Reduction of Plasma sCD40L and Stimulated MIP-1-Alpha Production by in vivo Beta-Adrenergic Stimulation

2007 ◽  
Vol 14 (5) ◽  
pp. 266-271 ◽  
Author(s):  
Kate M. Edwards ◽  
Suzi Hong ◽  
Barbara G. Woods ◽  
Paul J. Mills
Keyword(s):  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Alpha Production

Inotropic sensitivity to beta-adrenergic stimulation in early sepsis

1988 ◽  
Vol 255 (4) ◽  
pp. H699-H703 ◽  
Author(s):  
L. W. Smith ◽  
K. H. McDonough
Keyword(s):  
Contractile Function ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Maximal Increase ◽  
Beta Adrenergic ◽  
Arterial Blood ◽  
Myocardial Contractile ◽  
Early Sepsis

In early sepsis, maintenance of in vivo cardiovascular performance is at least partly dependent on sympathetic support to hearts with intrinsic contractile defects. Yet prolonged sympathetic stimulation, as occurs in sepsis, would be expected to alter the heart's ability to respond to this stimulation. We have investigated myocardial inotropic sensitivity to beta-adrenergic stimulation in a model of sepsis in which animals, at the time studied, exhibited bacteremia, normal arterial blood pressure and cardiac output, elevated heart rate, and elevated plasma catecholamines. Intrinsic myocardial contractile function, as assessed by the maximal rate of left ventricular pressure development (LV dP/dtmax) in an isovolumically contracting heart preparation, was significantly depressed in septic animals. To determine whether hearts from septic animals could respond normally to beta-adrenergic stimulation, we studied inotropic response to a bolus of isoproterenol in these isolated hearts. With maximal isoproterenol stimulation, hearts from septic animals were able to attain the same dP/dtmax as were hearts from control animals. With lower levels of isoproterenol, there was also no difference in inotropic indexes between the two groups when response was expressed as a percent of the maximal increase in dP/dtmax achieved with isoproterenol. These results suggest that in early sepsis, despite intrinsic myocardial contractile dysfunction, the ability of the heart to modulate its inotropic state in response in beta-adrenergic stimulation is intact.

scholarly journals In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure

2013 ◽  
Vol 57 ◽  
pp. 47-58 ◽  
Author(s):  
Anuradha Guggilam ◽  
Kirk R. Hutchinson ◽  
T. Aaron West ◽  
Amy P. Kelly ◽  
Maarten L. Galantowicz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Volume Overload ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Cardiac Responses

scholarly journals Energy metabolism in trout red cells: consequences of adrenergic stimulation in vivo and in vitro

1989 ◽  
Vol 143 (1) ◽  
pp. 133-147 ◽  
Author(s):  
R. A. Ferguson ◽  
B. L. Tufts ◽  
R. G. Boutilier
Keyword(s):  
Ph Regulation ◽  
Red Cells ◽  
Red Cell ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Extracellular Acidosis ◽  
Metabolic Functions ◽  
The Face

beta-Adrenergic stimulation of salmonid red cells results in a rapid decrease (within 5 min) in the nucleotide triphosphate:haemoglobin ratio (NTP:Hb), which is thereafter maintained at a constant level, presumably through increased ATP turnover via matched aerobic metabolism and energy-consuming processes. Addition of the beta-adrenergic agonist isoproterenol to rainbow trout red cells in vitro leads to a rise in intracellular pH (pHi), a corresponding decrease in extracellular pH (pHe) and an increase in red cell oxygen consumption (MO2). Moreover, the extent to which red cell pHi is maintained constant in the face of an acute extracellular acidosis in vitro or in vivo is proportional to the adrenergically stimulated increase in red cell MO2. In the absence of oxygen, these red cells remain capable of pH regulation, but cannot maintain NTP:Hb constant. As a result, membrane and metabolic functions become uncoupled in the stimulated deoxygenated cells.

Inhibition of nitric oxide synthase augments myocardial contractile responses to beta-adrenergic stimulation

1996 ◽  
Vol 271 (6) ◽  
pp. H2646-H2652 ◽  
Author(s):  
J. F. Keaney ◽  
J. M. Hare ◽  
J. L. Balligand ◽  
J. Loscalzo ◽  
T. W. Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Contractility ◽  
Adrenergic Stimulation ◽  
Maximum Increase ◽  
Beta Adrenergic ◽  
Before And After ◽  
Nos Inhibitor ◽  
Oxide Synthase

Recent in vitro evidence suggests a role for nitric oxide (NO) in the modulation of myocardial contractility. The specific role of NO in the control of cardiac function in vivo, however, remains unclear. We investigated the effect of NO synthase (NOS) inhibition on myocardial contractility in response to beta-adrenergic stimulation in autonomically blocked dogs. Intracoronary infusions of dobutamine (1-50 micrograms/min) and isoproterenol (0.1 and 0.5 microgram/min) were performed before and after the intracoronary administration of the specific NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Intracoronary dobutamine resulted in a dose-dependent increase in peak first derivative of pressure (dP/dtmax) to a maximum of 195 +/- 10% (P < 0.001). After inhibition of NOS with intracoronary L-NAME at rates of 0.1 and 1 mg/min, the response to dobutamine was significantly enhanced with dP/dtmax, increasing 276 +/- 17 and 317 +/- 26%, respectively (P < 0.001). Intracoronary isoproterenol resulted in a maximum increase in dP/dtmax of 116 +/- 15% (P < 0.001) that further increased to 154 +/- 17 and 157 +/- 18% after NOS inhibition with 0.1 and 1 mg/min L-NAME, respectively (both P < 0.002). L-NAME had no effect on baseline dP/dtmax but did produce a reduction in myocardial guanosine 3',5'-cyclic monophosphate content. These results suggest a role for NO in the control of myocardial contractility in response to beta-adrenergic stimulation in vivo.

