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The dose of propranolol varied from 80 to 160 mg/day. The proportional decrease in basal heart frequency varied from 20 to 33%, with an average of 25.4 +/- 3.9% in the propranolol group, maintaining a mean of 24.3 +/- 3.6% decrease in the postoperative period. Differences on clinical recovery of the postoperative ileus were not found. Significant differences on electromyographic patterns were not observed between the groups, except for the presence of a greater number of short-duration contractions in the second postoperative day in the beta-blocked group.
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Cardiovascular responses during a graded lower body negative pressure (LBNP) protocol were compared before and after atropine and propranolol administration to test the hypothesis that both sympathetic and parasympathetic control of cardio-acceleration are associated with syncopal predisposition to orthostatic stress in healthy subjects. Eleven men were categorized into two groups having high (HT, N = 6) or low (LT, N = 5) tolerance based on their total time before the onset of presyncopal symptoms. HT and LT groups were similar in physical characteristics, fitness, and baseline cardiovascular measurements. Atropine treatment had no effect on LBNP tolerance or mean arterial pressure at presyncope, despite an atropine-induced increase in heart rate. Propranolol treatment reduced (p<0.05) LBNP tolerance in both groups. Diminished LBNP tolerance after propranolol administration was associated with reductions in cardiac output, whereas increase in systemic peripheral resistance from baseline to presyncope was unaffected by propranolol. Reduction in cardiac output and LBNP tolerance after beta blockade reflected a chronotropic effect because lower LBNP tolerance for the HT (-50%) and LT (-39%) groups was associated with dramatic reductions (p <0.05) in the magnitude of LBNP-induced tachycardia without significant effects on stroke volume at presyncope. Absence of an atropine-induced difference in cardiac output and systemic peripheral resistance between HT and LT groups failed to support the notion that cardiac vagal withdrawal represents a predominant mechanism that could account for differences in orthostatic tolerance. Because a reduction in LBNP tolerance in both HT and LT groups after propranolol treatment was most closely associated with reduced tachycardia, the data suggest that a primary autonomically mediated mechanism for maintenance of mean arterial pressure and orthostatic tolerance in healthy subjects is beta adrenergic-induced tachycardia.
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The correlation coefficient between pLD and EM (0.86) was significantly less than that between cLD and EM (0.96), however it was not significantly different from that between TD and EM (0.85). The precision value of pLD (0.14) was the same as that of TD (0.14).
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Swimming increased plasma lactate concentration less (P<0.05) in rats fed omega-3PUFA than rats fed omega-6PUFA. Swimming increased plasma concentrations of glucose and glucagon, cyclic adenosine monophosphate (cAMP) concentration and phosphoenolypruvate carboxykinase mRNA in the liver, and cAMP concentration in the hindlimb muscle more (P<0.05) in rats fed omega-3PUFA than in rats fed omega-6PUFA. Phentolamine and propranolol enhanced swim-induced lactacidemia in the omega-3PUFA group, while they decreased the lactacidemia in the omega-6PUFA group. Propranolol enhanced swimming-induced hyperglycemia in the omega-6PUFA group more than in the omega-3PUFA group.
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A challenge dose of nicotine (0.4 mg kg-1 s.c.) produced a long-lasting potentiation (LLP) of field EPSPs evoked in the dentate gyrus by stimulation of the medial perforant path of urethane-anaesthetized rats primed four weeks previously with seven daily injections of nicotine (0.8 mg kg-1 s.c.). The same dose of nicotine did not alter EPSPs evoked in rats primed with saline vehicle. Systemic injection of either mecamylamine or propranolol, 30 min before nicotine challenge, prevented induction of LLP without affecting baseline EPSPs but neither drug affected LLP when given after it was established. Since the nicotine-priming regime is known to increase tyrosine hydroxylase activity and hippocampal noradrenaline release in response to nicotine challenge, the results suggest that systemic injection of nicotine released sufficient noradrenaline in nicotine-primed rats to induce a beta-adrenoceptor-mediated LLP.
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Eight anaesthetized pigs (43+/-4 kg) were studied at rest and after IV â-blockade (10 mg propranolol) before and after MCP. Muscular counterpulsation was performed on both thighs using trains (75 ms duration) of multiple biphasic electrical impulses with a width of 1 ms and a frequency of 200 Hz at low (10 V) and high (30 V) amplitude. ECG-triggering was used to synchronize stimulation to a given time point. LV pressure-volume relations were determined using the conductance catheter. After baseline measurements, MCP was carried out for 10 minutes at low and high stimulation amplitude. The optimal time point for MCP was determined from LV pressure-volume loops using different stimulation time points during systole and diastole. Best results were observed during end-systole and, therefore, this time point was used for stimulation.
