Hemodynamic effects of low-dose atipamezole in isoflurane-anesthetized cats receiving an infusion of dexmedetomidine

2017 ◽  
Vol 20 (6) ◽  
pp. 571-577 ◽  
Author(s):  
Manuel Martin-Flores ◽  
Daniel M Sakai ◽  
Juhana Honkavaara ◽  
Luis Campoy
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Low Dose ◽  
Healthy Adult ◽  
Cardiovascular Effects ◽  
Low Doses ◽  
Arterial Blood ◽  
Target Plasma ◽  
Target Plasma Concentration ◽  
Baseline Values

Objectives The objective of this study was to evaluate the cardiovascular effects of low-dose atipamezole administered intravenously to isoflurane-anesthetized cats receiving dexmedetomidine. We hypothesized that atipamezole would increase heart rate (HR) and reduce arterial blood pressure in isoflurane-anesthetized cats receiving dexmedetomidine. Methods Six healthy adult domestic shorthair cats were anesthetized with isoflurane and instrumented for direct arterial pressures and cardiac output (CO) measurements. The cats received a target-controlled infusion of dexmedetomidine (target plasma concentration 10 ng/ml) for 30 mins before administration of atipamezole. Two sequential doses of atipamezole (15 and 30 μg/kg IV) were administered at least 20 mins apart, during dexmedetomidine administration. The effects of dexmedetomidine and each dose of atipamezole on HR, mean arterial blood pressure (MAP), CO and systemic vascular resistance (SVR) were documented. Results Dexmedetomidine reduced the HR by 22%, increased MAP by 78% (both P ⩽0.01), decreased CO by 48% and increased SVR by 58% (both P ⩽0.0003). Administration of atipamezole 15 and 30 μg/kg intravenously increased HR by 8% ( P = 0.006) and 4% ( P = 0.1), respectively. MAP decreased by 39% and 47%, respectively (both P ⩽0.004). Atipamezole 30 μg/kg returned CO and SVR to baseline values. Conclusions and relevance Low doses of atipamezole (15 and 30 μg/kg) administered intravenously to anesthetized cats decreased arterial blood pressure with only marginal increases in HR. Atipamezole 30 μg/kg restored CO and SVR to baseline values before dexmedetomidine administration.

scholarly journals Maternal and Foetal Cardiovascular Effects of the Anaesthetic Alfaxalone in 2-Hydroxypropyl-β-cyclodextrin in the Pregnant Ewe

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Anna Andaluz ◽  
Laura Santos ◽  
Félix García ◽  
Rosa I. Ferrer ◽  
Laura Fresno ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Uneventful Recovery ◽  
Entire Study ◽  
Arterial Blood ◽  
Pregnant Sheep ◽  
Systolic Arterial Blood Pressure ◽  
Baseline Values ◽  
Pregnant Ewe

The objective of this study was to determine the pharmacodynamics effects of the anaesthetic alfaxalone in 2-hydroxypropyl-β-cyclodextrin in pregnant sheep after the intravenous injection of a 2 mg/kg weight dose. Six pregnant Ripollesa sheep, weighing 47.1 ± 4.4 kg, were used. Twenty-four hours after instrumentation, sheep were anaesthetized with intravenous alfaxalone in cyclodextrin. Time to standing from anaesthesia was 30.0 ± 10.81 min. Foetal heart rate increased significantly during the first 5 min after alfaxalone administration. Significant differences were observed in maternal diastolic arterial blood pressure between minute 10 and minutes 90, 120, 150, 180, 210, and 240. Significant differences were observed for foetal systolic arterial blood pressure between 5 and 30 min after alfaxalone administration. Significant differences in foetal pH were detected during the entire study period, whereas maternal pH returned to baseline values by 60 min after alfaxalone administration. The present study indicated that alfaxalone in 2-hydroxypropyl-β-cyclodextrin administered as an intravenous bolus at 2 mg/kg body weight produced minimal adverse effects and an uneventful recovery from anaesthesia in pregnant sheep and their foetus.

scholarly journals Cardiovascular effects of epidural morphine or ropivacaine in isoflurane-anaesthetised pigs during surgical devascularisation of the liver

