1
40
8
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
595–599
Volume
1
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Aspirin attenuation of alcohol-induced flushing and intoxication in Oriental and Occidental subjects.
Publisher
An entity responsible for making the resource available
Alcohol and alcoholism (Oxford, Oxfordshire). Supplement
Date
A point or period of time associated with an event in the lifecycle of the resource
1987
1905-6
Subject
The topic of the resource
Humans; Blood Pressure/drug effects; European Continental Ancestry Group; Heart Rate/drug effects; Asian Continental Ancestry Group; *Alcoholic Intoxication; Aspirin/*pharmacology; Ethanol/*antagonists & inhibitors/pharmacology; Flushing/*chemically induced; Skin Temperature/drug effects
Creator
An entity primarily responsible for making the resource
Truitt E B Jr; Gaynor C R; Mehl D L
Description
An account of the resource
Aspirin (ASA) was tested in a group of 8 Oriental and 3 Occidental subjects who were shown in a previous study to respond to small doses of ethanol (0.06-0.25 g/kg) with facial flushing. They were compared to a similar group of 11 non-flushing Occidental subjects following a larger ethanol dose (0.37 g/kg) to determine if similar effects could be produced in less sensitive individuals. Control tests of blood ethanol and acetaldehyde (AcH) levels (calculated from breath), facial and neck skin temperatures, body sway (Romberg test), blood pressure, heart rate and 10 Subjective High Assessment Scales (SHAS-Judd, 1977) were conducted before and at 15, 30, 60 and 90 minutes after drinking ethanol as vodka in orange juice. The tests were repeated one week later one hour after receiving 0.64 gm of ASA orally. ASA produced slight changes in the early absorption of ethanol and small decreases in AcH levels in the flushing and non-flushing groups. Facial flushing was markedly reduced in the flushing group, but was slightly increased in the non-flushing Occidentals. Body sway was reduced by ASA in both groups. An alcohol-induced increase in heart rate in the flushing group was reduced with no change in blood pressure. SHAS subjective parameters were widely variable, but indicated that ASA produced reduced sleepiness and earlier relaxation in the flushing group. It is concluded that ASA can block alcohol-induced facial flushing in sensitive subjects and also reduces body sway in the Romberg test and alters some subjective feelings of alcohol intoxication.
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Alcoholic Intoxication
1987
Alcohol and alcoholism (Oxford, Oxfordshire). Supplement
Asian Continental Ancestry Group
Aspirin/*pharmacology
Blood Pressure/drug effects
Ethanol/*antagonists & inhibitors/pharmacology
European Continental Ancestry Group
Flushing/*chemically induced
Gaynor C R
Heart Rate/drug effects
Humans
Mehl D L
Skin Temperature/drug effects
Truitt E B Jr
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Pages
267–273
Issue
2
Volume
24
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Methamphetamine-gonadal steroid hormonal interactions: effects upon acute toxicity and striatal dopamine concentrations.
