An Assessment of the Anti-Anginal Effect of Tolamolol, a New Beta-Blocking Agent

1975 ◽  
Vol 3 (6) ◽  
pp. 399-406 ◽  
Author(s):  
A Williams ◽  
M C Holt
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Side Effects ◽  
Open Study ◽  
Laboratory Tests ◽  
Statistical Significance ◽  
Blocking Agent ◽  
Anginal Attack ◽  
Routine Laboratory ◽  
Beta Blocking

The anti-anginal activity of a new beta-blocking agent, tolamolol, was investigated in an open study. Seventeen patients ( fourteen males, three females) from two centres were given tolamolol in doses varying from 150 mg to 800 mg daily for periods of between one and thirty-four weeks. Records were made of the number of attacks of angina and of the consumption of sublingual glyceryl trinitrate ( GTN). Blood pressure and heart rate were monitored together with possible side-effects and the results of routine laboratory tests. There was an over-all reduction in anginal attack rates and the number of GTN tablets used, although these did not reach statistical significance in the small numbers concerned. Heart rate and blood pressure were similarly reduced. Side-effects were of mild severity and were tolerated or disappeared with continued treatment.

A Multicentre Study Examining the Substitution of Trasidrex for the Free Combination of Slow-Trasicor and Navidrex-K

1979 ◽  
Vol 7 (6) ◽  
pp. 524-527 ◽  
Author(s):  
A F Ebbutt ◽  
R W Elsdon Dew
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
General Practice ◽  
Essential Hypertension ◽  
Side Effects ◽  
Open Study ◽  
Global Assessment ◽  
Pressure Control ◽  
Time Intervals ◽  
The Mean

A multicentre, open study of general practice patients with essential hypertension who were currently being treated with oxprenolol and cyclopenthiazide was undertaken in which the patients were transferred to Trasidrex for 12 weeks. Weight, blood pressure, heart rate and side-effects were assessed pre-trial and at 4-week intervals. A global assessment was also made at the same time intervals. The mean serum potassium remained virtually unchanged after 12 weeks treatment with Trasidrex. Blood pressure control was marginally improved during the study and it is thought possible that better patient compliance might explain this. Trasidrex was tolerated equally as well as the free combination.

Rapid cardiovascular effects of dexamethasone in rabbits with meconium-induced acute lung injury

2008 ◽  
Vol 86 (11) ◽  
pp. 804-814 ◽  
Author(s):  
Daniela Mokra ◽  
Ingrid Tonhajzerova ◽  
Juraj Mokry ◽  
Anna Drgova ◽  
Maria Petraskova ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Side Effects ◽  
Rabbit Model ◽  
Intratracheal Instillation ◽  
Cardiovascular Effects ◽  
Meconium Aspiration Syndrome ◽  
Cardiovascular Side Effects ◽  
Acute Side Effects ◽  
Systemic Glucocorticoids

Glucocorticoids may improve lung function in newborns with meconium aspiration syndrome (MAS), but information on the acute side effects of glucocorticoids in infants is limited. In this study using a rabbit model of MAS, we addressed the hypothesis that systemic administration of dexamethasone causes acute cardiovascular changes. Adult rabbits were treated with 2 intravenous doses of dexamethasone (0.5 mg/kg each) or saline at 0.5 h and 2.5 h after intratracheal instillation of human meconium or saline. Animals were oxygen-ventilated for 5 h after the first dose of treatment. Blood pressure, heart rate, and short-term heart rate variability (HRV) were analyzed during treatment, for 5 min immediately after each dose, and for the 5 h of the experiment. In the meconium-instilled animals, dexamethasone increased blood pressure, decreased heart rate, increased HRV parameters, and caused cardiac arrhythmia during and immediately after administration. In the saline-instilled animals, the effect of dexamethasone was inconsistent. In these animals, the acute effects of dexamethasone on blood pressure and cardiac rhythm were reversed after 30 min, whereas heart rate continued to decrease and HRV parameters continued to increase for 5 h after the first dose of dexamethasone. These effects were more pronounced in meconium-instilled animals. If systemic glucocorticoids are used in the treatment of MAS, cardiovascular side effects of glucocorticoids should be considered.

Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats

1991 ◽  
Vol 261 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Control ◽  
Area Postrema ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Blocking Agent ◽  
Adrenergic Blockade ◽  
Neural Pathways ◽  
Heart Rate Control

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

scholarly journals Fentanyl Pretreatment Modifies Anaesthetic Induction with Etomidate

1988 ◽  
Vol 16 (2) ◽  
pp. 171-176 ◽  
Author(s):  
R. J. Stockham ◽  
T. H. Stanley ◽  
N. L. Pace ◽  
S. Gillmor ◽  
F. Groen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Side Effects ◽  
Linear Regression ◽  
Anaesthetic Induction ◽  
Arterial Blood ◽  
Group I ◽  
Haemodynamic Changes ◽  
Induction Of Anaesthesia ◽  
Fentanyl Group

Haemodynamic changes and side-effects of induction of anaesthesia with etomidate were evaluated in 60 ASA Class I or II patients. The objective was to find an optimal pre-induction dose of fentanyl which eliminated haemodynamic changes and side-effects during induction and intubation without introducing other problems. Patients were randomly assigned to four groups according to the pretreatment dose of fentanyl (Group I= 2 ml normal saline; Group II= 100 μg of fentanyl; Group III= 250μg of fentanyl; Group IV = 500 μg of fentanyl) administered intravenously five minutes prior to induction of anaesthesia with etomidate, 0.3 mg/kg. There was an increasing incidence of apnoea (53, 87, 87 and 100% in Groups I-IV respectively) and a decreasing incidence of myoclonus (60, 33, 13 and 0% in Groups I-IV respectively) and injection pain (53, 13, 7 and 0% in Groups I-IV respectively), P< 0.002 chi-square test for linear trends, with increasing fentanyl dosage. The incidences of postoperative nausea and vomiting were similar in the four groups. There were also significant linear regression relationships (P< 0.01 ANOVA for linear regression) between increasing doses of fentanyl administered before etomidate and the prevention of increases in systolic blood pressure and heart rate during the induction-intubation sequence. The data demonstrate that increasing pre-induction doses of fentanyl are more effective at minimising side-effects and preventing increases in systolic arterial blood pressure and heart rate but also increase the incidence of apnoea during induction. The results suggest that 500 μg of fentanyl is an ideal pretreatment dose in fit patients prior to anaesthetic induction with etomidate.

