Rat vasopressin cell responses to simulated hemorrhage: stimulus-dependent role for A1 noradrenergic neurons

1995 ◽  
Vol 268 (5) ◽  
pp. R1336-R1342 ◽  
Author(s):  
D. W. Smith ◽  
J. R. Sibbald ◽  
S. Khanna ◽  
T. A. Day
Keyword(s):  
Supraoptic Nucleus ◽  
Area Postrema ◽  
Vena Cava ◽  
Electrophysiological Recording ◽  
Moderate Intensity ◽  
Cell Group ◽  
Gamma Aminobutyric Acid ◽  
Electrophysiological Studies ◽  
Simulated Hemorrhage

c-fos expression mapping and electrophysiological recording experiments were done to clarify the role of the A1 noradrenergic cell group in the vasopressin response to hypotensive hemorrhage. In pentobarbital-anesthetized rats, moderate and severe hypotensive hemorrhages were simulated by brief occlusion of the inferior vena cava sufficient to reduce mean arterial pressure to approximately 50 or 30 mmHg, respectively. Both stimuli significantly increased the number of A1 region catecholamine cells displaying Fos-like immunoreactivity, this effect being most prominent at the level of the area postrema. Both stimuli also increased the number of supraoptic nucleus vasopressin cells displaying Fos-like immunoreactivity. Accordingly, electrophysiological studies involving separate animals confirmed that both moderate and severe caval occlusion significantly increased the firing of functionally identified vasopressin cells recorded in the supraoptic nucleus. However, although interruption of A1 region neuronal function by injection of gamma-aminobutyric acid at the level of the area postrema eliminated the increase in vasopressin cell firing elicited by moderate caval occlusion, it did not block the response to severe caval occlusion. These findings suggest that, in the rat, the vasopressin response to an acute reduction in central blood volume, such as that produced by hemorrhage, depends on the A1 projection only if the stimulus is of moderate intensity. Severe stimuli appear to involve activation of both the A1 projection and an additional vasopressin-stimulatory pathway that bypasses the A1 region.

Effects of High Intensity Statin Therapy in the Treatment of Diabetic Dyslipidemia in Patients with Coronary Artery Disease

2018 ◽  
Vol 24 (4) ◽  
pp. 427-441 ◽  
Author(s):  
Marija Vavlukis ◽  
Sasko Kedev
Keyword(s):  
Statin Therapy ◽  
High Intensity ◽  
Statistical Significance ◽  
Incident Diabetes ◽  
Moderate Intensity ◽  
Protective Effects ◽  
Pcsk9 Inhibitors ◽  
Diabetic Dyslipidemia ◽  
Patients With Diabetes

Background: Diabetic dyslipidemia has specifics that differ from dyslipidemia in patients without diabetes, which contributes to accelerated atherosclerosis equally as dysglycemia. The aim of this study was to deduce the interdependence of diabetic dyslipidemia and cardiovascular diseases (CVD), therapeutic strategies and the risk of diabetes development with statin therapy. Method: We conducted a literature review of English articles through PubMed, PubMed Central and Cochrane, on the role of diabetic dyslipidemia in atherosclerosis, the antilipemic treatment with statins, and the role of statin therapy in newly developed diabetes, by using key words: atherosclerosis, diabetes mellitus, diabetic dyslipidemia, CVD, statins, nicotinic acid, fibrates, PCSK9 inhibitors. Results: hyperglycemia and dyslipidemia cannot be treated separately in patients with diabetes. It seems that dyslipidemia plays one of the key roles in the development of atherosclerosis. High levels of TG, decreased levels of HDL-C and increased levels of small dense LDL- C particles in the systemic circulation are the most specific attributes of diabetic dyslipidemia, all of which originate from an inflated flux of free fatty acids occurring due to the preceding resistance to insulin, and exacerbated by elevated levels of inflammatory adipokines. Statins are a fundamental treatment for diabetic dyslipidemia, both for dyslipidemia and for CVD prevention. The use of statin treatment with high intensity is endorsed for all diabetes-and-CVD patients, while a moderate - intensity treatment can be applied to patients with diabetes, having additional risk factors for CVD. Statins alone are thought to possess a small, although of statistical significance, risk of incident diabetes, outweighed by their benefits. Conclusion: As important as hyperglycemia and glycoregulation are in CVD development in patients with diabetes, diabetic dyslipidemia plays an even more important role. Statins remain the cornerstone of antilipemic treatment in diabetic dyslipidemia, and their protective effects in CVD progression overcome the risk of statin- associated incident diabetes.

scholarly journals Coughing as a potentially effective induction method of atrial tachycardia: a case report

