Alpha-2 adrenergic agonists.
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Adrenergic alpha-2 Receptor Agonists↗
Biomedical subjects
T Kamibayashi
Publications and source records attributed to T Kamibayashi.
The involvement of pertussis toxin-sensitive G proteins in the post receptor mechanism of central I1-imidazoline receptors.
1. To elucidate the possible involvement of pertussis toxin (PTX)-sensitive G proteins in the post receptor mechanism of alpha 2-adrenoceptors and imidazoline receptors, we examined the effect of pretreatment of the central nervous system with PTX on the antidysrhythmic effect of dexmedetomidine, a selective alpha 2-adrenoceptor agonist, and rilmenidine, a selective I1-imidazoline receptor agonist on halothane-adrenaline dysrhythmias in rats. 2. Dexmedetomidine (0, 1.0, 2.0, 5.0 micrograms kg-1 min-1.i.v.) and rilmenidine (0, 1.0, 3.0, 10, 20 micrograms kg-1, i.v.) prevented the genesis of halothane-adrenaline dysrhythmias in a dose-dependent fashion. Both idazoxan (10, 20 micrograms kg-1, intracerebroventricularly (i.c.v.)), an alpha 2-adrenoceptor antagonist with high affinity for imidazoline receptors, and rauwolscine, (40 micrograms kg-1, i.c.v.), an alpha 2-adrenoceptor antagonist with low affinity for imidazoline receptors inhibited the action of dexmedetomidine (5.0 micrograms kg-1, min-1, i.v.), but the inhibitory potency of idazoxan was much greater than that of rauwolscine. While the pretreatment with PTX (0.1, 0.5, 1.0 micrograms kg-1, i.c.v.) did not change the dysrhythmogenecity of adrenaline, this treatment completely blocked the antidysrhythmic property of rilmenidine (20 micrograms kg-1, i.v.) as well as dexmedetomidine (5.0 micrograms kg-1 min-1, i.v.). 3. It is suggested that central I1-imidazoline receptors as well as alpha 2-adrenoceptors may be functionally coupled to PTX-sensitive G proteins.
Adrenergic alpha-2 Receptor Agonists↗
Laser Doppler skin blood flow and sympathetic nervous responses to surgical incision during halothane and isoflurane anesthesia.
The aim of the present study was to evaluate whether a sudden decrease in skin blood flow measured using a laser Doppler velocimeter reflects sympathetic nervous response to surgical skin incision during halothane (n = 17) and isoflurane (n = 16) anesthesia in 33 ASA physical status I or II patients scheduled for laparotomy. Plasma norepinephrine concentrations in the responding patients who showed a sudden decrease in the skin blood flow after surgical incision increased significantly and continued to increase 1-10 min after skin incision under halothane and isoflurane anesthesia. Although plasma norepinephrine concentrations in the nonresponders did not increase after surgical incision with halothane, the concentrations increased significantly at 1 min, but not at 3 and 10 min, after skin incision with isoflurane. The results indicate that the sudden decrease in laser Doppler flow reflects the sympathetic response to surgical incision. However, these also suggest that the factors that control the skin blood flow may not be simply sympathetic but may reflect other modulators as well. Plasma epinephrine concentration increased during skin incision, but the concentrations did not differ between the patients with and without a sudden decrease in skin blood flow. Increases in systolic blood pressure and rate-pressure product on skin incision were also significantly more in patients with skin blood flow response compared with those without the response. The magnitude of changes in plasma norepinephrine concentration and hemodynamic variables with skin incision was greater with isoflurane than with halothane at the same minimum alveolar anesthetic concentration level.
Adult↗
The effect of imidazoline receptors and alpha2-adrenoceptors on the anesthetic requirement (MAC) for halothane in rats.
BACKGROUND: Recent evidences have documented that several pharmacologic actions of alpha2-adrenoceptor agonists are mediated via activation of not only alpha2-adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia. METHODS: Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 microg/kg, intraperitoneally [IP]), a selective alpha2-adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated. RESULTS: Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane. CONCLUSIONS: The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2- adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.
