Our previous studies have shown that electroacupuncture (EA) at the Jianshi-Neiguan acupoints (P5-6, overlying the median nerve) attenuates sympathoexcitatory responses through its influence on neuronal activity in the rostral ventrolateral medulla (rVLM). The nucleus tractus solitarii (NTS) receives input from somatic nerve stimulation. Connections between the NTS and the rVLM during EA stimulation have not been investigated and thus were the focus of the present study. Seven to ten days after unilateral microinjection of a rhodamine-conjugated microsphere retrograde tracer (100 nl) into the rVLM, rats were subjected to EA or sham-EA without electrical stimulation. EA was performed for 30 min at the P5-6 acupoints bilaterally. Perikarya containing the microsphere tracer were found in the NTS of both groups. Compared to controls (needle placement without electrical stimulation, n = 7), c-Fos immunoreactivity and neurons double-labeled with c-Fos, an immediate early gene, and the tracer were significantly increased in the NTS of EA-treated rats (all P < 0.05; n = 8), particularly, in the medial and lateral subdivisions of NTS at subpostremal and obex levels. These results suggest that EA at the P5-6 acupoints activates NTS neurons. Furthermore, EA-activated NTS neurons directly project to the rVLM and likely influence the rVLM activity.

Our previous studies have shown that electroacupuncture (EA) at the Jianshi-Neiguan acupoints (P5-6, overlying the median nerve) attenuates sympathoexcitatory responses through its influence on neuronal activity in the rostral ventrolateral medulla (rVLM). The nucleus tractus solitarii (NTS) receives input from somatic nerve stimulation. Connections between the NTS and the rVLM during EA stimulation have not been investigated and thus were the focus of the present study. Seven to ten days after unilateral microinjection of a rhodamine-conjugated microsphere retrograde tracer (100 nl) into the rVLM, rats were subjected to EA or sham-EA without electrical stimulation. EA was performed for 30 min at the P5-6 acupoints bilaterally. Perikarya containing the microsphere tracer were found in the NTS of both groups. Compared to controls (needle placement without electrical stimulation, n = 7), c-Fos immunoreactivity and neurons double-labeled with c-Fos, an immediate early gene, and the tracer were significantly increased in the NTS of EA-treated rats (all P < 0.05; n = 8), particularly, in the medial and lateral subdivisions of NTS at subpostremal and obex levels. These results suggest that EA at the P5-6 acupoints activates NTS neurons. Furthermore, EA-activated NTS neurons directly project to the rVLM and likely influence the rVLM activity.

Electroacupuncture (EA) can be used to lower high blood pressure (BP) in clinical practice. However, precise mechanisms underlying its effects on elevated BP remain unclear. Our previous studies have shown that EA at the P5-6 acupoints, overlying the median nerve, attenuates elevated BP induced by gastric distension (GD) through influence on rostral ventrolateral medulla (rVLM). Although adenosine is released during neuronal activation in the rVLM, its role in acupuncture-cardiovascular regulation is unknown. The purinergic system is involved in cardiovascular pressor and depressor responses, including via selective activation of A₁ and A_{2 a} rVLM receptors, respectively. The action of A_{2 a} receptor stimulation in the central nervous system may be further regulated through an endogenous opioid mechanism. However, it is uncertain whether this putative action occurs in the rVLM. We hypothesized that adenosine in the rVLM contributes to EA modulation of sympathoexcitatory reflexes through an A_{2 a} but not an A₁ adenosine receptor-opioid mechanism. EA or sham-EA was applied at the P5-6 acupoints in Sprague-Dawley male rats subjected to repeated GD under anesthesia. We found that EA (n = 6) but not sham-EA (n = 5) at P5-6 significantly (P < 0.05) attenuated GD-induced elevations in BP. EA modulation of sympathoexcitatory cardiovascular reflexes was reversed significantly after rVLM microinjection (50 nl) of 8-SPT (10 mM; non-selective adenosine receptor antagonist; n = 7) or SCH 58261 (1 mM; A_{2 a} receptor antagonist; n = 8; both P < 0.05), but not by DPCPX (3 mM; A₁ receptor antagonist; n = 6) or the vehicle (5% dimethylsulfoxide; n = 6). Moreover, microinjection of an A_{2 a} receptor agonist, CGS-21680 (0.4 mM; n = 8) into the rVLM attenuated GD-induced pressor responses without EA, which mimicked EA's inhibitory effects (P < 0.05). After blockade of opioid receptors with naloxone (1 mM) in the rVLM, SCH 58261's reversal of EA's effect on GD-induced pressor responses was blunted, and CGS-21680-mediated inhibitory effect on pressor responses was not observed. Furthermore, neurons labeled with adenosine A_{2 a} receptors were anatomically co-localized with neurons stained with enkephalin in the rVLM. These data suggest that the involvement of rVLM adenosine A_{2 a} receptors in EA modulation of GD-induced pressor reflexes is, at least in part, dependent on the presence of endogenous opioids.

