Ma huang and alpha subtype adrenoceptors in the cat pulmonary vascular bed.

Objective: To test the hypothesis that ma huang induces a pressor response in the pulmonary vascular bed of the cat and identify the alpha (1)-adrenoceptor subtype pathway(s) involved in the mediation or modulation of these effects.

Design: Prospective vehicle controlled study.

Setting: University research laboratory.

The role of cyclooxygenase in the feline pulmonary vascular bed.

Objective: There are extensive data on roles of cyclooxygenase 1 (COX 1) and cyclooxygenase 2 (COX 2) enzymes in temperature, coagulation, and inflammatory modulation. There is little known of the function of these enzymes in regulating tone in pulmonary vasculature. The purpose of this investigation was to elucidate the roles of COX 1 and 2 enzymes in the feline pulmonary vascular bed.

Analysis of the effects of fentanyl in the feline pulmonary vascular bed.

The objective of this study was to test the hypothesis that fentanyl induces a depressor response in the pulmonary vascular bed of the cat and to identify the receptors involved in the mediation or modulation of these effects. The authors conducted a prospective vehicle-controlled study at a university research laboratory using intact chest preparation in adult mongrel cats. In separate experiments, the effects of diphenhydramine (histamine receptor blocker), glibenclamide (ATP-sensitive K+ channel blocker), L-N5-(1-Iminoethyl) ornithine hydrochloride (L-NIO) (nitric oxide synthase inhibitor), nimesulide (selective cyclooxygenase [COX]-2 inhibitor), and naloxone (opiate receptor antagonist) were investigated on pulmonary arterial responses to fentanyl and other agonists in the pulmonary vascular bed of the cat.

The effects of meperidine in the pulmonary vascular bed of the cat.

Objective: The purpose of this study was to test the hypothesis that meperidine induces a dilator response in the feline pulmonary vascular bed, and to identify receptors involved in the mediation or modulation of these effects.

Design: Prospective vehicle controlled study.

Setting: University research laboratory.

Analysis of responses to kava kava in the feline pulmonary vascular bed.

This study was designed to test the hypothesis that kava kava induces a depressor response in the pulmonary vascular bed of the cat and to identify the pathways involved in the mediation or modulation of these effects. In separate experiments, the effects of L-N5-(1-iminoethyl)ornithine hydrochloride (L-NIO), a nitric oxide synthase inhibitor, glibenclamide, an ATP-sensitive K+ channel blocker, meclofenamate, a nonselective cyclooxygenase inhibitor, nicardipine, a calcium channel blocker, bicuculline, a gamma-aminobutyric acid (GABA)A receptor antagonist, and saclofen, a GABAB antagonist, were investigated on pulmonary arterial responses to kava kava (kava), pinacidil, an ATP-sensitive K+ channel activator, bradykinin, an inducer of nitric oxide synthase, 3-aminopropyl(methyl)phosphinic acid hydrochloride (SKF-97541), a GABAB receptor agonist, and muscimol, a GABAA receptor agonist. Lobar arterial perfusion pressure and systemic pressure were continuously monitored, electronically averaged, and recorded.

The effects of sufentanil in the feline pulmonary vascular bed.

The purpose of this prospective vehicle controlled study was to test the hypothesis that sufentanil induces a depressor response in the pulmonary vascular bed of the cat and identify the receptors involved in the mediation or modulation of these effects. In separate experiments, the effects of diphenydramine (histamine receptor blocker), glibenclamide (ATP-sensitive K+ channel blocker), L-N5-(1-Iminoethyl) ornithine hydrochloride (L-NIO) (nitric oxide synthase inhibitor), nimesulide (selective cyclooxygenase (COX)-2 inhibitor), and naloxone (opiate receptor antagonist) were investigated on pulmonary arterial responses to sufentanil and other agonists in the feline pulmonary vascular bed. The lobar arterial perfusion pressures were continuously monitored, electronically averaged, and recorded.