2010 ◽  
Vol 81 (3) ◽  
Author(s):  
G.F. Stegmann
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Abdominal Surgery ◽  
Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Group Differences ◽  
Epidural Administration ◽  
Isoflurane Anaesthesia ◽  
Treatment Groups ◽  
Arterial Blood

The cardiovascular effects of non-abdominal and abdominal surgery during isoflurane anaesthesia (A-group) or isoflurane anaesthesia supplemented with either epidural ropivacaine (AR-group; 0.75 % solution, 0.2 mℓ/kg) or morphine (AM-group; 0.1 mg/kg diluted in saline to 0.2mℓ/kg) were evaluated in 28 healthy pigs with a mean body weight of 30.3 kg SD ± 4.1 during surgical devascularisation of the liver. Anaesthesia was induced with the intramuscular injection of midazolam (0.3 mg/kg) and ketamine (10 mg/kg). Anaesthesia was deepened with intravenous propofol to enable tracheal intubation and maintained with isoflurane on a circle rebreathing circuit. The vaporiser was set at 2.5% for the A-group and 1.5% for the AR- and AM-groups. Differences between treatment groups were not statistically significant (P>0.05) for any of the variables. Differences between AM- and AR-groups were marginally significant heart rate (HR) (P = 0.06) and mean arterial blood pressure (MAP) (P = 0.08). Within treatment groups, differences for the A-group were statistically significant (P<0.05) between non-abdominal and abdominal surgery for HR, systolic blood pressure, diastolic blood pressure (DIA) and MAP. Within the AM-group differences were statistically significant (P < 0.05) for DIA and MAP, and within the AR group differences for all variables were not statistically significant (P > 0.05). It was concluded that in isoflurane-anaesthetised pigs, the epidural administration of ropivacaine decreased heart rate and improved arterial blood pressure during surgery.

Chronic regulation of arterial blood pressure by ANP: role of endogenous vasoactive endothelial factors

1998 ◽  
Vol 275 (5) ◽  
pp. H1826-H1833 ◽  
Author(s):  
L. G. Melo ◽  
A. T. Veress ◽  
U. Ackermann ◽  
H. Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Synthetic Activity ◽  
Arterial Blood

Atrial natriuretic peptide (ANP) exerts a chronic hypotensive effect due to a decrease in total peripheral resistance (TPR). This study examines if chronic ANP-dependent vasodilation is attributable to differences in the cardiovascular regulatory activity of vascular endothelium (VE), based on evidence that ANP affects synthesis/release and target cardiovascular effects of endothelin-1 (ET-1), C-type natriuretic peptide (CNP), and nitric oxide (NO). To determine if the synthetic activity of resistance vasculature VE is chronically altered by plasma ANP activity, we measured ET-1, CNP, and endothelial constitutive NO synthase (ecNOS) concentration and total NOS enzyme activity in homogenates of kidney, heart, lung, hindquarter skeletal muscle, and brain from hypotensive transgenic mice with elevated plasma ANP, hypertensive knockout mice (−/−) characterized by the absence of ANP, and the corresponding normotensive wild-type (NT, +/+) mice. Tissue distribution and abundance patterns of ET-1, CNP, ecNOS, and NOS enzyme activity were comparable between the different genotypes and did not differ significantly between mutant and control mice. Antagonism of ETA/B receptors in −/− and +/+ mice in vivo with SB-209670 reduced arterial blood pressure (ABP) significantly and comparably in both genotypes (−27 ± 4 and −25 ± 2% change for −/− and +/+ mice, respectively) independent of any significant changes in heart rate (HR) (−6 ± 8 and −4 ± 4% change for −/− and +/+ mice, respectively). Immunoneutralization of CNP-specific guanylate cyclase-linked receptors (GC-B) with monoclonal antibodies (3G12) increased ABP slightly, but not significantly, by similar relative amounts in both −/− (10 ± 6% change) and +/+ mice (8 ± 3% change), without changing HR significantly (4 ± 1% change for both +/+ and −/− mice). Inhibition of NOS activity (by N G-nitro-l-arginine methyl ester) significantly increased ABP, but the changes were comparable between −/− (53 ± 5% change) and +/+ mice (50 ± 6% change) and occurred in the absence of significant changes in HR (−1 ± 5 and 7 ± 5% change for −/− and +/+ mice, respectively). We conclude that the differences in ABP associated with chronic variations in endogenous ANP activity are not due to alterations in synthesis or responsiveness of the cardiovascular system to the effects of ET-1, CNP, or NO.