Adrenergic alpha-Agonists↗
Antiarrhythmic action of rilmenidine on adrenaline-induced arrhythmia via central imidazoline receptors in halothane-anaesthetized dogs.
1. To elucidate the role of central imidazoline receptors in the genesis of adrenaline-induced arrhythmias under halothane anaesthesia, we investigated the effects of rilmenidine, a selective agonist at imidazoline receptors, on this type of arrhythmia in dogs. Rilmenidine (1, 3, 10 micrograms kg-1, i.v.) did not affect basal haemodynamic parameters (heart rate and blood pressure), but dose-dependently inhibited adrenaline-induced arrhythmias under halothane anaesthesia. 2. Although, rilmenidine has a weak affinity for alpha(2)-adrenoceptors, pretreatment with idazoxan (10 micrograms kg-1, intracisternally i.c.), an imidazoline receptor antagonist which has also alpha(2)-adrenoceptor blocking potency, blocked the antiarrhythmic effect of rilmenidine (10 micrograms kg-1, i.v.). In contrast, pretreatment with rauwolscine (20 micrograms kg-1, i.c.), a classical alpha(2)-adrenoceptor antagonist with little affinity for imidazoline receptors, did not affect the effect of rilmenidine (10 micrograms kg-1, i.v.). Furthermore, bilateral vagotomy completely blocked the antiarrhythmic action of rilmenidine (10 micrograms kg-1, i.v.). 3. It is suggested that the antiarrhythmic action of rilmenidine is due to the activation of central imidazoline receptors and that vagal tone is critical for this action of rilmenidine.
Adrenergic alpha-Agonists↗
Adrenoceptor mechanism involved in thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs.
Although thiopental is known to potentiate halothane-epinephrine arrhythmias, the precise mechanism of this potentiation is obscure. The authors investigated the comparative role of alpha 1 and beta adrenergic actions in the thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs. Adult mongrel dogs were anesthetized with halothane alone (1.3%) or thiopental (20 mg kg-1) plus halothane and monitored continuously for systemic arterial pressures and for premature ventricular contractions. The arrhythmogenic doses of phenylephrine and isoproterenol were determined during the two anesthetic methods and the effect of thiopental on the arrhythmogenic action of alpha 1 and beta agonists was examined. Thiopental failed to exert a significant potentiation of arrhythmogenic effect of phenylephrine or isoproterenol, when these agents were administered separately. On the other hand, the potentiation of arrhythmogenicity by thiopental was remarkable in the case of combined administration of both the agonists, that is, thiopental enhanced the synergistic interaction between phenylephrine and isoproterenol for inducing arrhythmias during halothane anesthesia. In addition, the potentiation was more prominent when a low dose of isoproterenol and a high dose of phenylephrine was combined than that when a high dose of isoproterenol and a low dose of phenylephrine was given in combination. The results indicate that thiopental significantly potentiates the arrhythmogenic interaction of alpha 1 and beta adrenergic agonists administered concurrently, although individual potentiation of these agonists is not significant.
Anesthetics↗
Role of imidazoline receptors in halothane-epinephrine arrhythmias.
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Animals↗
Mandibular reconstruction using the double barrel fibular graft.
Five patients underwent mandibular reconstruction using the double barrel fibular graft from 1989 to 1994. Bony defects ranged from 7 to 14 cm. In three patients, two skin flaps were taken with the fibular graft for composite reconstruction. In order to overcome the main disadvantage of the fibular graft, i.e., small circumference of the bone, a harvested fibula was osteotomized into several portions, folded into two parallel lengths, and fixed along the inferior border of the mandible and the alveolar ridge. The double barrel fibular graft provided more than 4-cm alveolar height without damaging bone viability. In Orientals, a fibula is approximately 1.5 cm thick, and using a single fibular strut for mandibular reconstruction may result in subsequent difficulty in wearing conventional dentures or osseointegrated implants. All patients acquired good mandibular contour and enough thickness of the alveolar ridge, and could wear a conventional denture and eat a solid diet. This procedure seems to be superior to the iliac bone graft for major mandibular reconstruction because of its length, the possibility of three-dimensional composite reconstruction, increased bone thickness, and minimal donor-site morbidity.