Electroacupuncture (EA) can be used to lower high blood pressure (BP) in clinical practice. However, precise mechanisms underlying its effects on elevated BP remain unclear. Our previous studies have shown that EA at the P5-6 acupoints, overlying the median nerve, attenuates elevated BP induced by gastric distension (GD) through influence on rostral ventrolateral medulla (rVLM). Although adenosine is released during neuronal activation in the rVLM, its role in acupuncture-cardiovascular regulation is unknown. The purinergic system is involved in cardiovascular pressor and depressor responses, including via selective activation of A1 and A2 a rVLM receptors, respectively. The action of A2 a receptor stimulation in the central nervous system may be further regulated through an endogenous opioid mechanism. However, it is uncertain whether this putative action occurs in the rVLM. We hypothesized that adenosine in the rVLM contributes to EA modulation of sympathoexcitatory reflexes through an A2 a but not an A1 adenosine receptor-opioid mechanism. EA or sham-EA was applied at the P5-6 acupoints in Sprague-Dawley male rats subjected to repeated GD under anesthesia. We found that EA (n = 6) but not sham-EA (n = 5) at P5-6 significantly (P < 0.05) attenuated GD-induced elevations in BP. EA modulation of sympathoexcitatory cardiovascular reflexes was reversed significantly after rVLM microinjection (50 nl) of 8-SPT (10 mM; non-selective adenosine receptor antagonist; n = 7) or SCH 58261 (1 mM; A2 a receptor antagonist; n = 8; both P < 0.05), but not by DPCPX (3 mM; A1 receptor antagonist; n = 6) or the vehicle (5% dimethylsulfoxide; n = 6). Moreover, microinjection of an A2 a receptor agonist, CGS-21680 (0.4 mM; n = 8) into the rVLM attenuated GD-induced pressor responses without EA, which mimicked EAs inhibitory effects (P < 0.05). After blockade of opioid receptors with naloxone (1 mM) in the rVLM, SCH 58261s reversal of EAs effect on GD-induced pressor responses was blunted, and CGS-21680-mediated inhibitory effect on pressor responses was not observed. Furthermore, neurons labeled with adenosine A2 a receptors were anatomically co-localized with neurons stained with enkephalin in the rVLM. These data suggest that the involvement of rVLM adenosine A2 a receptors in EA modulation of GD-induced pressor reflexes is, at least in part, dependent on the presence of endogenous opioids.

Carotid intima-media thickness (CIMT) is a well-established predictor of cardiovascular disease events. Not well described, however, is the prevalence of plaque and stenosis severity and how this varies according to extent of CIMT, age, and gender. We evaluated the extent of carotid plaque and stenosis severity according to CIMT, age, and gender in a large CIMT screening registry. We studied 9,347 women and 12,676 men (n = 22,023) who received carotid ultrasound scans. The presence and severity of both carotid plaque and stenosis was compared according to extent of CIMT (≥1 mm vs <1 mm), age, and gender using the chi-square test of proportions. Among those aged <45 to ≥80 years, the prevalence of CIMT ≥1 mm ranged from 0.13% to 29.3% in women and 0.6% to 40.1% in men, stenosis ≥50% from 0.1% to 14.9% in women and 0.1% to 13.2% in men, and mixed and/or soft plaque from 7.1% to 66.5% in women, and 9.2% to 65.8% in men (all p <0.001 across age groups). Even when CIMT levels were <1 mm, >30% of patients demonstrated mixed or soft plaque potentially prone to rupture. Of those with CIMT ≥1 mm, more than 70% had such mixed or soft plaque and more than 40% demonstrated stenoses of 30% or greater. In conclusion, we describe in a large CIMT registry study a substantial age-related increase in both men and women of increased CIMT, plaque presence, and severity, and stenosis. Even in those with normal CIMT, mixed or soft plaque was common, further demonstrating the value in assessing for plaque when doing carotid ultrasound.

