Pentagastrin-induced hemoconcentration in healthy volunteers and patients with panic disorder: effect of pretreatment with ethinyl estradiol.

Panic disorder has been associated with both an increased risk of coronary events as well as an increased risk of stroke. Hemoconcentration, with both a decrease in plasma volume and an increase in plasma viscosity, is a possible contributor to the risk of acute ischemic events. Our objectives were to demonstrate the process of hemoconcentration in response to induced panic symptoms and to assess the effect of pretreatment with ethinyl estradiol on panic-induced hemoconcentration.

Delayed increase in LDL cholesterol following pentagastrin-induced panic attacks.

Objective: Panic disorder (PD) has been associated with an increased risk for cardiovascular (CV) morbidity and mortality. There are inconsistent reports of increased low-density lipoprotein cholesterol (LDL-C) in patients with PD. Studies have reported a correlation between cholesterol levels and the intensity and frequency of panic attacks (PAs), suggesting that an elevation in cholesterol could be due to physiological and neurochemical changes that occur during and after a PA.

Alteration of decreased plasma NO metabolites and platelet NO synthase activity by paroxetine in depressed patients.

Although major depression (MD) and cardiovascular disease (CVD) have been conclusively linked in the literature, the mechanism associating MD and CVD is yet undetermined. The purpose of this paper is to further investigate a potential mechanism involving nitric oxide (NO) and to examine the effect of the selective serotonin reuptake inhibitor paroxetine on NO production by both platelets and the endothelium. In total, 17 subjects with MD and 12 healthy controls (HCs) with no known history of cardiovascular illness completed the study.

Decreased platelet nitric oxide synthase activity and plasma nitric oxide metabolites in major depressive disorder.

Background: Major depression (MD) has been associated with increased cardiovascular mortality in patients with coronary heart disease (CHD) and has been described as an independent risk factor for the development of CHD in healthy subjects; however, the mechanism of the association between MD and CHD remains to be determined. Nitric oxide (NO) plays a major role in cardiovascular regulation, and decreased NO production has been associated with several cardiovascular risk factors. We hypothesized that in patients with MD, NO production by both platelets and the endothelium would be reduced when compared with healthy control subjects (HCs).

Increased cholesterol levels during paroxetine administration in healthy men.

Background: Despite the frequent use of selective serotonin reuptake inhibitors in patients with coronary heart disease (CHD), their effects on plasma lipid levels have not been systematically investigated. Our objective was to assess the effects of 8 weeks of paroxetine administration on plasma cholesterol and triglyceride levels.

Method: Blood samples were collected at baseline, after 8 weeks of paroxetine administration, and post-discontinuation in 18 healthy male volunteers.

Paroxetine-induced increase in metabolic end products of nitric oxide.

Decreased production of endothelium-derived nitric oxide (NO) has been implicated in the pathogenesis of cardiovascular diseases. Metabolic end products of nitric oxide (NOx) are often used as markers for endothelial NO production in humans. Decreased endothelium-derived NO has been suggested to mediate some of the deleterious effects of conventional cardiovascular risk factors such as hypercholesterolemia, smoking, and physical inactivity because they induce a decrease in plasma NOx.

Paroxetine-induced increase in metabolic end products of nitric oxide.

Decreased production of endothelium-derived nitric oxide has been implicated in the pathogenesis of cardiovascular diseases. Metabolic end products of nitric oxide (NO(x)) are often used as markers for endothelial nitric oxide production in humans. Decreased endothelium-derived nitric oxide has been suggested to mediate some of the deleterious effects of conventional cardiovascular risk factors such as hypercholesterolemia, smoking, and physical inactivity.

Pulmonary and systemic nitric oxide measurements during CCK-5-induced panic attacks.

Nitric oxide (NO) plays a major role in cardiopulmonary regulation as illustrated by the alterations of the NO system described in cardiopulmonary illnesses. Recent studies have found an association between panic disorder and cardiovascular death and illness, as well as pulmonary diseases. Our objective was to investigate whether pulmonary or systemic NO production was altered during induced panic attacks (PAs).

Pentagastrin-induced release of free fatty acids in healthy volunteers and patients with panic disorder: effect of pretreatment with ethinyl estradiol.

Objective: The primary objective of this study was to assess whether pentagastrin-induced panic symptoms are associated with release of free fatty acids (FFAs) in a manner that could explain the mechanism of correlations observed between serum cholesterol levels and frequency and severity of panic attacks in patients with panic disorder (PD). A secondary objective was to assess whether pretreatment with ethinyl estradiol (EE) attenuates pentagastrin-induced release of FFAs.

Methods: A double-blind, crossover, placebo-controlled study was conducted in which patients with PD and healthy volunteers received 2 injections of pentagastrin, 7-10 days apart, with randomization of the order of pretreatment with placebo and EE.

Neuroactive steroid changes in response to challenge with the panicogenic agent pentagastrin.

Background: Female hormones and female hormone derivatives, including neuroactive steroids (NASs) have been suspected to play a role in the pathophysiology of panic disorder (PD). The panicogenic agent CO(2) has been shown to induce a delayed release of NASs in both brain and plasma of rats. In the present study, we measured NASs plasma levels in response to challenge with another panicogenic agent, pentagastrin, and assessed the effect of ethynil estradiol (EE) pretreatment.