Adolescent↗
Thoracic epidural anesthesia attenuates halothane-induced myocardial sensitization to dysrhythmogenic effect of epinephrine in dogs.
BACKGROUND: The autonomic nervous system plays a critical role in the central modulation of cardiac dysrhythmias. Because sympathetic blockade by thoracic epidural anesthesia has been documented to protect patients from various stress responses, the authors speculate that epidural anesthesia can attenuate the dysrhythmogenic interaction between halothane and epinephrine. METHODS: In adult mongrel dogs anesthetized with halothane, the dysrhythmogenic dose (DD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, was determined in the presence of thoracic epidural mepivacaine or saline. To address the effect of circulating mepivacaine after epidural administration, the authors examined the DD of epinephrine in the presence of intravenous mepivacaine. They also investigated the effect of thoracic epidural anesthesia in bilaterally vagotomized dogs. RESULTS: Epidural mepivacaine significantly increased the DD of epinephrine compared with epidural saline. However, intravenous mepivacaine did not affect the DD of epinephrine, even when the plasma concentration of mepivacaine during the dysrhythmias was twice that in the epidural mepivacaine group. The beneficial effect of epidural mepivacaine was not seen in bilaterally vagotomized dogs. CONCLUSIONS: Thoracic epidural anesthesia attenuated the myocardial sensitization by halothane, and vagal activity had an essential role in this action.
Anesthesia, Epidural↗
Role of the vagus nerve in the antidysrhythmic effect of dexmedetomidine on halothane/epinephrine dysrhythmias in dogs.
BACKGROUND: Dexmedetomidine, an alpha 2-adrenergic agonist, can prevent the genesis of halothane/epinephrine dysrhythmias through the central nervous system. Because stimulation of alpha 2 adrenoceptors in the central nervous system enhances vagal neural activity and vagal stimulation is known to inhibit digitalis-induced dysrhythmias, dexmedetomidine may exert the antidysrhythmic property through vagal stimulation. To address this hypothesis, the effect of dexmedetomidine in vagotomized dogs was examined and compared with that in intact dogs. In addition, the effect of vagotomy on the antidysrhythmic action of doxazosin, an alpha 1 antagonist, was studied. METHODS: Adult mongrel dogs were anesthetized with halothane (1.3%) and monitored continuously for systemic arterial pressure and premature ventricular contractions. Animals were divided into two groups receiving bilateral vagotomy or sham operation. The dysrhythmia threshold was expressed by the dysrhythmogenic dose of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, and plasma concentration of epinephrine at the time when the dysrhythmogenic dose was reached. The threshold was determined in the presence of dexmedetomidine (a selective alpha 2 agonist that crosses the blood-brain barrier) and doxazosin (a selective alpha 1 antagonist that does not penetrate the blood-brain barrier) in the two groups. In addition, the effect of dexmedetomidine in the presence of atropine methylnitrate instead of vagotomy was examined. RESULTS: Vagotomy did not affect the basal vulnerability to halothane/epinephrine dysrhythmias significantly. Although dexmedetomidine dose-dependently prevented the genesis of the dysrhythmias in intact dogs, the beneficial effect of dexmedetomidine was abolished in both the vagotomized and the atropine-treated dogs. On the other hand, vagotomy did not change the antidysrhythmic property of doxazosin. CONCLUSIONS: The vagus nerve plays an important role in the prevention of halothane/epinephrine dysrhythmias by dexmedetomidine in dogs. However, resting vagal tone neither modulates the onset of halothane/epinephrine dysrhythmias nor affects the antidysrhythmic action of doxazosin.
Adrenergic alpha-Agonists↗
Further characterization of the receptor mechanism involved in the antidysrhythmic effect of dexmedetomidine on halothane/epinephrine dysrhythmias in dogs.