OBJECTIVES: To determine in-hospital mortality differences in individuals with dementia and acute myocardial infarction (AMI) when using invasive coronary procedures. DESIGN: Retrospective cohort study. SETTING: 2009 Nationwide Inpatient Sample. PARTICIPANTS: Individuals admitted with a primary diagnosis of AMI (N = 631,734) to 1,045 hospitals in 44 states during 2009. MEASUREMENTS: Dementia status and procedural use of diagnostic catheterization, percutaneous intervention (PCI), and coronary artery bypass grafts (CABG) as indicated by International Classification of Diseases, Ninth Revision, codes. The primary outcome was in-hospital mortality. Using multivariable analysis adjusted for covariates, associations were made between coronary procedural use in individuals with dementia and in-hospital mortality. Additional multivariable analysis identified the association between utilization of coronary procedures and in-hospital mortality in AMI patients with dementia. RESULTS: Dementia diagnosis (n = 15,335) was associated with greater likelihood of in-hospital mortality (odds ratio (OR) = 1.22, 95% confidence interval (CI) = 1.15-1.29, P < .001) and less use of diagnostic catheterization (OR = 0.37, 95% CI = 0.35-0.40, P < .001), PCI (OR = 0.37, 95% CI = 0.35-0.40, P < .001), and CABG (OR = 0.19, 95% CI = 0.16-0.22, P < .001). There was less likelihood of in-hospital mortality in participants with dementia who received diagnostic catheterization (OR = 0.36, 95% CI = 0.16-0.78, P < .001), PCI (OR = 0.57, 95% CI = 0.47-0.70, P < .001), or CABG (OR = 0.22, 95% CI = 0.08-0.56, P < .001) than in those not receiving respective interventions. CONCLUSION: Dementia is a significant predictor of in-hospital mortality for hospitalized individuals with AMI and is associated with less use of invasive coronary procedures. Beyond differing care patterns for individuals with AMI and dementia, these results indicate that individuals with dementia are at substantially greater risk for in-hospital mortality when they do not receive procedural interventions.

OBJECTIVE: Ruptured aortic aneurysm is a condition with a high rate of mortality that requires prompt surgical intervention. It has been noted that in some conditions requiring such prompt intervention, in-hospital mortality is increased in patients admitted on the weekends compared with patients admitted on weekdays. We sought to determine if this was indeed the case for both ruptured thoracic aortic aneurysms (TAA) and abdominal aortic aneurysms (AAA) and to elucidate the possible reasons. METHODS: Using the Nationwide Inpatient Sample, a publicly available database of inpatient care, we analyzed the incidence of mortality among 7200 patients admitted on the weekends compared with weekdays for ruptured aortic aneurysm. Among these patients, 19% had a TAA and 81% had an AAA, and each group was analyzed for differences in mortality during the hospitalization. We adjusted for demographics, comorbid conditions, hospital characteristics, rates of surgical intervention, timing of surgical intervention, and use of additional therapeutic measures. RESULTS: Patients admitted on the weekend for both ruptured TAA and AAA had a statistically significant increase in mortality compared with those admitted on the weekdays (TAA: odds ratio, 2.55; 95% confidence interval, 1.77-3.68; P = .03; AAA: odds ratio, 1.32; 95% confidence interval, 1.13-1.55; P = .0004). Among those with TAA, a surgical intervention was performed on day of admission in 62.1% of weekday admissions vs 34.9% of weekend admissions (P < .0001). This difference was much smaller among those with an aortic aneurysm; 79.6% had a surgical intervention on day of admission on a weekday vs 77.2% on the weekend (P < .0001). CONCLUSIONS: Weekend admission for ruptured aortic aneurysm is associated with an increased mortality compared with admission on a weekday, and this is likely due to several factors including a delay in prompt surgical intervention.