Effect of beta-adrenergic stimulation on experimental canine anaphylaxis in vivo

1983 ◽  
Vol 71 (1) ◽  
pp. 62-70 ◽  
Author(s):  
T MJORNDAL ◽  
S CHESROWN ◽  
M FREY ◽  
B REED ◽  
S LAZARUS ◽  
...  
Keyword(s):  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Experimental Canine

A61. Ablation of cMyBP-C diminishes in vivo responsiveness to beta-adrenergic stimulation

2006 ◽  
Vol 40 (6) ◽  
pp. 873
Author(s):  
Daniel Fitzsimons ◽  
Stacey Brickson ◽  
Timothy Hacker ◽  
Mary Bister ◽  
Richard Moss
Keyword(s):  
Adrenergic Stimulation ◽  
Beta Adrenergic

scholarly journals EFFECTS OF CHRONIC IN VIVO β-ADRENERGIC STIMULATION ON RAT ADIPOCYTES

1987 ◽  
Vol 36 (3) ◽  
pp. 147-155
Author(s):  
TETSUYA IZAWA ◽  
TAKAO KOMABAYASHI ◽  
KAZUHIRO SUDA ◽  
EIZI KOSHIMIZU ◽  
MINORU TSUBOI
Keyword(s):  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Rat Adipocytes

Autonomic neural regulation of intact Purkinje system of dogs

1990 ◽  
Vol 258 (5) ◽  
pp. H1420-H1426 ◽  
Author(s):  
D. J. Wendt ◽  
J. B. Martins
Keyword(s):  
Nerve Stimulation ◽  
Refractory Period ◽  
Vagal Stimulation ◽  
Neural Regulation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Purkinje System ◽  
Phenylephrine Infusion ◽  
Adrenergic Activation

To characterize autonomic influences on the Purkinje system in vivo, we measured Purkinje relative refractory period (PRRP) in response to sympathetic (SNS) and vagal nerve stimulation (VNS). Effects of SNS on PRRP were primarily mediated via beta-adrenergic mechanisms because shortening of PRRP during SNS [from 215 +/- 7 (SE) to 202 +/- 8 ms, P less than 0.01] was entirely blocked by metoprolol (1 mg/kg). Vagal influences in the ambient state did not prolong PRRP, even when effective refractory period of adjacent muscle did prolong. When VNS was augmented with physostigmine, PRRP prolonged from 205 +/- 12 to 212 +/- 13 ms, P less than 0.05. Similar provocation of parasympathetic effects on PRRP occurred when VNS was performed during SNS; PRRP prolonged from 188 +/- 9 to 193 +/- 9 ms, P less than 0.05. Also, when alpha-adrenergic stimulation was produced by phenylephrine infusion (25 micrograms.kg-1.min-1) in the presence of metoprolol (1 mg/kg), which prolonged PRRP from 242 +/- 8 to 246 +/- 9 ms, P less than 0.05, the addition of VNS further prolonged PRRP from 246 +/- 9 to 253 +/- 9 ms, P less than 0.05. Thus some refractory period responses in the Purkinje system were similar to adjacent muscle, because beta-adrenergic activation shortened refractory period and vagal stimulation antagonized the shortening. Findings unique to Purkinje tissue were refractory period prolongation by vagal stimulation when facilitated by concurrent prolongation of refractory period during alpha-adrenergic stimulation.

Beta-adrenergic stimulation of renin expression in vivo

1997 ◽  
Vol 15 (12) ◽  
pp. 1471-1479 ◽  
Author(s):  
Stephan R. Holmer ◽  
Brigitte Kaissling ◽  
Kurt Putnik ◽  
Michael Pfeifer ◽  
Bernhard K. Krämer ◽  
...  
Keyword(s):  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Stimulation Of

Experimental canine anaphylaxis: cyclic nucleotides, histamine, and lung function

1979 ◽  
Vol 46 (5) ◽  
pp. 919-926 ◽  
Author(s):  
S. C. Lazarus ◽  
S. E. Chesrown ◽  
M. J. Frey ◽  
B. R. Reed ◽  
T. O. Mjorndal ◽  
...  
Keyword(s):  
Cyclic Nucleotides ◽  
Physiological Effects ◽  
Adrenergic Stimulation ◽  
Physiological Mechanisms ◽  
Beta Adrenergic ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Experimental Canine

We studied the effects of Ascaris suum antigen (iv) in 32 natively allergic, anesthetized dogs. After thoracotomy, bilateral cervical vagotomy, and propranolol, samples of peripheral lung frozen in situ were obtained for measurement of cyclic nucleotides and histamine. Following Ascaris, lung histamine decreased 20.4 +/- 3.7% (mean +/- SE), cAMP increased 391 +/- 122%, and cGMP increased 110 +/- 20% with increased plasma histamine and physiological changes of anaphylaxis. No significant changes occurred in 10 control dogs. Release of histamine, reflecting immunological degranulation of mast cells, correlated closely with the physiological effects of anaphylaxis. beta-Adrenergic stimulation with isoproterenol prevented these physiological effects of anaphylaxis in three dogs studied. Furthermore, the level of cAMP induced in lung tissue by beta-adrenergic stimulation in these dogs correlated with the degree of inhibition of immunologically induced histamine release. These results illustrate the suitability of this experimental preparation to study the biochemical and physiological mechanisms of anaphylaxis in vivo.

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