Direct Effects of Ropivacaine and Bupivacaine on Spinal Pial Vessels in Canine 

1997 ◽  
Vol 87 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Hiroki Iida ◽  
Yukinaga Watanabe ◽  
Shuji Dohi ◽  
Tadahiko Ishiyama
Keyword(s):  
Topical Application ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Beta Adrenoceptor ◽  
Pial Vessels ◽  
Arterial Blood ◽  
Before And After ◽  
Pial Arterioles ◽  
Anesthetized Dogs ◽  
Pial Vessel

Background Ropivacaine produces a vasoconstriction of cutaneous vessels in contrast to vasodilation produced by bupivacaine. To evaluate direct spinal microvascular actions of these local anesthetics, the authors investigated the concentration-related effects of ropivacaine and bupivacaine on spinal pial vascular diameters using the spinal window technique. Methods Anesthetized dogs (n = 14) divided into two groups (ropivacaine, n = 7; bupivacaine, n = 7) were prepared for measurement of spinal pial vessel diameters by intravital microscopy in a spinal window preparation. The authors administered six concentrations of each drug (10(-8)-10(-3) M) under the window and directly measured the spinal pial arteriolar and venular diameters at sequential times. Physiologic data including mean arterial blood pressure (MAP) and heart rate (HR) were determined before and after topical application of each concentration of the drugs. In additional experiments (n = 18), the action of topical ropivacaine and bupivacaine solution on spinal vessels was evaluated in the presence of yohimbine, prazosin, and propranolol. Results Ropivacaine significantly constricted whereas bupivacaine dilated pial arterioles and venules, both in a concentration-dependent manner. Microvascular alteration was not blocked with any of the adrenoceptor antagonists tested (yohimbine, prazosin, propranolol), each of which per se did not affect pial vessel diameters. Topical application of ropivacaine or bupivacaine did not induce any change in MAP or HR. Conclusions The present results indicate that ropivacaine constricts and bupivacaine dilates the pial vessels of the spinal cord in a concentration-dependent fashion, and the mechanisms involved in such actions do not seem to be mediated via alpha- or beta-adrenoceptor of spinal vasculature.

Direct Effects of α1-and α2-AdrenergicAgonists on Spinal and Cerebral Pial Vessels in Dogs 

1999 ◽  
Vol 91 (2) ◽  
pp. 479-485 ◽  
Author(s):  
Hiroki Iida ◽  
Hiroto Ohata ◽  
Mami Iida ◽  
Yukinaga Watanabe ◽  
Shuji Dohi
Keyword(s):  
Topical Administration ◽  
Vessel Diameter ◽  
Dependent Manner ◽  
Adrenergic Agonists ◽  
Concentration Dependent Manner ◽  
Cranial Window ◽  
Pial Vessels ◽  
Cerebral Arterioles ◽  
Pial Vessel

Background The effects of adrenergic agonists, often used as local anesthetic additives or spinal analgesics, on spinal vessels have not been firmly established. The authors investigated the effects of alpha2- and alpha1-adrenergic agonists on spinal and cerebral pial vessels in vivo. Methods Pentobarbital-anesthetized dogs (n = 28) were prepared for measurement of spinal pial-vessel diameter in a spinal-window preparation. The authors applied dexmedetomidine, clonidine, phenylephrine, or epinephrine in three different concentrations (0.5, 5.0, and 50 microg/ml; [2.1, 1.9, 2.5, and 2.3] x [10(-6), 10(-5), and 10(-4)] M, respectively) under the window (one drug in each dog) and measured spinal pial arteriolar and venular diameters in a sequential manner. To enable the comparison of their effects on cerebral vessels, the authors also administered these drugs under a cranial window. Results On topical administration, each drug constricted spinal pial arterioles in a concentration-dependent manner. Phenylephrine and epinephrine induced a significantly larger arteriolar constriction than dexmedetomidine or clonidine at 5 microg/ml (8%, 11%, 0%, and 1%, respectively). Spinal pial venules tended to be less constricted than arterioles. In cerebral arterioles, greater constrictions were induced by dexmedetomidine and clonidine than those induced by phenylephrine and epinephrine (14%, 8%, 0%, and 1%, respectively). Cerebral pial venules tended to exhibit larger constrictions than cerebral arterioles (unlike in spinal vessels). Conclusion Dexmedetomidine and clonidine constricted spinal vessels in a concentration-dependent manner, but such vasoconstrictions were smaller than those induced by phenylephrine and epinephrine.