BACKGROUND: alpha 2 Adrenoceptors in the central nervous system mediate various physiologic processes, including cardiovascular control. Recently, some of these actions have been reported to be mediated by a nonadrenergic receptor, namely an imidazoline receptor. The authors previously reported that dexmedetomidine, a selective alpha 2 agonist, prevents the genesis of halothane-epinephrine dysrhythmias through a central mechanism. Because dexmedetomidine also binds to imidazoline receptors, we performed the current study to examine the precise receptor mechanism involved in the antidysrhythmic property of dexmedetomidine. METHODS: Adult mongrel dogs were anesthetized with halothane (1.3%) and monitored continuously for systemic arterial pressure and premature ventricular contractions. The dysrhythmogenic dose of epinephrine was defined as the smallest dose producing four or more premature ventricular contractions within 15-s period. We examined the antidysrhythmic action of dexmedetomidine in the presence of two kinds of alpha 2 antagonists, that is, agents that label imidazoline receptors and exert a pharmacologic action through imidazoline receptors (idazoxan and atipamezole) and agents that are nonimidazoline compounds and are lacking in pharmacologic action through imidazoline receptors (rauwolscine and L-659,066). They were given cerebroventricularly. RESULTS: Idazoxan and atipamezole significantly inhibited the antidysrhythmic action of dexmedetomidine, whereas rauwolscine and L-659,066 did not. CONCLUSIONS: Because alpha 2 antagonists having imidazoline or imidazole structures inhibited the antidysrhythmic action of dexmedetomidine, and the inhibition produced by the non-imidazoline alpha 2 antagonists was not significant, imidazoline receptors in the central nervous system are more responsible for the antidysrhythmic action of dexmedetomidine than are alpha 2 adrenoceptors.
Adrenergic alpha-Agonists↗
Rilmenidine prevents epinephrine-induced arrhythmias in halothane-anesthetized dogs.
Stimulation of central alpha 2-adrenoceptors has been known to prevent epinephrine-induced arrhythmias in halothane-anesthetized dogs. Because recent studies suggested that several physiological processes that were traditionally attributed to activation of alpha 2-adrenoceptors, such as hypotensive action, are mediated through imidazoline receptors (IRs), it may be likely that IRs are involved in the antiarrhythmic action. We investigated the hypotensive effect of rilmenidine, a selective IR agonist (1, 3, and 10 micrograms/kg i.v.), and the antiarrhythmic effects of the drug on epinephrine-induced arrhythmias during halothane anesthesia in dogs. Although the hypotensive effect of rilmenidine was not remarkable in the dose range we tested, rilmenidine increased the arrhythmogenic threshold for epinephrine in a dose-dependent manner during halothane anesthesia, achieving statistical significance at 10 micrograms/kg, the highest dose we examined. These results suggest that rilmenidine prevents epinephrine-induced arrhythmias during halothane anesthesia and that this effect is more potent than its hypotensive action.
Adrenergic alpha-Agonists↗
Decrease in vecuronium infusion dose requirements by nicardipine in humans.
This study was designed to analyze quantitatively the interaction of nicardipine with vecuronium using a constant infusion technique. Forty-seven patients undergoing elective otolaryngeal surgery were anesthetized with isoflurane (1% end-tidal) and nitrous oxide (67%). Patients were randomly assigned to receive one of four doses of nicardipine (0, 1, 2, and 3 micrograms.kg-1.min-1). Vecuronium infusion dose requirement was determined as a constant infusion rate which maintained 90% depression of control twitch tension. Nicardipine significantly decreased the vecuronium requirement in a dose-dependent manner, i.e., the vecuronium doses were 0.70 +/- 0.03, 0.55 +/- 0.04, 0.42 +/- 0.04, and 0.37 +/- 0.05 micrograms.kg-1.min-1 at nicardipine doses of 0, 1, 2, and 3 micrograms.kg-1.min-1, respectively. Nicardipine also reduced both the plasma concentration of vecuronium to maintain the 90% depression and the total plasma clearance of vecuronium. The reversal of the vecuronium effect with neostigmine was not influenced by nicardipine. The results indicate that the vecuronium infusion dose requirements are reduced as much as 53% by a clinical dose of nicardipine.
Adult↗
Role of imidazoline-preferring receptors in the genesis of epinephrine-induced arrhythmias in halothane-anesthetized dogs.