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.

Naturally occurring hypertension in New World nonhuman primates: potential role of the perifornical hypothalamus

2007 ◽  
Vol 292 (2) ◽  
pp. R937-R945 ◽  
Author(s):  
Orville A. Smith ◽  
Cliff A. Astley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
New World ◽  
Critical Role ◽  
Cardiovascular Responses ◽  
Routine Laboratory ◽  
New World Primates ◽  
Naturally Occurring

Hypertension is a prominent underlying factor in the genesis of cardiovascular-related morbidity and mortality. A major impediment to the investigation into the causes of the disease is the paucity of naturally occurring animal models of the disease. There is evidence that some species of New World primates spontaneously become hypertensive. We used chronically implanted pressure transducers to assess normally occurring blood pressure and heart rate levels at rest and during routine laboratory procedures in a group of one of these New World primates ( Aotus sp.). Resting mean arterial pressure ranged from 72 to 130 mmHg. Three animals were judged to have resting mean arterial pressure levels in the hypertensive range (≥110 mmHg). In all of the animals, pressor responses to routine laboratory events were exaggerated (average highest mean pressure during 1 min from any session was 97–196 mmHg). Subsequently, the region of the perifornical/lateral hypothalamus known to produce elevated blood pressure and heart rate responses to electrical stimulation was removed, and the blood pressure responses to the laboratory routines were significantly decreased and, in some cases, eliminated. Control lesions in nearby tissue had no effect on these responses. This region may play a critical role in initiating or exacerbating cardiovascular responses that contribute to the development of essential hypertension.

Phase I Safety Assessment of Intrathecal Neostigmine Methylsulfate in Humans 

1995 ◽  
Vol 82 (2) ◽  
pp. 331-343 ◽  
Author(s):  
David D. Hood ◽  
James C. Eisenach ◽  
Robin Tuttle
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Side Effects ◽  
Healthy Volunteers ◽  
Nausea And Vomiting ◽  
Severe Nausea ◽  
End Tidal Carbon Dioxide ◽  
End Tidal ◽  
Ice Water

Background In dogs, sheep, and rats, spinal neostigmine produces analgesia alone and enhances analgesia from alpha 2-adrenergic agonists. This study assesses side effects and analgesia from intrathecal neostigmine in healthy volunteers. Methods After institutional review board approval and informed consent, 28 healthy volunteers were studied. The first 14 volunteers received neostigmine (50-750 micrograms) through a #19.5 spinal needle followed by insertion of a spinal catheter. The remaining 14 volunteers received neostigmine through a #25 or #27 spinal needle without a catheter. Safety measurements included blood pressure, heart rate, oxyhemoglobin saturation, end-tidal carbon dioxide, neurologic evaluation, and computer tests of vigilance and memory. Analgesia in response to ice water immersion was measured. Results Neostigmine (50 micrograms) through the #19.5 needle did not affect any measured variable. Neostigmine (150 micrograms) caused mild nausea, and 500-750 micrograms caused severe nausea and vomiting. Neostigmine (150-750 micrograms) produced subjective leg weakness, decreased deep tendon reflexes, and sedation. The 750-micrograms dose was associated with anxiety, increased blood pressure and heart rate, and decreased end-tidal carbon dioxide. Neostigmine (100-200 micrograms) in saline, injected through a #25 or #27 needle, caused protracted, severe nausea, and vomiting. This did not occur when dextrose was added to neostigmine. Neostigmine by either method of administration reduced visual analog pain scores to immersion of the foot in ice water. Conclusions The incidence and severity of these adverse events from intrathecal neostigmine appears to be affected by dose, method of administration, and baricity of solution. These effects in humans are consistent with studies in animals. Because no unexpected or dangerous side effects occurred, cautious examination of intrathecal neostigmine alone and in combination with other agents for analgesia is warranted.

Clinical and Haemodynamic Study of Atenolol (Tenormin) in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 525s-526s
Author(s):  
H. Æ. Jensen ◽  
K. Rasmussen ◽  
N. Mosbæk
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Side Effects ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Blocking Agent ◽  
Pronounced Decrease ◽  
Daily Range ◽  
Haemodynamic Study

1. The β1-adrenoreceptor-blocking agent atenolol was studied in the treatment of twelve out-patients with essential hypertension. 2. With a mean dose of 110 mg of atenolol daily (range 75–200 mg/day) we observed a pronounced decrease in blood pressure. 3. Only minimal side effects were seen. 4. Cardiac output decreased from 4·6 to 3·4 l/min during treatment. This decrease did not correlate with the decrease in blood pressure but correlated well with the changes in calculated total peripheral resistance.

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.

scholarly journals Acute Cardiovascular Effects of Epidural Spinal Cord Stimulation

2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spinal Cord Stimulation ◽  
Statistical Significance ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Arterial Blood

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test

Sign in / Sign up

Export Citation Format

Share Document