Publisher
An entity responsible for making the resource available
Neurotoxicology and teratology
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-04
Subject
The topic of the resource
Female; Male; Animals; Mice; Sex Factors; Body Weight/drug effects; Organ Size/drug effects; Dopamine/*metabolism; Body Temperature/drug effects; Methamphetamine/*toxicity; Corpus Striatum/*metabolism; Orchiectomy; Ovariectomy; Drug Interactions; Estrogens/pharmacology/*physiology; Heart Rate/drug effects; Heart Ventricles/metabolism; Norepinephrine/metabolism; Pituitary Gland/anatomy & histology; Testosterone/pharmacology/*physiology; Inbred Strains
Creator
An entity primarily responsible for making the resource
Dluzen Dean E; Anderson Linda I; Pilati Charles F
Description
An account of the resource
Methamphetamine (MA)-related deaths and nigrostriatal dopaminergic (NSDA) neurotoxicity are greater in males. The exact basis for this gender difference is not known, but data, which show that estrogen (E) can function as a protectant of both the cardiovascular and NSDA systems, suggest an important role for gonadal steroids in modulating toxicity to this psychostimulant. In the present report, we examined the effects of treatment with the gonadal steroid hormones E and testosterone (T) upon MA-induced toxicity within intact and castrated female and male CD-1 mice. Treatment of intact males with E produced a severe acute toxicity to MA, with only 41% (7/17) males surviving at 24-h post-MA. This incidence of mortality was significantly different from that of nonhormonally treated mice receiving an identical regimen of MA [94% survival (16/17)]. None of the other treatment groups showed mortality rates, which differed significantly from the nonhormonally treated mice. Striatal dopamine (DA) concentrations of E-treated female mice (intact or castrated) were significantly greater than that of the nonhormonally treated mice, which failed to differ statistically among each other. In an attempt to understand some of the bases for the mortality rates in
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2002
Anderson Linda I
Animals
Body Temperature/drug effects
Body Weight/drug effects
Corpus Striatum/*metabolism
Dluzen Dean E
Dopamine/*metabolism
Drug Interactions
Estrogens/pharmacology/*physiology
Female
Heart Rate/drug effects
Heart Ventricles/metabolism
Inbred Strains
Male
Methamphetamine/*toxicity
Mice
Neurotoxicology and teratology
Norepinephrine/metabolism
Orchiectomy
Organ Size/drug effects
Ovariectomy
Pilati Charles F
Pituitary Gland/anatomy & histology
Sex Factors
Testosterone/pharmacology/*physiology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/01.hyp.26.4.676" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/01.hyp.26.4.676</a>
Pages
676–683
Issue
4
Volume
26
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Acute exercise attenuates cardiac autonomic regulation in hypertensive rats.
Publisher
An entity responsible for making the resource available
Hypertension (Dallas, Tex. : 1979)
Date
A point or period of time associated with an event in the lifecycle of the resource
1995
1995-10
Subject
The topic of the resource
*Physical Exertion; Adrenergic Agents/pharmacology; Animals; Autonomic Nervous System/*physiopathology; Blood Pressure/drug effects; Cholinergic Agents/pharmacology; Heart Conduction System/*physiopathology; Heart Rate/drug effects; Hypertension/*physiopathology; Inbred SHR; Male; Nitroglycerin/pharmacology; Parasympathetic Nervous System/physiopathology; Phenylephrine/pharmacology; Rats; Sympathetic Nervous System/physiopathology; Time Factors
Creator
An entity primarily responsible for making the resource
Chen Y; Chandler M P; DiCarlo S E
Description
An account of the resource
Dynamic exercise may be used as a safe, therapeutic approach to reduce sympathetic nerve activity at rest and thus may be beneficial for individuals with hypertension. Therefore, we tested the hypothesis that a single bout of mild to moderate dynamic exercise would decrease cardiac sympathetic tonus at rest. We designed two experimental protocols to test this hypothesis in male spontaneously hypertensive rats. In protocol 1 (n = 6) cardiac sympathetic tonus and parasympathetic tonus were determined before and after a single bout of dynamic exercise. We developed protocol 2 (n = 5) to determine the component of the autonomic nervous system responsible for the postexercise reduction in heart rate. Rats were instrumented with catheters inserted into the descending aorta for measurements of arterial pressure, mean arterial pressure, and heart rate and into the jugular vein for infusion of drugs. A single bout of mild to moderate dynamic treadmill exercise (12 m/min, 10% grade for 42 +/- 1 minutes, representing approximately 74% to 79% of maximal heart rate) resulted in a postexercise reduction in mean arterial pressure (163 +/- 7 to 149 +/- 5 mm Hg; P \textless .05). Associated with the postexercise hypotension was a reduction in sympathetic and parasympathetic tonus (47 +/- 12% and 71 +/- 12%, respectively). The reduction in heart rate during the early recovery phase was due to a withdrawal of sympathetic tonus, because beta 1-adrenergic receptor blockade significantly enhanced the postexercise reduction in heart rate, and muscarinic-cholinergic receptor blockade did not affect the postexercise decrease in heart rate until 20 minutes after exercise.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/01.hyp.26.4.676" target="_blank" rel="noreferrer noopener">10.1161/01.hyp.26.4.676</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Physical Exertion
1995
Adrenergic Agents/pharmacology
Animals
Autonomic Nervous System/*physiopathology
Blood Pressure/drug effects
Chandler M P
Chen Y
Cholinergic Agents/pharmacology
DiCarlo S E
Heart Conduction System/*physiopathology
Heart Rate/drug effects
Hypertension (Dallas, Tex. : 1979)
Hypertension/*physiopathology
Inbred SHR
Male
Nitroglycerin/pharmacology
Parasympathetic Nervous System/physiopathology
Phenylephrine/pharmacology
Rats
Sympathetic Nervous System/physiopathology
Time Factors
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/jappl.1991.71.3.1166" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jappl.1991.71.3.1166</a>
Pages
1166–1170
Issue
3
Volume
71
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Hemodynamic basis for cocaine-induced pulmonary edema in dogs.