Blood pressure lowering action of adenosine diphosphate and related compounds

1961 ◽  
Vol 201 (6) ◽  
pp. 1123-1125 ◽  
Author(s):  
David B. Gordon ◽  
Donald H. Hesse
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Intravenous Injection ◽  
Low Dose ◽  
Adenosine Diphosphate ◽  
Blood Pressure Lowering ◽  
Arterial Blood ◽  
Pressure Lowering ◽  
Dose Levels ◽  
Related Compounds

It was found upon intravenous injection of adenosine and its mono-, di-, and triphosphate in the rat that ADP produced the greatest fall in arterial blood pressure. At low dose levels ADP was about 147 times as potent as adenosine and about 45 times as potent as AMP or ATP on an equimolar basis. The rat is more sensitive to the blood pressure lowering action of the adenosine compounds than other species thus far tested.

Cardiovascular actions of trout urotensin II in the conscious trout, Oncorhynchus mykiss

1996 ◽  
Vol 271 (5) ◽  
pp. R1335-R1343 ◽  
Author(s):  
J. C. Le Mevel ◽  
K. R. Olson ◽  
D. Conklin ◽  
D. Waugh ◽  
D. D. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Urotensin Ii ◽  
Cardinal Vein ◽  
Vascular Rings ◽  
Arterial Blood ◽  
Dose Dependent

The central and peripheral cardiovascular effects of synthetic trout urotensin II (UII) were investigated in the conscious rainbow trout. Intracerebroventricular injection of 50 pmol UII produced a slight (3%) but significant (P < 0.05) increase in heart rate but had no effect on mean arterial blood pressure. Injection of 500 pmol UII icv produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak pressor effect of centrally administered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with significant (P < 0.05) effects on both parameters observed at a dose of 25 pmol. Higher doses of the peptide produced a sustained decrease in cardiac output that accompanied the bradycardia and rise in arterial blood pressure. The UII-induced bradycardia, but not the increase in pressure, was abolished by pretreatment with phentolamine. Trout UII produced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concentration producing maximal contraction (pD2) = 8.30] and celiacomesenteric (pD2 = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the pressor effect of UII in trout is mediated predominantly, if not exclusively, by an increase in systemic vascular resistance. The UII-induced hypertensive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of cardioinhibitory baroreflexes.

scholarly journals Hypotensive and Bradycardic Effects of Quinovic Acid Glycosides from Aspidosperma fendleri in Spontaneously Hypertensive Rats

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Omar Estrada ◽  
Juan M. González-Guzmán ◽  
María M. Salazar-Bookman ◽  
Alfonso Cardozo ◽  
Eva Lucena ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Triterpenoid Saponins ◽  
Spontaneously Hypertensive ◽  
Arterial Blood

The Aspidosperma genus (Apocynaceae) represents one of the largest sources of indole alkaloids widely associated with cardiovascular effects. Aspidosperma fendleri, a plant found mainly in Venezuela, has a single phytochemical report in which is revealed the presence of alkaloids in its seeds. This study explored the cardiovascular effects of an ethanolic extract of A. fendleri leaves (EEAF) in spontaneously hypertensive rats (SHR) and its potential bioactive compounds. Using bioguided fractionation, fractions and pure compounds were intravenously administered to SHR and their effects on mean arterial blood pressure (MABP) and heart rate (HR) monitored over time. EEAF induced hypotensive and bradycardic effects as shown by significant reductions in mean arterial blood pressure (MABP) and heart rate (HR), respectively. Bioactivity-guided fractionation led to the isolation of a mixture of two known isomeric triterpenoid glycosides identified by spectral evidence as quinovic acid 3- O-β-rhamnopyranoside and quinovic acid 3- O-β-fucopyranoside. This mixture of triterpenoid saponins induced reductions in MABP and HR similar to those induced by propranolol. Together, these findings indicate that the two quinovic acid glycosides are responsible for the hypotensive and bradycardic effects which suggest their potential use in cardiovascular therapy.