Effect of digitalis on the diaphragm in anesthetized dogs

1987 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
T. Chonan ◽  
H. Miki ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Stimulus Frequency ◽  
Dependent Manner ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Mechanically Ventilated ◽  
Before And After ◽  
Residual Capacity ◽  
Anesthetized Dogs

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Effects of estrogen on cerebral blood flow and pial microvasculature in rabbits

2000 ◽  
Vol 279 (3) ◽  
pp. H1208-H1214 ◽  
Author(s):  
M. T. Littleton-Kearney ◽  
D. M. Agnew ◽  
R. J. Traystman ◽  
P. D. Hurn
Keyword(s):  
Blood Flow ◽  
Estrogen Receptor ◽  
Cerebral Blood Flow ◽  
Receptor Activation ◽  
Receptor Subtypes ◽  
Dependent Manner ◽  
Pial Arteries ◽  
Concentration Dependent Manner ◽  
Cranial Window ◽  
Pial Arterioles

We tested the hypothesis that intracarotid estrogen infusion increases cerebral blood flow (CBF) in a concentration-dependent manner and direct application of estrogen on pial arterioles yields estrogen receptor-mediated vasodilation. Rabbits of both genders were infused with estrogen via a branch of the carotid artery. Estrogen doses of 20 or 0.05 μg · ml−1 · min−1 were used to achieve supraphysiological or physiological plasma estrogen levels, respectively. CBF and cerebral vascular resistance were determined at baseline, during the infusion, and 60-min postinfusion, and effects on pial diameter were assessed via a cranial window. Pial arteriolar response to estrogen alone and to estrogen after administration of tamoxifen (10−7), an antiestrogen drug that binds to both known estrogen receptor subtypes, was tested. No gender differences were observed; therefore, data were combined for both males and females. Systemic estrogen infusion did not increase regional CBF. Estradiol dilated pial arteries only at concentrations ranging from 10−4–10−7 M ( P ≤ 0.05). Pretreatment with tamoxifen alone had no effect on arteriolar diameter but inhibited estrogen-induced vasodilation ( P < 0.001). Our data suggest that estrogen does not increase CBF under steady-state conditions in rabbits. In the pial circulation, topically applied estradiol at micromolar concentrations dilates vessels. The onset is rapid and dependent on estrogen receptor activation.

Responsiveness of individual airways to methacholine in adult rat lung explants

1993 ◽  
Vol 75 (1) ◽  
pp. 364-372 ◽  
Author(s):  
R. J. Dandurand ◽  
C. G. Wang ◽  
N. C. Phillips ◽  
D. H. Eidelman
Keyword(s):  
Video Camera ◽  
Maximal Response ◽  
Dependent Manner ◽  
Response Curves ◽  
Concentration Dependent Manner ◽  
Lung Inflation ◽  
Adult Rat ◽  
Computerized Image Processing ◽  
Before And After ◽  
Area X

We used a modified adult lung explant technique to directly measure the area of individual airways before and after methacholine (MCh) administration. Lungs were removed from 12-wk-old male Lewis rats under sterile conditions, filled with an agarose-containing solution at 37 degrees C, and cooled to 4 degrees C. Transverse slices (0.5–1.0 mm thick) were cut and cultured overnight. Concentration-response curves to MCh were determined for explant airways from lungs inflated to 25, 50, 75, and 100% total lung capacity (TLC) with a 1.0% agarose solution and to 75% TLC with 0.5 and 2.0% agarose solutions. MCh was added to the medium to achieve final concentrations ranging from 10(-9) to 10(-2) M. Airways were imaged before and 10 min after each increase in MCh concentration with an inverted microscope and video camera, and airway area was determined by computerized image processing. The maximal response (MR) ([1-(minimal area/baseline area)] x 100) and concentration of MCh resulting in 50% MR (EC50) were determined. A total of 217 airways from 3–12 explants per rat constricted in a concentration-dependent manner. Baseline area was larger with both higher lung volumes and agarose concentrations. MR was greatest in the airways from the 25% TLC and 0.5% agarose explants. Although there was considerable heterogeneity toward MCh within rats (EC50 varied up to 5.46 x 10(5)-fold), the median EC50 was similar among all rats (range 1.96 x 10(-6)-5.87 x 10(-4) M). Lung inflation volume and agarose concentration affected baseline area and MR, suggesting that airway-parenchymal interdependence mechanisms are operative in this preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Epinephrine-induced hepatic potassium movements before and after adrenergic blockade