Publisher
An entity responsible for making the resource available
Journal of applied physiology (Bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
1991
1991-09
Subject
The topic of the resource
Animals; Blood Pressure/drug effects; Cardiac Output/drug effects; Cocaine/*toxicity; Coronary Circulation/drug effects; Dogs; Female; Heart Rate/drug effects; Hemodynamics/*drug effects; Male; Pulmonary Circulation/drug effects; Pulmonary Edema/chemically induced/*physiopathology; Stroke Volume/drug effects; Vascular Resistance/drug effects
Creator
An entity primarily responsible for making the resource
Lang S A; Maron M B
Description
An account of the resource
We tested the hypothesis that cocaine-induced impairment of left ventricular function results in cardiogenic pulmonary edema. Mongrel dogs, anesthetized with alpha-chloralose, were injected with two doses of cocaine (5 mg/kg iv) 27 min apart. Cocaine produced transient decreases in aortic and left ventricular systolic pressures that were followed by increases exceeding control. As aortic pressure recovered, left ventricular end-diastolic, left atrial (Pla), pulmonary arterial (Ppa), and central venous pressures rose. Cardiac output and stroke volume were reduced when measured 4-5 min after cocaine administration. Peak Ppa and Pla were 31 +/- 5 (SE) mmHg (range 17-51 mmHg) and 26 +/- 5 mmHg (range 12-47 mmHg), respectively. Increases in extravascular lung water content (4.10 to 6.24 g H2O/g dry lung wt) developed in four animals in which Pla exceeded 30 mmHg. Analysis of left ventricular function curves revealed that cocaine depressed the inotropic state of the left ventricle. Cocaine-induced changes in hemodynamics spontaneously recovered and could be elicited again by the second dose of the drug. Our results show that cocaine-induced pulmonary hypertension, associated with decreased left ventricular function, produces pulmonary edema if pulmonary vascular pressures rise sufficiently.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.1991.71.3.1166" target="_blank" rel="noreferrer noopener">10.1152/jappl.1991.71.3.1166</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1991
Animals
Blood Pressure/drug effects
Cardiac Output/drug effects
Cocaine/*toxicity
Coronary Circulation/drug effects
Dogs
Female
Heart Rate/drug effects
Hemodynamics/*drug effects
Journal of applied physiology (Bethesda, Md. : 1985)
Lang S A
Male
Maron M B
Pulmonary Circulation/drug effects
Pulmonary Edema/chemically induced/*physiopathology
Stroke Volume/drug effects
Vascular Resistance/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.1993.265.4.H1184" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1993.265.4.H1184</a>
Pages
H1184–1188
Issue
4
Volume
265
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine.