BACKGROUND: Drugs with a central alpha 2-adrenergic action can increase the threshold for halothane-epinephrine-induced arrhythmias. Recently, imidazoline-preferring receptors were shown to play a significant role in the hypotensive effect of alpha 2-adrenergic agonists containing an imidazole ring in their structure. To address the question of whether the antiarrhythmic property of the alpha 2-adrenergic agonists was caused by activation of alpha 2-adrenoceptors or imidazoline-preferring receptors in the central nervous system, the effect of an imidazoline (atipamezole) and a nonimidazoline (L-659,066 and yohimbine) alpha 2-adrenergic antagonist were examined as etiologic factors in the genesis of halothane-epinephrine-induced arrhythmias in dogs. METHODS: Adult mongrel dogs were anesthetized with halothane (1.3%) and monitored continuously for systemic arterial pressure and for premature ventricular contractions. The arrhythmogenic dose (AD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, was determined in the presence of atipamezole (an imidazoline compound that acrosses the blood-brain barrier), L-659,066 (a nonimidazoline compound that does not penetrate the blood-brain barrier), and yohimbine (a nonimidazoline compound that passes the blood-brain barrier). These drugs were administered either intravenously or into the cisterna magna to assess the site of action for changes in responsiveness. RESULTS: Intravenous atipamezole decreased the AD of epinephrine in the dose-dependent fashion. However, neither L-659,066 nor yohimbine, administered peripherally, decreased the AD of epinephrine. Central administration of atipamezole also decreased the AD of epinephrine, while L-659,066, even if administered centrally, did not affect the AD of epinephrine in the presence of halothane. CONCLUSIONS: Because the imidazoline ring-containing alpha 2-adrenergic antagonist (atipamezole) potentiated the halothane-epinephrine-induced arrhythmias and the nonimidazole alpha 2-adrenergic antagonist (L-659,066 and yohimbine) did not, it is possible that the imidazoline-preferring, rather than the alpha 2-adrenergic, receptor is responsible for the antiarrhythmic property of alpha 2-adrenergic agonists.
Adrenergic alpha-Antagonists↗
Comparative efficacy of antiarrhythmic agents in preventing halothane-epinephrine arrhythmias in rats.
BACKGROUND: Because the relative efficacy of antiarrhythmic agents on halothane-epinephrine arrhythmias has not been well characterized, this study was undertaken to comparatively evaluate the antiarrhythmic action of Na(+)-, K(+)- and Ca(2+)-channel blockers on epinephrine-induced ventricular arrhythmias during halothane anesthesia in rats. METHODS: Rats were anesthetized at random with either halothane (1.5%), isoflurane (2.0%), or pentobarbital (50 mg/kg intraperitoneally), and the lungs were mechanically ventilated with oxygen. The rats were studied in three consecutive protocols. Protocol I determined the arrhythmogenic thresholds of epinephrine during the three types of anesthesia in 33 rats. Protocol II determined the arrhythmogenic thresholds of epinephrine during halothane anesthesia in 64 rats receiving saline (control) or one of five antiarrhythmic agents. Protocol III measured the duration of epinephrine-induced arrhythmias during halothane anesthesia in 42 rats receiving saline (control) or one of five antiarrhythmic agents. RESULTS: In protocol I, the arrhythmogenic doses of epinephrine during halothane, isoflurane, or pentobarbital anesthesia were 1.7 +/- 3.2, 11.1 +/- 0.6, and 39.0 +/- 3.9 micrograms/kg, respectively, and the corresponding plasma concentrations were 4.3 +/- 0.8, 103.7 +/- 9.2, and 246.7 +/- 28.9 ng/ml, respectively. In protocol II, the arrhythmogenic doses were similar in rats receiving saline and in those receiving lidocaine. The arrhythmogenic doses in rats receiving verapamil, flecainide (Na(+)- and K(+)-channel blocker), E-4031 (K(+)-channel blocker), or amiodarone(K(+)-channel blocker with Na(+)-, Ca(2+)-, and beta-blocking activity) increased significantly, i.e., 4.2, 4.2, 5.5, and 31.7 times control (P < 0.01). In protocol III, lidocaine had no effect on the duration of arrhythmias. Flecainide, E-4031, and verapamil markedly reduced the duration of arrhythmias induced by epinephrine, 8 micrograms/kg intravenously (P < 0.01), whereas only amiodarone markedly reduced the duration of arrhythmias induced by epinephrine, 16 micrograms/kg intravenously (P < 0.01). CONCLUSIONS: It was concluded that agents with K(+)-channel blocking properties were the most effective in preventing halothane-epinephrine arrhythmias in rats.