1976 ◽  
Vol 54 (3) ◽  
pp. 347-356 ◽  
Author(s):  
Stephen D. Guthrie ◽  
Quillian R. Murphy
Keyword(s):  
Portal Vein ◽  
Superior Mesenteric Artery ◽  
Adrenergic Receptors ◽  
Mesenteric Artery ◽  
Adrenergic Blockade ◽  
Blood Flows ◽  
Arterial Blood ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Artery Flow

The epinephrine-induced loss and subsequent uptake of K+ by the liver was studied by measuring hepatic arterio–venous K+ differences and splanchnic blood flows in anesthetized dogs with chronically implanted portal vein catheters and celiac and superior mesenteric artery flow probes. When epinephrine was administered intraportally, neither α- nor β-adrenergic blockade, singly or in combination, had significant effects upon the hyper-kalemic or the hypokalemic phases in either hepatic venous or systemic arterial blood. It was concluded that the movements of K+ into and out of the liver caused by epinephrine are not mediated by the classical adrenergic receptors as defined by inhibition by specific blocking agents.

Exogenous NO inhibits basal NO release from vascular endothelium in vitro and in vivo

1996 ◽  
Vol 271 (5) ◽  
pp. H2045-H2051 ◽  
Author(s):  
X. L. Ma ◽  
B. L. Lopez ◽  
T. A. Christopher ◽  
D. S. Birenbaum ◽  
J. Vinten-Johansen
Keyword(s):  
In Vivo Studies ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
No Donor ◽  
Parent Molecule ◽  
Arterial Blood ◽  
No Release ◽  
Basal Release

This study tested the hypothesis that exogenous nitric oxide (NO) inhibits basal release of NO in isolated rat aortic rings and in vivo. Thoracic aortic rings were suspended in organ chambers with Krebs-Henseleit solution. In untreated rings, the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) markedly increased basal vascular tone by 34.6 +/- 5.2% of maximal force produced by 100 nM thromboxane A2 mimetic U-46619, indicating a basal release of NO. Other rings were pretreated with the exogenous NO donor S-nitroso-N-acetylpenicillamine (SNAP) for 20 min and then washed free of drug. In these rings, L-NAME-induced vasoconstriction was significantly attenuated in a concentration-dependent manner (from 34.6 +/- 5.2 to 25.7 +/- 2.9% at SNAP = 0.5 microM, 15.2 +/- 3.1% at 1 microM, and 11.9 +/- 2.5% at 5 microM), while having no effect on NO-independent phenylephrine-induced vasoconstriction (35.4 +/- 4.7 untreated vs. 41.3 +/- 4.3% SNAP pretreated, not significant). In addition, the nonnitrosylated parent molecule of SNAP, acetylpenicillamine, had no effect on the vasoconstriction induced by L-NAME. In the in vivo studies in anesthetized rats, L-NAME caused significant hypertensive responses (34 +/- 4-mmHg increase in mean arterial blood pressure). Subvasoactive doses of SNAP attenuated these hypertensive responses in a dose-dependent manner (20 +/- 3-mmHg increase with 10 micrograms/kg SNAP pretreatment and 16 +/- 4-mmHg increase with 20 micrograms/kg SNAP pretreatment), but any dose of acetylpenicillamine studied had no effect. Coadministration of superoxide dismutase and SNAP significantly potentiated the inhibitory effect of the NO donor on vasocontraction responses to L-NAME. Furthermore, SNAP did not attenuate the hypertensive responses to phenylephrine. These results indicate that exogenous NO significantly inhibits basal NO release both in vitro and in vivo, suggesting that NO plays an important negative-feedback regulatory role under physiological conditions.

