Beta2-mediated hypotension and myocardial injury

1982 ◽  
Vol 60 (8) ◽  
pp. 1144-1148 ◽  
Author(s):  
Alison Brown-Lukacsko ◽  
Peter Lukacsko
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Elevated Serum ◽  
Blocking Agent ◽  
Arterial Blood ◽  
Ganglionic Blocking ◽  
Elevated Heart Rate ◽  
Stimulation Of

This study was designed to investigate the importance of beta2 receptor mediated hypotension in the pathogenesis of myocardial injury. The effect of isoproterenol and the putative beta2 agonist albuterol on arterial blood pressure, heart rate, the myocardial content of ATP and cAMP, and the serum content of MB-CPK was examined in conscious rats. Isoproterenol (5.25 mg/kg, s.c.) and albuterol (45 mg/kg, s.c.) lowered blood pressure and elevated heart rate to the same extent. Also, both agonists increased the myocardial content of cAMP, decreased the myocardial content of ATP, and elevated serum MB-CPK. The beta1 antagonist practolol, but not the ganglionic blocking agent chlorisondamine, attenuated the elevation in heart rate to albuterol without reducing its effect on blood pressure. Practolol, but not chlorisondamine, abolished the effects of albuterol on cAMP, ATP, and MB-CPK. These data suggest that the myocardial injury which is associated with an increased heart rate and changes in cAMP, ATP, and MB-CPK following the administration of albuterol is not the result of beta2-mediated hypotension, but is due to stimulation of myocardial beta1 receptors.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Primary vagally mediated decelerations in heart rate during tonic rapid eye movement sleep in cats

1998 ◽  
Vol 274 (4) ◽  
pp. R1136-R1141 ◽  
Author(s):  
Richard L. Verrier ◽  
T. Rern Lau ◽  
Umesha Wallooppillai ◽  
James Quattrochi ◽  
Bruce D. Nearing ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Rem Sleep ◽  
Blocking Agent ◽  
Rapid Eye Movement ◽  
Arterial Blood ◽  
State Dependent ◽  
Hippocampal Theta

Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg iv) and the β-adrenergic blocking agent atenolol (0.3 mg/kg iv) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.

Cerebral blood flow and behavior during brain stimulation in the goat

1977 ◽  
Vol 232 (5) ◽  
pp. H495-H499
Author(s):  
M. Manrique ◽  
E. Alborch ◽  
J. M. Delgado
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Maxillary Artery ◽  
Internal Maxillary Artery ◽  
Arterial Blood ◽  
And Behavior ◽  
Stimulation Of

Cerebral blood flow, heart rate, arterial blood pressure, and behavior were studied in conscious goats during electrical stimulation of the diencephalon and mesencephalon. Stimulation of the subthalamic area produced a considerable increase in ipsilateral cerebral blood flow and heart rate, accompanied by either a small or a large increase in systemic arterial blood pressure. Cardiovascular effects were associated with changes in alertness. The increase in cerebral blood flow was partially abolished by previous administration of atropine directly into the internal maxillary artery. Stimulation of the mesencephalic reticular formation caused a marked increase in blood pressure with no change or with some decrease in cerebral blood flow. After administration of phentolamine into the internal maxillary artery, stimulation produced increase in cerebral blood flow. The behavioral response consisted of restlessness and attempted flight. These results suggest the existence of cholinergic vasodilator and adrenergic vasoconstrictor pathways to cerebral blood vessels that may be stimulated electrically.

scholarly journals Electrical stimulation of the midbrain increases heart rate and arterial blood pressure in awake humans

2002 ◽  
Vol 539 (2) ◽  
pp. 615-621 ◽  
Author(s):  
Judith M. Thornton ◽  
Tipu Aziz ◽  
David Schlugman ◽  
David J. Paterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Stimulation Of

scholarly journals Calabadion

2013 ◽  
Vol 119 (2) ◽  
pp. 317-325 ◽  
Author(s):  
Ulrike Hoffmann ◽  
Martina Grosse-Sundrup ◽  
Katharina Eikermann-Haerter ◽  
Sebastina Zaremba ◽  
Cenk Ayata ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Train Of Four ◽  
Complete Reversal ◽  
Blood Gas Parameters

Abstract Introduction: To evaluate whether calabadion 1, an acyclic member of the Cucurbit[n]uril family of molecular containers, reverses benzylisoquinoline and steroidal neuromuscular-blocking agent effects. Methods: A total of 60 rats were anesthetized, tracheotomized, and instrumented with IV and arterial catheters. Rocuronium (3.5 mg/kg) or cisatracurium (0.6 mg/kg) was administered and neuromuscular transmission quantified by acceleromyography. Calabadion 1 at 30, 60, and 90 mg/kg (for rocuronium) or 90, 120, and 150 mg/kg (for cisatracurium), or neostigmine/glycopyrrolate at 0.06/0.012 mg/kg were administered at maximum twitch depression, and renal calabadion 1 elimination was determined by using a 1H NMR assay. The authors also measured heart rate, arterial blood gas parameters, and arterial blood pressure. Results: After the administration of rocuronium, resumption of spontaneous breathing and recovery of train-of-four ratio to 0.9 were accelerated from 12.3 ± 1.1 and 16.2 ± 3.3 min with placebo to 4.6 ± 1.8 min with neostigmine/glycopyrrolate to 15 ± 8 and 84 ± 33 s with calabadion 1 (90 mg/kg), respectively. After the administration of cisatracurium, recovery of breathing and train-of-four ratio of 0.9 were accelerated from 8.7 ± 2.8 and 9.9 ± 1.7 min with placebo to 2.8 ± 0.8 and 7.6 ± 2.1 min with neostigmine/glycopyrrolate to 47 ± 13 and 87 ± 16 s with calabadion 1 (150 mg/kg), respectively. Calabadion 1 did not affect heart rate, mean arterial blood pressure, pH, carbon dioxide pressure, and oxygen tension. More than 90% of the IV administered calabadion 1 appeared in the urine within 1 h. Conclusion: Calabadion 1 is a new drug for rapid and complete reversal of the effects of steroidal and benzylisoquinoline neuromuscular-blocking agents.

Compression Stocking Length Effects on Arterial Blood Pressure and Heart Rate Following Head-Up Tilt in Healthy Volunteers

2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Arterial Blood Pressure ◽  
Compression Stocking ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Length Effects

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

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