Publisher
An entity responsible for making the resource available
The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
1993-10
Subject
The topic of the resource
*Physical Exertion; Animals; Arginine/analogs & derivatives/pharmacology; Blood Flow Velocity; Blood Pressure/drug effects; Blood Vessels/*drug effects; Dose-Response Relationship; Drug; Female; Heart Rate/drug effects; Iliac Artery/drug effects/physiology; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide/antagonists & inhibitors/*physiology; Phenylephrine/*pharmacology; Rats; Sprague-Dawley; Time Factors; Vasoconstriction/drug effects/physiology
Creator
An entity primarily responsible for making the resource
Patil R D; DiCarlo S E; Collins H L
Description
An account of the resource
The influence of the release of endothelium-derived nitric oxide (NO) on the vasoconstrictor response to phenylephrine (PE) was evaluated before and after a single bout of dynamic exercise. Each rat ran on a motor-driven treadmill at
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1993.265.4.H1184" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1993.265.4.H1184</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Physical Exertion
1993
Animals
Arginine/analogs & derivatives/pharmacology
Blood Flow Velocity
Blood Pressure/drug effects
Blood Vessels/*drug effects
Collins H L
DiCarlo S E
Dose-Response Relationship
Drug
Female
Heart Rate/drug effects
Iliac Artery/drug effects/physiology
Male
NG-Nitroarginine Methyl Ester
Nitric Oxide/antagonists & inhibitors/*physiology
Patil R D
Phenylephrine/*pharmacology
Rats
Sprague-Dawley
The American journal of physiology
Time Factors
Vasoconstriction/drug effects/physiology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.1993.265.4.H1179" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1993.265.4.H1179</a>
Pages
H1179–1183
Issue
4
Volume
265
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Attenuation of postexertional hypotension by cardiac afferent blockade.
Publisher
An entity responsible for making the resource available
The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
1993-10
Subject
The topic of the resource
*Heart Arrest; *Physical Exertion; Afferent Pathways/physiology; Animals; Blood Pressure/drug effects; Efferent Pathways/physiology; Heart Rate/drug effects; Hypotension/*physiopathology; Inbred SHR; Induced; Pressoreceptors/drug effects; Procainamide/pharmacology; Rats; Reference Values
Creator
An entity primarily responsible for making the resource
Collins H L; DiCarlo S E
Description
An account of the resource
Naloxone eliminates postexertional hypotension (PEH) in human and animal models. The effect of naloxone on sympathetic activity during hemorrhage and generation of arterial baroreflex function curves can be stimulated by blockade of cardiac afferent receptors. We tested the hypothesis that cardiac afferent blockade would eliminate PEH in eight spontaneously hypertensive rats (SHR). Rats were instrumented with a Silastic-tipped catheter inserted into the pericardial space. Four weeks later, a Teflon catheter was placed in the descending aorta via the left common carotid artery for measurement of mean arterial pressure (MAP) and heart rate (HR). MAP and HR were examined before (preexercise) and after (postexercise) a single bout of dynamic treadmill exercise (9-12.0 m/min, 10-18% grade for 30-40 min) under three experimental conditions: control, cardiac efferent blockade, and combined cardiac efferent and afferent blockade. MAP significantly decreased (29 +/- 5 and 25.6 +/- 4 mmHg) in the control and cardiac efferent blockade conditions after exercise. However, when cardiac afferents were blocked, the hypotensive response to mild dynamic exercise was significantly attenuated (-6 +/- 3 mmHg). Thus blockade of cardiac afferents eliminated PEH in the SHR. These data suggest that inhibitory influence of cardiac afferents on the circulation may be enhanced after exercise.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1993.265.4.H1179" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1993.265.4.H1179</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Heart Arrest
*Physical Exertion
1993
Afferent Pathways/physiology
Animals
Blood Pressure/drug effects
Collins H L
DiCarlo S E
Efferent Pathways/physiology
Heart Rate/drug effects
Hypotension/*physiopathology
Inbred SHR
Induced
Pressoreceptors/drug effects
Procainamide/pharmacology
Rats
Reference Values
The American journal of physiology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.1992.263.3.H784" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1992.263.3.H784</a>
Pages
H784–791
Issue
3
Volume
263
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Factors involved in left ventricular dysfunction after massive sympathetic activation.
