Enhanced vasoconstriction to α1-adrenoceptor stimulation during cooling in mouse cutaneous plantar arteries

Goto, Kazunori; Ishikawa, Tomohisa

doi:10.1016/j.ejphar.2014.08.014

Cited by 8 publications

(6 citation statements)

References 18 publications

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“…As previously described in the ICU, significant gradient is associated with higher doses of vasopressors [ 7 , 22 , 39 , 40 ]. The association with higher norepinephrine dosage is thought to be part of the physiological mechanism underlying this condition which is consistent with our findings [ 41 , 42 ]. In fact, vasoactive agents are known to create peripheral vasoconstriction of medium-size arteries [ 12 , 42 ] which may also explain the higher lactate that we observed.…”

Section: Discussionsupporting

confidence: 93%

Non-invasive detection of a femoral-to-radial arterial pressure gradient in intensive care patients with vasoactive agents

et al. 2021

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Background In patient requiring vasopressors, the radial artery pressure may underestimate the true central aortic pressure leading to unnecessary interventions. When using a femoral and a radial arterial line, this femoral-to-radial arterial pressure gradient (FR-APG) can be detected. Our main objective was to assess the accuracy of non-invasive blood pressure (NIBP) measures; specifically, measuring the gradient between the NIBP obtained at the brachial artery and the radial artery pressure and calculating the non-invasive brachial-to-radial arterial pressure gradient (NIBR-APG) to detect an FR-APG. The secondary objective was to assess the prevalence of the FR-APG in a targeted sample of critically ill patients. Methods Adult patients in an intensive care unit requiring vasopressors and instrumented with a femoral and a radial artery line were selected. We recorded invasive radial and femoral arterial pressure, and brachial NIBP. Measurements were repeated each hour for 2 h. A significant FR-APG (our reference standard) was defined by either a mean arterial pressure (MAP) difference of more than 10 mmHg or a systolic arterial pressure (SAP) difference of more than 25 mmHg. The diagnostic accuracy of the NIBR-APG (our index test) to detect a significant FR-APG was estimated and the prevalence of an FR-APG was measured and correlated with the NIBR-APG. Results Eighty-one patients aged 68 [IQR 58–75] years and an SAPS2 score of 35 (SD 7) were included from which 228 measurements were obtained. A significant FR-APG occurred in 15 patients with a prevalence of 18.5% [95%CI 10.8–28.7%]. Diabetes was significantly associated with a significant FR-APG. The use of a 11 mmHg difference in MAP between the NIBP at the brachial artery and the MAP of the radial artery led to a specificity of 92% [67; 100], a sensitivity of 100% [95%CI 83; 100] and an AUC ROC of 0.93 [95%CI 0.81–0.99] to detect a significant FR-APG. SAP and MAP FR-APG correlated with SAP (r2 = 0.36; p < 0.001) and MAP (r2 = 0.34; p < 0.001) NIBR-APG. Conclusion NIBR-APG assessment can be used to detect a significant FR-APG which occur in one in every five critically ill patients requiring vasoactive agents.

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Section: Discussionsupporting

confidence: 93%

Non-invasive detection of a femoral-to-radial arterial pressure gradient in intensive care patients with vasoactive agents

et al. 2021

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“…17,18) In response to vasoconstrictor agonists, a slowly developing monophasic contraction is induced in splanchnic arteries such as aorta and iliac arteries, whereas biphasic contraction is induced in cutaneous arteries such as plantar, tail, and ear arteries. 9,[19][20][21] The present study also showed that the pattern of depolarization-induced contraction depends on the type of artery: High K + -induced contraction was monophasic in the aorta and iliac artery and biphasic in the tail artery. It should be noted, however, that our results suggest the contribution of nerve-derived noradrenaline to high K + -induced contraction in the tail artery.…”

Section: Discussionmentioning

confidence: 63%

Differential Contribution of Nerve-Derived Noradrenaline to High K<sup>+</sup>-Induced Contraction Depending on Type of Artery