2020 ◽  
Author(s):  
Reina Tonegawa-Kuji ◽  
Kenichiro Yamagata ◽  
Kengo Kusano
Keyword(s):  
Pulmonary Vein ◽  
Atrial Tachycardia ◽  
Superior Vena ◽  
Vena Cava ◽  
P Wave ◽  
Induction Method ◽  
Voluntary Cough ◽  
Wave Morphology ◽  
The Right

Abstract Background  Cough-induced atrial tachycardia (AT) is extremely rare and its electrical origin remains largely unknown. Atrial tachycardias triggered by pharyngeal stimulation, such as swallowing or speech, appears to be more common and the majority of them originate from the superior vena cava or right superior pulmonary vein (PV). Only one case of swallow-triggered AT with right inferior pulmonary vein (RIPV) origin has been reported to date. Case summary  We present a case of a 41-year-old man with recurring episodes of AT in the daytime. He underwent electrophysiology study without sedation. Atrial tachycardia was not observed when the patient entered the examination room and could not be induced with conventional induction procedures. By having the patient cough periodically on purpose, transient AT with P-wave morphology similar to the clinical AT was consistently induced. Activation mapping of the AT revealed a centrifugal pattern with the earliest activity localized inside the RIPV. After successful radiofrequency isolation of the right PV, AT was no longer inducible. Discussion  In the rare case of cough-induced AT originating from the RIPV, the proximity of the inferior right ganglionated plexi (GP) suggests the role of GP in triggering tachycardia. This is the first report that demonstrates voluntary cough was used to induce AT. In such cases that induction of AT is difficult using conventional methods, having the patient cough may be an effective induction method that is easy to attempt.

scholarly journals Role of Inferior Vena Cava Filter Retrieval in Patients on Chronic Anticoagulation Therapy

2021 ◽  
Vol 23 (2) ◽  
Author(s):  
Savannah Fletcher ◽  
Adam Plotnik ◽  
Ravi N. Srinivasa ◽  
Jeffrey Forris Beecham Chick ◽  
John M. Moriarty
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena Cava Filter ◽  
Inferior Vena ◽  
Treatment Options ◽  
Anticoagulation Therapy ◽  
Vena Cava ◽  
Vena Cava Filter ◽  
Venous Thromboembolic

Abstract Purpose of review Describe the role of inferior vena cava filter (IVCF) retrieval in patients on chronic anticoagulation given the overlap of these treatment options in the management of patients with venous thromboembolic disease. Recent findings Despite the increase in IVCF retrievals since the Food and Drug Administration safety communications in 2010 and 2014, retrieval rates remain low. Previous studies have shown that longer filter dwell times are associated with greater risk for filter complications and more difficulty with filter retrievals. Recent findings suggest that complications are more frequent in the first 30 days after placement. Summary The decision to retrieve an optional IVCF is individualized and requires diligent follow-up with consistent re-evaluation of the need for the indwelling IVCF, particularly in those on long-term anticoagulation therapy.

Physical exercise and blood pressure with reference to the angiotensinogen M235T polymorphism

2002 ◽  
Vol 10 (2) ◽  
pp. 71-77 ◽  
Author(s):  
Rainer Rauramaa ◽  
Raimo Kuhanen ◽  
Timo A. Lakka ◽  
Sari B. Väisänen ◽  
Pirjo Halonen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Reference Group ◽  
Controlled Trial ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Blood Pressures ◽  
Agt Gene ◽  
M235t Polymorphism

We investigated the role of the angiotensinogen (AGT) gene M235T polymorphism in determining blood pressure (BP) response to moderate intensity exercise in a 6-yr randomized controlled trial in 140 middle-aged men. Sitting, supine, and standing blood pressures were measured annually. Of the randomized men, 86% participated in the trial for 6 yr. Submaximal cardiorespiratory fitness increased by 16% in the exercise group. In the M homozygotes, sitting systolic BP decreased by 1.0 mmHg in the exercise but increased by 14.6 mmHg in the reference group ( P = 0.007 for net effect). Sitting and supine diastolic BP decreased by 6.2 and 3.3 mmHg in the exercise but increased by 2.8 and 3.2 mmHg in the reference group ( P = 0.026 and 0.024 for net effects), respectively. Regular moderate intensity exercise attenuates aging-related increase in systolic BP and decreases diastolic BP among the M homozygotes of the AGT gene M235T polymorphism.

