EXPRESS: Intimacy, Contraception, and Pregnancy Prevention in Patients with Pulmonary Arterial Hypertension: Are We Counseling Our Patients?

Pulmonary arterial hypertension (PAH) is a serious, life-altering condition. Patients who are diagnosed are often of childbearing potential. Given the well-documented risks associated with this condition during pregnancy, as well as risks to the fetus from medications used to treat this disorder, patients should be strongly advised against pregnancy.

Safety, tolerability, and efficacy of overnight switching from sildenafil to tadalafil in patients with pulmonary arterial hypertension.

Aims: Tadalafil, a once-daily phosphodiesterase type 5 inhibitor (PDE-5I), offers clinicians an alternative to sildenafil, a 3-times-daily (t.i.d.

Systemic BP and heart rate as prognostic indicators in pulmonary arterial hypertension.

Background: Heart rate (HR) and systolic BP (SBP) are significant multivariate predictors of survival in patients with pulmonary arterial hypertension (PAH) as part of a 19-element formula. To what extent HR and BP alone predict survival and future hospitalization in patients with PAH is unknown.

Methods: We analyzed data from the Registry to Evaluate Early and Long-term PAH Disease Management (REVEAL Registry), a prospective, observational study of patients with PAH.

Impact of the removal of the monthly liver function test requirement for ambrisentan.

Background: The management of patients with pulmonary arterial hypertension (PAH) requires extensive coordination between patients, their support system, third-party payers, and healthcare professionals. For patients with PAH who are receiving endothelin receptor antagonists (ERAs), such cross-stakeholder coordination was needed to ensure compliance with a US Food and Drug Administration (FDA) Risk Evaluation and Mitigation Strategy (REMS) requirement for monthly liver function tests (LFTs). In March 2011, the FDA removed this requirement for ambrisentan (Letairis) in conjunction with a change to the product label.

Sex differences in the diagnosis, treatment, and outcome of patients with pulmonary arterial hypertension enrolled in the registry to evaluate early and long-term pulmonary arterial hypertension disease management.

Background: Pulmonary arterial hypertension (PAH) is a life-threatening disease that affects more women than men. The reasons for the female preponderance are unclear, and there are limited data available for men with PAH.

Methods: Data from the Registry to Evaluate Early and Long-term PAH Disease Management (REVEAL Registry) were analyzed to explore sex differences among patients with PAH with regard to 2-year survival from enrollment and 5-year survival from time of diagnosis.

Pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a rare and debilitating disease characterized by abnormal proliferation and contraction of pulmonary vascular smooth muscle cells. The resulting increase in pressure and pulmonary vascular resistance results in progressive right heart failure, low cardiac output, and ultimately death if left untreated. PAH is defined by a persistent elevation in pulmonary artery pressure with normal left-sided pressures, differentiating it from left-sided heart disease.

Nurse/physician collaboration: action research and the lessons learned.

Objective: Finding time to add to nursing knowledge while solving problems in a fast-paced healthcare environment is the ultimate challenge for nurse executives. At one hospital, use of an action research model to measure collaboration in nurse/physician led interdisciplinary teams improved the intervention and the approach to outcome measurement.

Background: Many hospital nurse executives promote collaborative practice, and yet, innovations introduced to foster collaboration are rarely studied prospectively.

A self-medication administration program for transplant recipients.

Cardiothoracic transplant recipients must follow a complex medication regimen after discharge. Patients, particularly heart transplant recipients who have a shorter postoperative length of stay than other organ recipients, have a limited time to master this regimen. The SMAP has shown benefits in patients' mastery of medication information, increased patient satisfaction, better preparation for discharge, and home adjustment.

Preliminary safety evaluation of parenterally administered sulfoalkyl ether beta-cyclodextrin derivatives.

Parenteral administration of beta-cyclodextrin (beta-CD) results in renal and/or local toxicity dependent on the mode of administration. In an attempt to alleviate these properties, a series of anionically charged sulfoalkyl ether cyclodextrin (SAE-beta-CD) derivatives have been developed. The parenteral safety of these derivatives was determined by survival of male mice after intraperitoneal (ip) injection, kidney histopathology, plasma urea nitrogen levels of mice determined 24 h after injection, relative in vitro hemolytic potential and activated partial thromboplastin times (APTT).

The effect of partial hepatectomy on the metabolism, distribution, and nephrotoxicity of para-methylthiobenzamide in the rat.

Para-Methylthiobenzamide (PMTB) produces injury to the liver and kidney. Toxicity is mediated via its biotransformation to a reactive S,S-dioxide metabolite. The objective of this study was to examine the role of hepatic metabolism in the production of PMTB-induced renal toxicity.

Determination of p-methylthiobenzamide and p-methylthiobenzamide-S-oxide from rat plasma using solid-phase extraction and high-performance liquid chromatography.

p-Methylthiobenzamide (PMTB) is a thiocarbonyl compound exhibiting marked hepatotoxicity and nephrotoxicity. We describe a high-performance liquid chromatographic method for analyzing PMTB and a metabolite, p-methylthiobenzamide-S-oxide (PMTBSO), from rat plasma using a solid-phase extraction technique. In this way, PMTB and PMTBSO can be extracted from 0.

Toxicity of alkyldihydrofurans to metabolically active organs in the mouse.