Ishida

Hishinuma

Ishikawa

2017

Biological & Pharmaceutical Bulletin

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High K -induced contraction of arterial smooth muscle is thought to be mediated by membrane depolarization and subsequent activation of voltage-dependent Ca 2 channels (VDCCs). In line with this, this study found that contraction induced by 80 mM K was almost abolished by nifedipine (1 µM), a VDCC inhibitor, in isolated rat aorta, and was markedly suppressed in the iliac artery. However, nifedipine (1 µM) only partially suppressed high K -induced contraction in the tail artery. The contractions remaining in the arteries were further reduced by non-selective cation channel (NSCC) inhibitors, including 2-aminoethoxydiphenyl borate (2-APB) (100 µM), SK&F96365 (10 µM), and 3,4-dihydro-6,7-dimethoxy-α-phenyl-N,N-bis[2-(2,3,4-trimethoxyphenyl)ethyl]-1-isoquinolineacetamide hydrochloride (LOE908) (10 µM). In particular, sustained tonic contraction was nearly abolished. Prazosin (0.3 µM), an α 1 -adrenoceptor antagonist, partially inhibited high K -induced contraction in the tail and iliac arteries, but had no effect in the aorta. Consistently, tyramine potently induced contraction in the tail and iliac arteries, but not in the aorta. Furthermore, the inhibition by prazosin and NSCC inhibitors of the high K -induced contraction in the presence of nifedipine was comparable. These results suggest that depending on the type of artery, high K -induced contraction is mediated by Ca 2 influx not only through VDCCs but also through NSCCs, the activation of which is due to the activation of α 1 -adrenoceptors by the released noradrenaline from sympathetic nerve terminals resulting from high K stimulation. Key words high K +; tail artery; non-selective cation channel; voltage dependent calcium channel; noradrenaline Ca 2+ elevation in cytosol causes contraction in smooth muscle. In arterial smooth muscle, the primary pathways of Ca 2+ influx from extracellular space are through L-type voltagedependent Ca 2+ channels (VDCCs) and non-selective cation channels (NSCCs). 1) Elevating extracellular K + concentration decreases the K + gradient between the inside and outside of the cell membrane, which in turn causes cell membrane depolarization. VDCCs are activated by this depolarization, which leads to Ca 2+ influx, thereby causing smooth muscle contraction. Therefore, high K + stimulation is frequently used as an estimation of VDCC-mediated contraction.2) It is interesting to note, however, that our preliminary study showed insufficient inhibition of high K + -induced contraction by the VDCC inhibitor nifedipine in isolated rat tail artery. We thus further investigated the mechanism underlying high K + -induced contraction in different types of arteries, i.e., the aorta, and the iliac and tail arteries. The present data show that, depending on the type of artery, high K + -induced contraction is mediated not only through VDCCs but also through NSCCs activated by noradrenaline released from sympathetic nerve terminals. MATERIALS AND METHODS Measurement of ContractionProtocols for animal use were reviewed and approved by the Institutio...

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“…A rather simple way to possibly cause local vasoconstriction is to inject the cooled local anesthetic solutions. Cooling causes significant peripheral vasoconstriction via adrenoceptors ( 21 ). There is another important aspect of the cooling of anesthetic solutions.…”

Section: Discussionmentioning

confidence: 99%

“…A simple way is to decrease the temperature of the anesthetic solution. Cooling has been shown to cause vasoconstriction in cutaneous arteries via α1-adrenoceptor and α2C-adrenoceptors ( 21 ). Moreover, cooling the solution can lead to a reversible block of the compound action potential of rat sciatic nerves ( 22 ).…”

Section: Introductionmentioning

confidence: 99%

Effect of Cooling of Lidocaine with Epinephrine on the Anesthetic Success of Supplementary Intraligamentary Injection after a Failed Primary Inferior Alveolar Nerve Block: A Randomized Controlled Trial

AGGARWAL

2023

Eur Endod J

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Objective The purpose of this prospective, randomized clinical trial was to evaluate the effect of cooling a 2% lidocaine solution with 1:200,000 epinephrine, administered as a supplementary intraligamentary injection to overcome a failed primary inferior alveolar nerve block (IANB). Methods The study was preceded by a pilot study to evaluate the anesthetic efficacy of plain lidocaine solutions given as intraligamentary injections. In the subsequent randomized clinical trial, one hundred and thirty-eight patients received IANB with 2% lidocaine with 1:80,000 epinephrine for endodontic management of a mandibular molar with symptomatic irreversible pulpitis. Eighty-eight patients reported pain greater than 54 mm on a visual analog scale (Heft-Parker VAS) were categorized as unsuccessful anesthesia. These patients received either of the following intraligamentary injections: 2% lidocaine with 1:200,000 epinephrine at room temperature; or 2% lidocaine with 1:200,000 epinephrine at 4°C. Anesthetic success was again evaluated after re-initiation of the endodontic treatment. The heart rates of the patients were measured using a finger pulse oximeter. The categorical success rates were statistically analyzed with the Pearson chi-square test at 5% significance levels. The heart rate measurements were analyzed using a t-test. Results The intraligamentary injections with anesthetic solutions at room temperature presented a success rate of 59.1%, while the injections with a solution at 4°C gave a success rate of 52.27%. There were no significant differences between the success rates of the groups (χ 2 =0.41, p=0.52). Regarding the heart rates, there were no differences between the two solutions at baseline (T=1.2, p=0.2) or after injections (T=0.64, p=0.52). Conclusion Reducing the temperature of 2% lidocaine with 1:200,000 epinephrine to 4°C does not affect the anesthetic efficacy of supplemental intraligamentary injections, given after a failed primary IANB.

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Enhanced vasoconstriction to α1-adrenoceptor stimulation during cooling in mouse cutaneous plantar arteries

Cited by 8 publications

References 18 publications

Non-invasive detection of a femoral-to-radial arterial pressure gradient in intensive care patients with vasoactive agents

Non-invasive detection of a femoral-to-radial arterial pressure gradient in intensive care patients with vasoactive agents

Differential Contribution of Nerve-Derived Noradrenaline to High K<sup>+</sup>-Induced Contraction Depending on Type of Artery

Effect of Cooling of Lidocaine with Epinephrine on the Anesthetic Success of Supplementary Intraligamentary Injection after a Failed Primary Inferior Alveolar Nerve Block: A Randomized Controlled Trial

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