Influence of ephedrine and the role of alpha subtype adrenoreceptors in the vascular bed of the cat lung.

In a university research laboratory and in separate experiments, the effects of phentolamine, the alpha-adrenergic antagonist; prazosin, an alpha1-adrenoceptor antagonist; 5-methyl-urapidil, the selective alpha1A-subtype adrenoceptor antagonist; chloroethylclonidine, an alpha1B- and alpha1D-subtype adrenoceptor antagonist; and BMY 7378, a selective alpha1D-subtype adrenoceptor antagonist were analyzed in an attempt to identify any significant effect on pulmonary arterial responses to ephedrine and other agonist agents in the pulmonary vascular bed of the cat. Under constant flow conditions, lobar arterial perfusion pressure and systemic pressure were continuously monitored, electronically averaged, and permanently recorded. In the isolated left lower lobe of the pulmonary feline vascular bed, ephedrine induced a dose-dependent vasoconstrictor response that was not significantly altered following administration of 5-methyl-urapidil.

An analysis of remifentanil in the pulmonary vascular bed of the cat.

In this investigation we sought to identify the role of remifentanil in the feline pulmonary vascular bed. Using adult mongrel cats in separate experiments, the effects of glibenclamide (adenosine triphosphate-sensitive K+ channel blocker), diphenhydramine (histamine H(1)-receptor antagonist), L-N5-(1-Iminoethyl) ornithine hydrochloride (nitric oxide synthase inhibitor), and naloxone (opioid receptor antagonist) were investigated in pulmonary arterial responses to remifentanil (opioid agonist), pinacidil (adenosine triphosphate-sensitive K+ channel activator), and bradykinin (nitric oxide synthase inducer). Under increased tone conditions in the isolated left lower lobe vascular bed of the cat, remifentanil induced a dose-dependent vasodepressor response that was not significantly altered after administration of glibenclamide and L-N5-(1-Iminoethyl) ornithine hydrochloride.

Influence of TMB-8 and thapsigargin on vasoconstrictor responses in the pulmonary vascular bed of the cat.

The effects of 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), a protein kinase C (PKC) inhibitor, and thapsigargin, a CaATPase inhibitor, on pressor responses were studied in the pulmonary vascular bed of the intact-chest anesthetized cat. Under conditions of constant lobar blood flow in the cat, injections of the angiotensin peptides (ANG II), norepinephrine (NE), serotonin (5-HT), Bay K 8644, and the thromboxane A2 mimic U46619 into the lobar arterial perfusion circuit caused dose-related increases in lobar arterial pressure and responses were reproducible with respect to time. Intravenous infusion of TMB-8 at 1.

Analysis of responses to St. John's Wort in the feline pulmonary vascular bed.

Objective: To test the hypothesis that St. John's wort induces a depressor response in the feline pulmonary vascular bed and identify the pathways involved in the mediation or modulation of these effects.

Design: Prospective vehicle controlled study.

Effects of norepinephrine on alpha-subtype receptors in the feline pulmonary vascular bed.

Objective: To test the hypothesis that norepinephrine induces a pressor response in the pulmonary vascular bed of the cat and identify the alpha-(1)adrenoceptor subtypes involved in the mediation or modulation of these effects.

Design: Prospective vehicle controlled study.

Setting: University research laboratory.

Analysis of gamma-aminobutyric acid-mediated responses in the pulmonary vascular bed of the cat.