Alkylfurans inflict toxicity in several mammalian species to lung, liver and kidney. Organ specificity of the alkylfurans is a sensitive function of the nature of the alkyl group. To determine if this toxicity requires an aromatic ring in the compound, we synthesized 4-methyl-2,3-dihydrofuran, 4-ethyl-2,3-dihydrofuran and 4-pentyl-2,3-dihydrofuran and determined their toxicity to lung, liver and kidney in mice.

Nephrotoxicity of para-substituted thiobenzamide derivatives in the rat.

Histological examination, plasma urea nitrogen levels (BUN), and renal cortical slice uptake of paminohippurate (PAH) or tetraethylammonium (TEA) were used to assess the nephrotoxicity of thiobenzamide and its para-substituted derivatives in Sprague-Dawley rats. Intraperitoneal injection of p-methylthiobenzamide (PMTB) to rats resulted in dose-dependent nephrotoxicity as judged by increased BUN levels, decreased TEA uptake and histologic examination of the kidney. Para-methoxythiobenzamide and PMTB were more potent nephrotoxins than thiobenzamide, which was itself minimally nephrotoxic.

Effect of reserpine on N-methylthiobenzamide-induced pulmonary edema: role of lung norepinephrine and hypothermia.

N-Methylthiobenzamide (NMTB) is a pneumotoxin which causes pulmonary edema and hydrothorax in rodents. Reserpine has been shown to attenuate the pneumotoxicity induced by NMTB. Some of that evidence suggests that the protection afforded by reserpine occurs independently of its capacity to reduce peripheral 5-hydroxytryptamine (5-HT).

Effect of 2-butanol and 2-butanone on rat hepatic ultrastructure and drug metabolizing enzyme activity.

The effect of a single oral dose of 2-butanol (2.2 ml/kg) or 2-butanone (1.87 ml/kg) on hepatic ultrastructure and drug-metabolizing enzyme activity was studied in the rat.

The involvement of serotonin in the pneumotoxicity induced by N-methylthiobenzamide.

N-Methylthiobenzamide (NMTB) and alpha-naphthylthiourea (ANTU) are pneumotoxicants which cause pulmonary edema and hydrothorax. Recently a role was assigned to serotonin (5-hydroxytryptamine, 5-HT) in the pneumotoxic response to ANTU (D.E.

Comparison of the toxicity of methylcyclopentadienyl manganese tricarbonyl with that of its two major metabolites.

Pneumotoxicity and lethality resulting from administration of methylcyclopentadienyl manganese tricarbonyl (MMT) and its 2 major metabolites in rats were compared. Following i.p.

The role of metabolism in N-methylthiobenzamide-induced pneumotoxicity.

N-Methylthiobenzamide (NMTB) produces pulmonary edema, hydrothorax, and death in rodents. The objectives of the present studies were to establish a relationship between the lethality of NMTB and its pneumotoxicity and to explore the role of S-oxidation in these events. Pulmonary injury was assessed by measuring [14C]thymidine incorporation into pulmonary DNA.

Oxidation of N-methylthiobenzamide and N-methylthiobenzamide S-oxide by liver and lung microsomes.

The in vitro oxidation of N-[14C]methylthiobenzamide (NMTB) and N-[14C]methylthiobenzamide S-oxide (NMTBSO) by rat lung and liver microsomes was studied. In the presence of an NADPH-generating system, NMTB was rapidly converted to NMTBSO and small amounts of N-methylbenzamide (NMBA) and covalently bound metabolites (CVB). Under similar conditions, NMTBSO was converted to NMBA and CVB.

The acute toxicity of cyclopentadienyl manganese tricarbonyl in the rat.

The acute toxicity of cyclopentadienyl manganese tricarbonyl (CMT) was studied in Sprague-Dawley rats. CMT was found to produce convulsions and pulmonary edema. The ED50s for convulsion were 32 mg/kg (95% C.

Effect of inhibitors of alpha-naphthylisothiocyanate-induced hepatotoxicity on the in vitro metabolism of alpha-naphthylisothiocyanate.

The role of S-oxidation in the toxic bioactivation of alpha-naphthylisothiocyanate (ANIT) was investigated. The effects of several thione compounds, inhibitors and an inducer of the cytochrome P-450-dependent mixed function oxidase systems on the in vitro metabolism of ANIT and aminopyrine were determined. Ethionamide, sodium diethyldithiocarbamate (Na-DDTC) and S-methyl diethyldithiocarbamate (Me-DDTC), three agents known to undergo metabolism by an S-oxidative pathway and diminish ANIT's toxicity, inhibited the in vitro enzymatic metabolism of ANIT by rat liver microsomes.

Toxicity-distribution relationships among 3-alkylfurans in mouse liver and kidney.

The present study was designed to extend previous observations regarding toxicity of furans and related compounds to liver and kidney. It was desired to test a series of homologous 3- alkylfurans , where changes in lipophilic character might be related to changes in toxicity. Additionally, it was desired to measure distribution of toxins to the target organs to ascertain whether organ selectivity might be determined by the concentrations attained in the target organs by the toxins.

Effect of thiocarbonyl compounds on alpha-naphthylisothiocyanate-induced hepatotoxicity and the urinary excretion of [35S]alpha-naphthylisothiocyanate in the rat.

The effect of disulfiram (DSF), sodium diethyldithiocarbamate (DDTC), methyl diethyldithiocarbamate (Me-DDTC), and ethionamide on the hepatotoxic response of alpha-naphthylisothiocyanate (ANIT) was studied in the rat. The hyperbilirubinemic response of ANIT was significantly inhibited by ip or po DSF pretreatment. A more marked inhibition of toxicity occurred when DSF was given via ip injection.