Renal Vascular Responses to Dopamine: Haemodynamic and Angiographic Observations in Normal Man

1973 ◽  
Vol 45 (6) ◽  
pp. 733-742 ◽  
Author(s):  
N. K. Hollenberg ◽  
D. F. Adams ◽  
P. Mendell ◽  
H. L. Abrams ◽  
J. P. Merrill
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Cardiovascular Effects ◽  
Normal Subjects ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Normal Man ◽  
Renal Vascular

1. The renal vascular response to intravenously administered dopamine was assessed in normal man by selective renal arteriography and xenon washout. Infusion of 3 μg min−1 kg−1 induced renal vasodilatation with an increase in the cortical component of blood flow. Arterial blood pressure was not influenced and a systemic effect was not demonstrable. Lower doses did not induce a renal response. Increasing dosage raised arterial blood pressure and induced subjective symptoms, but did not result in a further increase in renal blood flow. 2. Renal vascular resistance increased with increasing age in the normal subjects. A significant inverse relationship was found between the initial vascular resistance and the renal vasodilator response to dopamine. It thus appears that the vascular effects of increasing age (nephrosclerosis) may limit the dilator response to dopamine. 3. It is concluded that dopamine is an effective renal cortical vasodilator when administered intravenously at doses which are free from other systemic cardiovascular effects. The dose-response relationship must be considered in attempts at reversal of conditions characterized by renal vasoconstriction.

Sedation Effects

2018 ◽  
pp. 50-53
Author(s):  
Jeffrey Linzer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Drug Administration ◽  
Cardiovascular Effects ◽  
Cardiac Work ◽  
Underlying Condition ◽  
Arterial Blood

While respiratory concerns tend to be the first consideration with sedation medications, many can have important effects on the cardiovascular system that need to be managed. Changes in heart rate, blood pressure, and cardiac work have to be considered. While most of these medications will affect arterial blood pressure in one way or another, some will have no effect on heart rate. While one agent may work well in majority of patients, that same medication could have potentially devastating effects because of a patient’s underlying condition. Additionally, simply changing the rate of drug administration can potentially reduce or increase the cardiovascular effects.

Cardiovascular effects of atrial extracts in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 819-826 ◽  
Author(s):  
Uwe Ackermann ◽  
Terumi G. Irizawa ◽  
Susan Milojevic ◽  
Harald Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
Direct Stimulation ◽  
Arterial Blood ◽  
Cardiopulmonary Receptors

Tissue extracts derived from atria or ventricles of Sprague–Dawley rats were injected into Inactin-anesthetized assay rats. Compared with ventricular extracts, atrial extracts produced a 20 mmHg (1 mmHg = 133.322 Pa) fall in mean arterial blood pressure. This fall resulted from failure to increase cardiac output in compensation for peripheral vasodilation. Two factors were responsible: depression of heart rate (by 25 beats/min) and failure to increase cardiac performance. The time patterns and magnitudes of changes in cardiovascular parameters after cardiac extracts were not changed by prior atropinization. However, assay rats that were vagotomized showed no cardiac slowing after atrial extract and showed a significantly smaller decrease in mean arterial blood pressure than did sham-vagotomized or intact rats. Another group of assay rats was vagotomized as well as carotid-sinus-denervated before extract injection. In these rats the degree of hypotension caused by atrial extract was significantly greater than that observed after vagotomy alone and was not significantly different from that observed in rats with intact innervation. The results suggest that the hypotension that is caused by atrial extract, but not by ventricular extracts, results in part from the reflex effects of direct stimulation of chemosensitive cardiopulmonary receptors with vagal afferents and partly from the reflex effects of baroreceptor unloading. Ventricular extract had no hypotensive effect in any group of assay rats.

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