Publisher
An entity responsible for making the resource available
The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1992
1992-09
Subject
The topic of the resource
*Ventricular Function; Animals; Blood Pressure/drug effects/physiology; Catecholamines/physiology; Female; Heart Conduction System/*physiology; Heart Diseases/*physiopathology; Heart Rate/drug effects; In Vitro Techniques; Left; Male; Rabbits; Sympathetic Nervous System/drug effects/*physiology; Veratrine/pharmacology
Creator
An entity primarily responsible for making the resource
Pilati C F; Bosso F J; Maron M B
Description
An account of the resource
We sought to determine whether catecholamines are responsible for the depressed left ventricular (LV) function that follows massive sympathetic nervous system (SNS) activation and whether the additional myocardial energy demands of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1992.263.3.H784" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1992.263.3.H784</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Ventricular Function
1992
Animals
Blood Pressure/drug effects/physiology
Bosso F J
Catecholamines/physiology
Female
Heart Conduction System/*physiology
Heart Diseases/*physiopathology
Heart Rate/drug effects
In Vitro Techniques
Left
Male
Maron M B
Pilati C F
Rabbits
Sympathetic Nervous System/drug effects/*physiology
The American journal of physiology
Veratrine/pharmacology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpendo.1989.256.3.E345" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpendo.1989.256.3.E345</a>
Pages
E345–351
Issue
3
Volume
256
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Oxygen consumption after massive sympathetic nervous system discharge.
Publisher
An entity responsible for making the resource available
The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1989
1989-03
Subject
The topic of the resource
*Blood Pressure; *Oxygen Consumption/drug effects; Adrenal Glands/physiology; Animals; Cardiac Output/drug effects; Dogs; Epinephrine/blood; Female; Heart Rate/drug effects; Male; Norepinephrine/blood; Pulmonary Artery/drug effects/physiology/physiopathology; Pulmonary Edema/physiopathology; Reference Values; Sympathetic Nervous System/*physiology/physiopathology; Veratrine/pharmacology
Creator
An entity primarily responsible for making the resource
Lang S A; Maron M B; Signs S A
Description
An account of the resource
We evaluated the possibility that massive, sympathetic nervous system (SNS) activation [as may precede the development of neurogenic pulmonary edema (NPE)] increases O2 demand. O2 consumption (VO2) and plasma concentrations of the calorigenic agents, epinephrine (EPI) and norepinephrine (NE) were measured in alpha-chloralose-anesthetized dogs under control conditions and for 3 h after the administration of either 1) intracisternal (ic) veratrine to activate the SNS, 2) intravenous (iv) veratrine, 3) ic saline, or 4) ic veratrine, after clamping the adrenal blood vessels. VO2 increased 31.7 +/- 3.6% (SE), and EPI and NE increased to, respectively, 30,853 +/- 8,347 and 8,176 +/- 2,104 pg/ml in the ic veratrine group. No increases in VO2 and EPI and attenuated increases in NE were observed in the ic veratrine animals with clamped adrenals. No significant increases in VO2 or catecholamine concentrations were observed after ic saline or iv veratrine administration. These data suggest that the elevated VO2 may have been mediated by adrenal catecholamines and that an increased metabolic rate may complicate the ability of patients with severe NPE to balance O2 supply with demand.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpendo.1989.256.3.E345" target="_blank" rel="noreferrer noopener">10.1152/ajpendo.1989.256.3.E345</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Blood Pressure
*Oxygen Consumption/drug effects
1989
Adrenal Glands/physiology
Animals
Cardiac Output/drug effects
Dogs
Epinephrine/blood
Female
Heart Rate/drug effects
Lang S A
Male
Maron M B
Norepinephrine/blood
Pulmonary Artery/drug effects/physiology/physiopathology
Pulmonary Edema/physiopathology
Reference Values
Signs S A
Sympathetic Nervous System/*physiology/physiopathology
The American journal of physiology
Veratrine/pharmacology