̇o2, reduced O2def in fentanyl versus placebo within HF (13 ± 4 vs. 22 ± 15 ml/W, P = 0.04) was accounted for by a rapid phase II τ of V̇o2 in fentanyl versus placebo within HF (45 ± 11 vs. 57 ± 14 s, P = 0.04), respectively. In an integrative manner, these data demonstrate important effects of abnormal locomotor muscle afferents coupled to pulmonary and circulatory dysfunction in determining impaired exercise V̇o2 in HF. Effects of abnormal muscle afferents on impaired exercise V̇o2 and hence exercise intolerance may not be discernable by independently assessing steady-state V̇o2 in HF. NEW & NOTEWORTHY Inhibition of locomotor muscle afferents results in rapid primary-component O2 uptake (V̇o2) on-kinetics accounting for the decreased O2 deficit in heart failure (HF). This study revealed that abnormal musculoskeletal–neural afferents couple with pulmonary and circulatory dysfunction to provoke impaired exercise V̇o2 in HF. Steady-state V̇o2 cannot properly phenotype abnormal muscle afferent contributions to impaired exercise V̇o2 in HF.

Abstract Introduction Pre-pouch ileitis or afferent limb inflammation is generally considered to be suggestive of de novo Crohn’s disease in patients with ileal pouch. However, the data on whether these patients progress to develop CD-like complications is limited. We aim to study the evolution of pre-pouch ileitis in this study. Methods All patients who underwent an IPAA surgery by an expert surgeon between 1990 and 2018 for diagnosis of ulcerative colitis (UC) or inflammatory bowel disease-unclassified (IBD-U) at our institution and later went to develop pre-pouch ileitis were included. Patient charts were reviewed were reviewed subsequent to the diagnosis of pre-pouch ileitis to assess development of CD-like complications (non-anastomotic strictures and fistulae developing &gt;6 months after ileostomy closure) or requirement of J-pouch surgery or ileostomy. Pre-pouch ileitis was defined by presence of erosions or ulcers in the afferent limb. Results 58 patients with J-pouch developed pre-pouch ileitis at a median of 21 months (range 1–216 months) from ileostomy closure. Baseline characteristics are shown in table 1. Median follow up duration after the diagnosis of pre-pouch ileitis was 48 months (range 2–204 months). 54/58 (93%) patients had concomitant pouchitis with pre-pouch ileitis. 36/58 (62%) patients were initiated on biologic therapy during their follow up course and 3/58 (5%) were treated with an immunomodulator. 20/58 (35%) patients developed Crohn’s disease-like complications (10 developed non-anastomotic strictures and 10 developed perianal complications) at a median follow up of 17 months (range 2–85 months) from the diagnosis of pre-pouch ileitis. 5/58 (8.6%) needed endoscopic stricture dilation and 6/58 (10%) needed perianal surgery for fistula or abscess. Pouch failure occurred in 5/58 (9%) of patients (3 with pouch resection, 1 with pouch revision and 1 with permanent ileostomy), while 3/58 (5%) patients required temporary ileostomy. Conclusions Patients who develop pre-pouch ileitis are at high risk of developing CD-like complications (non-anastomotic strictures and perianal complications). The risk of pouch failure and requirement for endoscopic procedures or surgery in this cohort also appears to higher than traditionally reported in patients with pouchitis. Hence, pre-pouch ileitis should be considered suggestive of Crohn’s disease and treated aggressively.

This chapter describes the appropriate clinical approach to take when presented with a patient reporting a neurological symptom. Just under 10 per cent of the population consult their general practitioner about a neurological symptom each year in the United Kingdom. About 10 per cent of these are referred for a specialist opinion, usually to a neurologist. Nine conditions account for roughly 75 per cent of general neurological referrals and are diagnosed initially on purely clinical grounds, with the other 25 per cent representing the full range of other, potentially very rare, neurological disorders.This chapter underlines the importance of a thorough and informative history to achieve successful diagnosis. Crucial facets for a good history include information on the time course of symptom development, whether symptoms are negative or positive, previous neurological history (both personal and familial), as well as other potentially contributory general medical disorders. The general neurological examination is also described, as are specific examination manoeuvres that may be added to the general neurological examination in specific clinical circumstances.Reflexes play an important role in diagnostic neurology because they reflect the integrity of, or alterations in, the neural structures responsible for their arc. Loss of a reflex may be due to interruption of the afferent path by a lesion involving the first sensory neurone in the peripheral nerves, plexuses, spinal nerves, or dorsal roots, by damage to the central paths of the arc in the brainstem or spinal cord, by lesions of the lower motor neurone at any point between the anterior horn cells and the muscles, of the muscles themselves, or by the neural depression produced by neural shock. In clinical practice, the most useful and oft-elicited reflexes are the tendon reflexes of the limbs, the jaw jerk, the plantar response, the superficial abdominal reflexes, the pupil-light response, and in infants, the Moro reflex. The place of these particular reflexes in the routine neurological examination is outlined, and the elicitation and significance of these reflexes and of a wide variety of others which are used occasionally are described.Examinations that allow localization lesions that are responsible for muscle weaknesses and the assessment of somatosensory abnormalities are described, as are neurological disorders that result in identifiable gait disorders. The clinical signs and examinations relevant to autonomic disorders are also discussed.Intensive care may be required for patients critically ill either as a result of primary neurological disease, or in those in whom a neurological disorder is a component of, or secondary to, a general medical disorder. Indications for admission to neurological intensive care have been defined (Howard et al. 2003): impaired consciousness, bulbar muscle failure, severe ventilatory respiratory failure, uncontrolled seizures, severely raised intracranial pressure, some monitoring and interventional treatments, and unforeseen general medical complications. Naturally specific treatments indicated for the particular diagnosis should be instituted along with general intensive care measures.Finally, the discussion of diagnoses of chronic or terminal conditions with patients is discussed, with particular focus on the best way to present the diagnosis to the patient.