Abstract 17344: Increasing Calcium-activated Potassium Current Shortens and Stabilizes Repolarization in Chronic Heart Failure

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Ingrid M Bonilla ◽  
Victor Long ◽  
Kent Mowrey ◽  
Karsten Schober ◽  
Raul Weiss ◽  
...  
Keyword(s):  
Heart Failure ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Canine Model ◽  
Ventricular Repolarization ◽  
Resting Membrane Potential ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Before And After ◽  
Normal Controls

Heart failure (HF) is a chronic disease resulting in abnormal prolongation and instability of ventricular repolarization. IKCa has been suggested to stabilize repolarization in HF as IKca blockade has shown pro-arrhythmic effects in the failing ventricle. We tested the hypothesis that an SK channel (IKCa) agonist CyPPA, would shorten and stabilize ventricular repolarization in HF ventricular myocytes. Methods: A tachypacing - induced 4 month HF canine model was used (LVFS: 15.9 ± 2.5%), and LV midwall myocytes were isolated and compared to normal controls. Action potential duration at 50 (APD50), and 90% (APD90) repolarization and APD instability (beat to beat variability of repolarization, a measure of arrhythmia risk) were measured before and after the application of CyPPA (0.001nM-20uM) in control ventricular, and in 4 months HF ventricular myocytes (n=10-15 per group). Results: In control myocytes, CyPPA shortened action potential APD50 and APD90 in a concentration dependent manner (0.001nM-20uM, p<0.05 vs baseline at 20uM, Figure). In HF myocytes, CyPPA also shortened APD50 and APD90, but at lower concentrations than in controls. Notably, In addition to APD shortening, CyPPA significantly decreased repolarization instability (P<0.05 vs baseline at 1 Hz) in HF. CyPPA did not affect resting membrane potential in either group. Conclusions: HF myocytes are more sensitive to IKCa agonism than control myocytes. An IKCa agonist attenuates electrophysiologic remodeling and stabilizes repolarization in failing ventricular myocytes, suggesting a therapeutic role for this approach in HF.

Deactivation of Norepinephrine by Peroxynitrite as a New Pathogenesis in the Hypotension of Septic Shock

2003 ◽  
Vol 98 (4) ◽  
pp. 928-934 ◽  
Author(s):  
Ko Takakura ◽  
Wen Xiaohong ◽  
Kenji Takeuchi ◽  
Yoshikazu Yasuda ◽  
Satoru Fukuda
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Rate Constant ◽  
Phosphate Buffer Solution ◽  
Dependent Manner ◽  
Buffer Solution ◽  
Concentration Dependent Manner ◽  
Sodium Phosphate Buffer ◽  
Arterial Blood ◽  
Anesthetized Rats

Background Vascular hyporeactivity to catecholamines limits successful treatment of hypotension in septic shock. Large amounts of nitric oxide (NO) and superoxide anion (O(2)(-1).) are produced in response to bacterial endotoxins and/or inflammatory cytokines. NO reacts with O(2)(-1). to form the potentially toxic NO metabolite, peroxynitrite (ONOO(-1)). The purpose of this study was to investigate whether ONOO(-1) decreases the vasocontractile activity of norepinephrine. Methods Norepinephrine was treated with ONOO(-1) or 3-morpholinosydonimine-N-ethyl-carbamine (SIN-1; an ONOO(-1) producer) in a 5 x 10(-2) m sodium phosphate buffer solution at pH 7.4, and absorbance of the product was measured spectrophotometrically at 295 and 370 nm. Norepinephrine pretreated with ONOO(-1) was administered to isolated rat thoracic aortas to observe contractions in functional experiments. The rate constant between norepinephrine and ONOO(-1) was determined via a competition assay with cysteine in functional experiments. Norepinephrine pretreated with ONOO(-1) was injected intravenously into anesthetized rats to measure blood pressure. Results Norepinephrine pretreated with ONOO(-1) was confirmed spectrally as oxidized norepinephrine. Norepinephrine pretreated with ONOO(-1) decreased its vasocontractile force in an ONOO(-1) (10(-6), up to 3 x 10(-4) m) concentration-dependent manner (EC(50) = 5.1 x 10(-5) m). The decrease in its force was lower at pretreatment with ONOO(-1) in a lower pH buffer. A rate constant for the ONOO(-1)-norepinephrine reaction was 6 x 10(2) m/s. Norepinephrine (10(-7) m) incubated with SIN-1 (10(-3) m) decreased its vasocontractile force in an incubation time-dependent manner. Administration of norepinephrine pretreated with ONOO(-1) to anesthetized rats caused no significant change in arterial blood pressure. Conclusions These results indicate that norepinephrine was oxidized and deactivated by ONOO(-1). This deactivation may, at least in part, account for the hyporeactivities of vasocontraction to norepinephrine in septic shock.

