Neurovascular coupling is not influenced by lower body negative pressure in humans.

Cerebral blood flow is tightly coupled with local neuronal activation and metabolism, i.e., neurovascular coupling (NVC). Studies suggest a role of sympathetic nervous system in the regulation of cerebral blood flow. However, this is controversial, and the sympathetic regulation of NVC in humans remains unclear. Since impaired NVC has been identified in several chronic diseases associated with a heightened sympathetic activity, we aimed to determine whether reflex-mediated sympathetic activation via lower body negative pressure (LBNP) attenuates NVC in humans. NVC was assessed using a visual stimulation protocol (5 cycles of 30 s eyes closed and 30 s of reading) in 11 healthy participants (aged 24 ± 3 yr). NVC assessments were made under control conditions and during LBNP at -20 and -40 mmHg. Posterior (PCA) and middle (MCA) cerebral artery mean blood velocity (Vmean) and vertebral artery blood flow (VAflow) were simultaneously determined with cardiorespiratory variables. Under control conditions, the visual stimulation evoked a robust increase in PCAVmean (∆18.0 ± 4.5%), a moderate rise in VAflow (∆9.6 ± 4.3%), and a modest increase in MCAVmean (∆3.0 ± 1.9%). The magnitude of NVC response was not affected by mild-to-moderate LBNP (all P > 0.05 for repeated-measures ANOVA). Given the small change that occurred in partial pressure of end-tidal CO2 during LBNP, this hypocapnia condition was matched via voluntary hyperventilation in absence of LBNP in a subgroup of participants (n = 8). The mild hypocapnia during LBNP did not exert a confounding influence on the NVC response. These findings indicate that the NVC is not influenced by LBNP or mild hypocapnia in humans.NEW & NOTEWORTHY Visual stimulation evoked a robust increase in posterior cerebral artery velocity and a modest increase in vertebral artery blood flow, i.e., neurovascular coupling (NVC), which was unaffected by lower body negative pressure (LBNP) in humans. In addition, although LBNP induced a mild hypocapnia, this degree of hypocapnia in the absence of LBNP failed to modify the NVC response.

Management of suspected acute coronary syndrome patients admitted to cardiology or non-cardiology services at Auckland City Hospital: implications for future national data collection.

AIMS: To review the number, characteristics and clinical management of suspected ACS patients admitted to cardiology and non-cardiology services at Auckland City Hospital, to assess differences between these services and to assess the number who would potentially be enrolled in the All New Zealand Acute Coronary Syndrome (ACS) Quality Improvement Programme (ANZACS-QI) database. METHODS: Auckland City Hospital patient data was extracted from the Australia and New Zealand ACS 'SNAPSHOT' audit, performed over 14 days in May 2012. RESULTS: There were 121 suspected ACS admissions to Auckland City hospital during the audit period, with 45 (37%) patients directly managed by the cardiology service, and 76 (63%) patients cared for by non-cardiology services. Based on the subsequent discharge diagnosis, the cardiology service had more patients with definite ACS than the non-cardiology services; 27/45 (60%) compared to 16/76 (21%), difference (95%CI) 39% (22-56), P<0.0001). Cardiology ACS patients were more likely to undergo echocardiography; 15/27 (56%) compared to 2/16 (13%), difference 42% (18-68), P=0.0089), coronary angiography; 21/27 (78%) compared to 3/16 (19%), difference (95%CI) 59% (34-84), P=0.0003), coronary revascularisation; 18/27 (67%) compared to 3/16 (19%), difference (95%CI) 48% (22-74), P=0.004, and be discharged on two antiplatelet agents; 18/26 (69%) compared to 3/15 (20%), difference (95%CI) 49% (22-76), P=0.0036, or an ACEI/ARB; 20/26 (77%) compared to 5/15 (33%), difference (95%CI) 44% (15-72), P=0.0088. CONCLUSIONS: In patients with a discharge diagnosis of definite ACS, those managed by non-cardiology services were less likely to receive guideline-recommended investigations, and management, in this relatively small cohort study. About one-third of all ACS patients are managed by non-cardiology services and would not be recorded by the ANZACS-QI database.

An unusual case of chronic meningitis.

BACKGROUND: Chronic meningitis is defined as symptoms and signs of meningeal inflammation and persisting cerebrospinal fluid abnormalities such as elevated protein level and pleocytosis for at least one month. CASE PRESENTATION: A 62-year-old woman, of unremarkable past medical history, was admitted to hospital for investigation of a four-week history of vomiting, malaise an associated hyponatraemia. She had a low-grade pyrexia with normal inflammatory markers. A CT brain was unremarkable and a contrast MRI brain revealed sub-acute infarction of the right frontal cortex but with no evidence of meningeal enhancement. Due to increasing confusion and patient clinical deterioration a lumbar puncture was performed at 17 days post admission. This revealed gram-negative coccobacilli in the CSF, which was identified as Neisseria meningitidis group B. The patient made a dramatic recovery with high-dose intravenous ceftriaxone antibiotic therapy for meningococcal meningitis. CONCLUSIONS: 1) Chronic bacterial meningitis may present highly atypically, particularly in the older adult. 2) There may be an absent or reduced febrile response, without a rise in inflammatory markers, despite a very unwell patient. 3) Early lumbar puncture is to be encouraged as it is essential to confirm the diagnosis.4) Despite a delayed diagnosis appropriate antibiotic therapy can still lead to a good outcome.

Barium reduces resting blood flow and inhibits potassium-induced vasodilation in the human forearm.

BACKGROUND: Increasing extracellular K+ concentration within and just above the physiological range hyperpolarizes and relaxes vascular smooth muscle in vitro. These actions involve inwardly rectifying potassium channels (K(IR)) and Na+/K+ ATPase, which are inhibited, respectively, by Ba2+ and ouabain. The role (if any) of K(IR) in controlling human resistance vessel tone is unknown, and we investigated this in the forearm. METHODS AND RESULTS: Blood flow was measured by plethysmography in healthy men. Drugs and electrolytes were infused through the brachial artery. BaCl2 (4 micromol/min, also used in subsequent experiments) increased Ba2+ plasma concentration in the infused forearm to 50+/-0.8 micromol/L (mean+/-SEM) and reduced blood flow by 24+/-4% (n=8, P<0.001) without causing systemic effects. Ouabain (2.7 nmol/min), alone and with BaCl2, reduced flow by 10+/-2% and 28+/-3%, respectively (n=10). Incremental infusions of KCl (0.05, 0.1, and 0.2 mmol/min) increased flow from baseline by 1.0+/-0.2, 2.0+/-0.4, and 4.2+/-0.5 mL/min per deciliter forearm, respectively. Responses to KCl (0.2 mmol/min) were inhibited by BaCl2, alone and plus ouabain, by 60+/-9% and 88+/-6%, respectively (both P< or =0.01). In control experiments, norepinephrine (240 pmol/min) reduced blood flow by 24+/-2% but had no significant effect on K+-induced vasodilation. BaCl2, alone or with ouabain, did not significantly influence responses to verapamil or nitroprusside. CONCLUSIONS: Ba2+ increases forearm vascular resistance. K+-induced vasodilation is selectively inhibited by Ba2+ and almost abolished by Ba2+ plus ouabain, suggesting a role for K(IR) and Na+/K+ ATPase in controlling basal tone and in K+-induced vasorelaxation in human forearm resistance vessels.