In this investigation, we sought to identify the role of gamma-aminobutyric acid (GABA)(A) and GABA(B) receptors in the feline pulmonary vascular bed. Using adult mongrel cats and in separate experiments, we investigated the effects of l-N(5)-(1-iminoethyl) ornithine hydrochloride (l-NIO) (a nitric oxide synthase inhibitor), glibenclamide (an adenosine triphosphate (ATP)-sensitive K(+) channel blocker), meclofenamate (a nonselective cyclooxygenase inhibitor), bicuculline (a GABA(A) receptor antagonist), and saclofen (a GABA(B) receptor antagonist) on pulmonary arterial responses to pinacidil (an ATP-sensitive K(+) channel activator), bradykinin (a nitric oxide synthase inducer), muscimol (a GABA(A) receptor agonist), and 3-aminopropyl(methyl)phosphinic acid, hydrochloride (SKF-97541; a GABA(B) receptor agonist). Under increased tone conditions in the isolated left lower lobe vascular bed of the cat, muscimol induced a dose-dependent vasodepressor response that was not significantly altered after the administration of l-NIO, glibenclamide, meclofenamate, and saclofen.

The effects of load on systolic mitral annular velocity by tissue Doppler imaging.

Tissue Doppler Imaging (TDI) provides information on systolic function through its systolic mitral annulus velocity wave (Sm), reflecting the peak velocity of shortening of the myocardial fibers oriented in the longitudinal direction. In this study, we evaluated the effect of load changes on Sm. Forty-two cardiac surgical patients with left ventricular ejection fraction >60% were consecutively evaluated.

Analysis of responses to valerian root extract in the feline pulmonary vascular bed.

Objectives: This study was undertaken to investigate pulmonary vascular response to valerian (Valeriana officinalis) in the feline pulmonary vasculature under constant flow conditions.

Design: In separate experiments, the effects of NG-L-nitro-L-arginine methyl ester (L-NIO), a nitric oxide synthase inhibitor, glibenclamide, an adenosine triphosphate (ATP)-sensitive potassium (K+) channel blocker, meclofenamate, a nonselective cyclooxygenase (COX) inhibitor, bicuculline, a GABA(A) receptor antagonist, and saclofen, a GABA(B) antagonist, were investigated on pulmonary arterial responses to various agonists in the feline pulmonary vascular bed. These agonists included valerian, muscimol, a GABA(A) agonist, SKF-97541 a GABA(B) agonist, acetylcholine (ACh), and bradykinin, both inducers of nitric oxide synthase, arachidonic acid, a COX substrate, and pinacidil, an ATP-sensitive K+ channel activator, during increased tone conditions induced by the thromboxane A2 mimic, U46619.

Pulmonary vascular responses to ma huang extract.

Objective: To test the hypothesis that ma huang induces a pressor response in the pulmonary vascular bed of the cat by activating alpha(1)-adrenergic receptors

Design: Prospective vehicle-controlled study.

Setting: Research laboratory at Texas Tech University School of Medicine, Lubbock, TX.

Subjects: Intact chest preparation; adult mongrel cats.

An analysis of responses to levosimendan in the pulmonary vascular bed of the cat.

Unlabelled: Calcium-sensitizing drugs, such as levosimendan, are a novel class of drug therapy for heart failure. We investigated the hypothesis that levosimendan is a pulmonary vasodepressor mediated through inhibition of phosphodiesterase, adenosine triphosphate (ATP)-dependent potassium channels, or both. We investigated responses to the calcium sensitizer levosimendan in the pulmonary vascular bed of the cat under conditions of controlled pulmonary blood flow and constant left atrial pressure when lobar arterial pressure was increased to a high steady level with the thromboxane A(2) analog U-46619.

Inhibitory Effects of LY301875 on Responses to Angiotensin Peptides in Pulmonary Vascular Bed of the Cat.

The effects of the nonpeptide angiotensin receptor antagonist LY301875 on responses to angiotensin II, angiotensin III, and angiotensin IV were investigated in the pulmonary vascular bed of the intact cat chest. Under conditions of controlled blood flow, injections of the angiotensin peptides into the perfused lobar artery caused dose-related increases in lobar arterial pressure, and LY301875 decreased pressor responses to angiotensin II, angiotensin III, and angiotensin IV. The duration of the blockade was related to the dose of the antagonist, and LY301875 had no significant effect on pressor responses to U-46619, norepinephrine, serotonin or BAY K 8644.