scholarly journals Activation of opioid μ-receptors in medullary raphe depresses sighs

2009 ◽  
Vol 296 (5) ◽  
pp. R1528-R1537 ◽  
Author(s):  
Zhenxiong Zhang ◽  
Fadi Xu ◽  
Cancan Zhang ◽  
Xiaomin Liang
Keyword(s):  
Intravenous Administration ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Medullary Raphe ◽  
Before And After ◽  
Chemical Stimuli ◽  
Spontaneously Breathing ◽  
Ventilatory Response To Hypoxia ◽  
Μ Receptor

Sighs, a well-known phenomenon in mammals, are substantially augmented by hypoxia and hypercapnia. Because (d-Ala2,N-Me-Phe4,Gly-ol)-enkephalin (DAMGO), a μ-receptor agonist, injected intravenously and locally in the caudal medullary raphe region (cMRR) decreased the ventilatory response to hypoxia and hypercapnia, we hypothesized that these treatments could inhibit sigh responses to these chemical stimuli. The number and amplitude of sighs were recorded during three levels of isocapnic hypoxia (15%, 10%, and 5% O2 for 1.5 min) or hypercapnia (3%, 7%, and 10% CO2 for 4 min) to test the dependence of sigh responses on the intensity of chemical drive in anesthetized and spontaneously breathing rats. The role of μ-receptors in modulating sigh responses to 10% O2 or 7% CO2 was subsequently evaluated by comparing the sighs before and after 1) intravenous administration of DAMGO (100 μg/kg), 2) microinjection of DAMGO (35 ng/100 nl) into the cMRR, and 3) intravenous administration of DAMGO after microinjection of d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 100 ng/100 nl), a μ-receptor antagonist, into the cMRR. Hypoxia and hypercapnia increased the number, but not amplitude, of sighs in a concentration-dependent manner, and the responses to hypoxia were significantly greater than those to hypercapnia. Systemic and local injection of DAMGO into the cMRR predominantly decreased the number of sighs, while microinjection into the rostral and middle MRR had no or limited effects. Microinjecting CTAP into the cMRR significantly diminished the systemic DAMGO-induced reduction of the number of sighs in response to hypoxia, but not to hypercapnia. Thus we conclude that hypoxia and hypercapnia elevate the number of sighs in a concentration-dependent manner in anesthetized rats, and this response is significantly depressed by activating systemic μ-receptors, especially those within the cMRR.

Renal vascular response to angiotensin and other vasoactive agents in endotoxin shock

1964 ◽  
Vol 207 (6) ◽  
pp. 1260-1264 ◽  
Author(s):  
Thomas E. Emerson ◽  
Charles M. Brake ◽  
Lerner B. Hinshaw
Keyword(s):  
Renal Artery ◽  
Endotoxin Shock ◽  
Vasoactive Agents ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Before And After ◽  
Vascular Responsiveness ◽  
Anesthetized Dogs ◽  
Renal Vascular

Renal vascular responsiveness to angiotensin, epinephrine, norepinephrine, and histamine was investigated before and after endotoxin shock in 25 anesthetized dogs. Drugs were injected into the renal artery inflow tubing in constant-flow, isolated kidney preparations. Mean renal vascular responses were compared for both peak elevation of renal artery pressure (RAP) and area under the RAP curve. In situ kidney preparations in which angiotensin and norepinephrine were infused intravenously after endotoxin were utilized in several experiments. Renal blood flow (RBF) and the dog's arterial blood pressure (ABP) were measured in both groups. Renal vascular responsiveness to angiotensin was virtually abolished within 1 hr after endotoxin. The RAP elevation produced by epinephrine and the decreased RAP following histamine injections were not significantly altered. In the in situ kidney studies, angiotensin was initially effective in elevating ABP after endotoxin, but RBF was further depressed; by approximately 1 hr after endotoxin, angiotensin infusion was ineffective. Norepinephrine infusion maintained the animal's ABP at a normotensive level and did not seriously reduce RBF.

Sign in / Sign up

Export Citation Format

Share Document