Reassessment of the Role of Inferior-Vena-Cava Ligation in Venous Thromboembolism

1965 ◽  
Vol 273 (23) ◽  
pp. 1250-1253 ◽  
Author(s):  
Donald C. Nabseth ◽  
John M. Moran
Keyword(s):  
Venous Thromboembolism ◽  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Vena Cava

scholarly journals LPS Primes Brain Responsiveness to High Mobility Group Box-1 Protein

2021 ◽  
Vol 14 (6) ◽  
pp. 558
Author(s):  
Verena Peek ◽  
Lois M. Harden ◽  
Jelena Damm ◽  
Ferial Aslani ◽  
Stephan Leisengang ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Area Postrema ◽  
High Mobility ◽  
High Mobility Group ◽  
Direct Access ◽  
Significant Release ◽  
Factor Α ◽  
Culture Supernatants

High mobility group box (HMGB)1 action contributes to late phases of sepsis, but the effects of increased endogenous plasma HMGB1 levels on brain cells during inflammation are unclear. Here, we aimed to further investigate the role of HMGB1 in the brain during septic-like lipopolysaccharide-induced inflammation in rats (LPS, 10 mg/kg, i.p.). HMGB-1 mRNA expression and release were measured in the periphery/brain by RT-PCR, immunohistochemistry and ELISA. In vitro experiments with disulfide-HMGB1 in primary neuro-glial cell cultures of the area postrema (AP), a circumventricular organ with a leaky blood–brain barrier and direct access to circulating mediators like HMGB1 and LPS, were performed to determine the direct influence of HMGB1 on this pivotal brain structure for immune-to-brain communication. Indeed, HMGB1 plasma levels stayed elevated after LPS injection. Immunohistochemistry of brains and AP cultures confirmed LPS-stimulated cytoplasmatic translocation of HMGB1 indicative of local HMGB1 release. Moreover, disulfide-HMGB1 stimulation induced nuclear factor (NF)-κB activation and a significant release of interleukin-6, but not tumor necrosis factor α, into AP culture supernatants. However, only a few AP cells directly responded to HMGB1 with increased intracellular calcium concentration. Interestingly, priming with LPS induced a seven-fold higher percentage of responsive cells to HMGB1. We conclude that, as a humoral and local mediator, HMGB1 enhances brain inflammatory responses, after LPS priming, linked to sustained sepsis symptoms.

scholarly journals Effect of P2 receptor blockade on cutaneous vasodilation during rest and exercise in the heat in young men

2018 ◽  
Vol 43 (3) ◽  
pp. 312-315
Author(s):  
Naoto Fujii ◽  
Robert D. Meade ◽  
Jeffrey C. Louie ◽  
Pegah Akbari ◽  
Pierre Boulay ◽  
...  
Keyword(s):  
Heat Exposure ◽  
P2 Receptors ◽  
Moderate Intensity ◽  
Receptor Blockade ◽  
P2 Receptor ◽  
Moderate Intensity Exercise ◽  
Cutaneous Vasodilation ◽  
Oxide Synthase ◽  
Rest And Exercise

We assessed the role of purinergic P2 receptors in the regulation of cutaneous vasodilation in young adults at rest and during intermittent moderate-intensity exercise in the heat (35 °C). P2 receptor blockade augmented resting cutaneous vasodilation but had no influence during and following exercise. This increase was partly diminished by nitric oxide synthase inhibition. These results suggest a functional role of P2 receptors in the regulation of cutaneous vascular tone during ambient heat exposure at rest.

Role of the AMP-activated protein kinase in regulating fatty acid metabolism during exerciseThis paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.

2009 ◽  
Vol 34 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Gregory R. Steinberg
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Protein Kinase ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Moderate Intensity ◽  
Amp Activated Protein Kinase

During moderate-intensity exercise, fatty acids are the predominant substrate for working skeletal muscle. The release of fatty acids from adipose tissue stores, combined with the ability of skeletal muscle to actively fine tune the gradient between fatty acid and carbohydrate metabolism, depending on substrate availability and energetic demands, requires a coordinated system of metabolic control. Over the past decade, since the discovery that AMP-activated protein kinase (AMPK) was increased in accordance with exercise intensity, there has been significant interest in the proposed role of this ancient stress-sensing kinase as a critical integrative switch controlling metabolic responses during exercise. In this review, studies examining the role of AMPK as a regulator of fatty acid metabolism in both adipose tissue and skeletal muscle during exercise will be discussed. Exercise induces activation of AMPK in adipocytes and regulates triglyceride hydrolysis and esterfication through phosphorylation of hormone sensitive lipase (HSL) and glycerol-3-phosphate acyl-transferase, respectively. In skeletal muscle, exercise-induced activation of AMPK is associated with increases in fatty acid uptake, phosphorylation of HSL, and increased fatty acid oxidation, which is thought to occur via the acetyl-CoA carboxylase-malony-CoA-CPT-1 signalling axis. Despite the importance of AMPK in regulating fatty acid metabolism under resting conditions, recent evidence from transgenic models of AMPK deficiency suggest that alternative signalling pathways may also be important for the control of fatty acid metabolism during exercise.

Sign in / Sign up

Export Citation Format

Share Document