Amiodarone↗
Effect of local anaesthetics on the stimulus-secretion coupling in bovine adrenal chromaffin cells.
This study was carried out to determine the relative potencies of local anesthetics to inhibit the cholinergic synaptic transmission using cultured bovine adrenal chromaffin cells, and to clarify if the inhibitory action would correlate with biophysical and pharmacological properties. Local anaesthetics (bupivacaine, etidocaine, tetracaine, lignocaine and procaine; 0.02-2 mM) inhibited carbachol-induced catecholamine release from the cells in a concentration-dependent manner. This inhibition was completely reversible. IC50 (concentration of 50% inhibition) of each anaesthetic showed no correlation with the lipid solubility. The local anaesthetics showed greater inhibitory potency at a higher extracellular pH. The results suggest that clinically relevant concentrations of local anaesthetics inhibit the stimulus-secretion coupling in the chromaffin cells. The un-ionized based form plays a major role, and the inhibitory potency does not depend on the lipid solubility of the anaesthetics.
Adrenal Medulla↗
Adrenoceptor mechanism involved in thiopental-epinephrine-induced arrhythmias in dogs.
The authors investigated the role of alpha 1- and beta-adrenoceptors on induction of ventricular arrhythmias during thiopental anesthesia in dogs and compared with that during halothane anesthesia. Throughout this study, arrhythmogenic threshold of epinephrine during thiopental anesthesia was designed to be comparable with that during halothane anesthesia. Phenylephrine, an alpha 1-agonist, and isoproterenol, a beta-agonist, consistently failed to provoke arrhythmias during thiopental or halothane anesthesia. The interaction between phenylephrine and isoproterenol in inducing arrhythmias was synergistic and additive during halothane and thiopental anesthesia, respectively, indicating that adrenoceptor mechanism in thiopental-epinephrine arrhythmias is different from that in halothane-epinephrine arrhythmias. During thiopental anesthesia, incidence of arrhythmias with blood pressure elevation by epinephrine, phenylephrine, or angiotensin II was not different, and increasing heart rate by electrical pacing did not replace isoproterenol in the arrhythmogenic interaction between isoproterenol and phenylephrine. The results indicate that blood pressure elevation due to the combined inotropic action of alpha 1- and beta-adrenoceptor agonists is a critical factor in the genesis of thiopental-epinephrine arrhythmias.
Adrenergic alpha-Agonists↗
Quantitative analysis of pulmonary clearance of exogenous dopamine after cardiopulmonary bypass in humans.
The contribution of the lung to the clearance of exogenous dopamine after cardiopulmonary bypass (CPB) was analyzed quantitatively in humans and compared with the contribution of the lung before CPB. The pulmonary and arterial plasma concentration of dopamine and the pulmonary plasma flow were measured simultaneously during infusion of dopamine. Contribution of the pulmonary circulation was defined as the ratio between clearance through the pulmonary circulation and the total plasma clearance of dopamine. The calculated contribution values after CPB were 12.0, 10.7, 11.4, 16.2, and 16.7% at the doses of 3.0, 4.0, 5.0, 6.0, and 7.0 micrograms.kg-1.min-1, respectively. Those values before CPB were 15.6% and 17.4% at the doses of 1.0 and 2.0 micrograms.kg-1.min-1, respectively. The comparison of the values before and after CPB did not achieve statistical significance. Furthermore, there were no significant correlations between the pulmonary clearance after CPB and mean pulmonary arterial pressure, pulmonary vascular resistance, or CPB time. The results suggest that the pulmonary clearance mechanism for dopamine after CPB is maintained as effectively as that before CPB and is not influenced by pulmonary hypertension or CPB time.
Adult↗