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There were 53 infantile haemangioma cases treated with oral propranolol. Treatment responses occurred as early as two weeks after propranolol administration in 91.5% of the follow-up patients, with all 53 cases achieving the desired treatment responses two months after propranolol was initiated. No significant differences in treatment responses were found between propranolol as a mono-therapy or as a combination therapy with prednisolone at the two-week (p value 0.13) and one-month follow-ups (p value 0.98). Complications were documented in three cases (5.6%) when the propranolol dose was increased, and these were asymptomatic hypoglycaemia in two cases and one case of hypotension.
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Intragastric Dai-Kenchu-To induced phasic contractions in the antrum, duodenum, and jejunum. Zanthoxylum fruit elicited phasic contractions mainly in the duodenum and jejunum, whereas dried ginger rhizome induced phasic contractions in the antrum. Ginseng root had no effect. Phasic contractions induced by intragastric Dai-Kenchu-To were inhibited by atropine and hexamethonium at all sites, although ondansetron inhibited these contractions in the antrum and duodenum.
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Burn trauma is known to induce a significant rise in circulating catecholamine levels and despite catecholamines being potent endogenous vasoactive agents with known actions on microvascular permeability, their effect on burn edema has been poorly investigated. The present study in rats investigated the role and importance of adrenergic receptor subtypes in the regulation of basal capillary permeability in normal skin and hyperpermeability in partial- and full-thickness skin burns. Edema was quantified by spectrophotometric analysis of extravasated Evans blue-albumin. Evaluation was based on intravenous administration of the following adrenergic agonists and antagonists: l-phenylephrine (alpha(1)-receptor agonist), prazosin (alpha(1)-receptor antagonist), clonidine (alpha(2)-receptor agonist), yohimbine (alpha(2)-receptor antagonist), prenalterol (beta(1)-receptor agonist), terbutaline (beta(2)-receptor agonist), or propranolol (beta(1)- and beta(2)-receptor antagonist). Results showed increased capillary permeability in normal skin following administration of terbutaline (p<0.01) and yohimbine (p<0.01). In partial-thickness burns, clonidine significantly (p<0.05) reduced edema formation, whereas in full-thickness burns edema was significantly reduced by clonidine (p<0.05) and l-phenylephrine (p<0.01). In conclusion, the inhibition of postburn edema induced by stimulation of alpha(1)-receptors (l-phylephrine) and alpha(2)-receptors (clonidine) could be secondary to increased vascular resistance and reduced tissue perfusion pressure and/or suppressed inflammatory reaction in the burn injury. In the treatment of burn patients, clonidine is particularly interesting since the agent has previously been proven to induce potent analgesia in thermally injured.
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To check the relationship of impaired glucose tolerance with the other atherosclerotic risk factors, fasting blood sugar and the standard two hour glucose tolerance test, serum tryglyceride, serum cholesterol, cyclosporine through level (in renal transplant recipients) and hemoglobin A1C were measured in 55 stable renal transplant recipients, 55 hemodialysis patients and 55 healthy controls with similar demographic characteristics. Patients with diabetes mellitus and propranolol consumers were excluded. The mean age and female to male ratio were 39 +/- 7 years and 23/22, respectively.
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This study used monophasic action potential (MAP) to examine the effect of nicorandil, a K+ channel opener, on repolarization abnormalities induced by epinephrine in the LQT1 form of congenital long-QT syndrome in which the KvLQT1 mutation underlies the defect in the channel responsible for the slowly activating component of the delayed rectifier potassium current.
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Our experiments demonstrate a significant increase in NNK-induced PAC multiplicity in animals chronically exposed to the beta-adrenergic agonist epinephrine or theophylline which causes intracellular accumulation of the beta-adrenergic second messenger cAMP. On the other hand, our data show that administration of the beta-adrenergic antagonist propranolol prior to each NNK injection significantly inhibited the development of PACs.
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Pharmaceuticals, among them the β-adrenoceptor blocker propranolol, are an important group of environmental contaminants reported in European waters. Laboratory exposure to pharmaceuticals on marine species has been performed without considering the input of the ecosystem flow. To unravel the ecosystem response to long-term exposure to propranolol we have performed long-term exposure to propranolol and low salinity in microcosms. We applied shotgun proteomic analysis to gills of Mytilus edulis from those Baltic Sea microcosms and identified 2071 proteins with a proteogenomic strategy. The proteome profiling patterns from the 587 highly reproductive proteins among groups define salinity as a key factor in the mussel's response to propranolol. Exposure at low salinity drives molecular mechanisms of adaptation based on a decrease in the abundance of several cytoskeletal proteins, signalling and intracellular membrane trafficking pathway combined with a response towards the maintenance of transcription and translation. The exposure to propranolol combined with low salinity modulates the expression of structural proteins including cilia functions and decreases the expression of membrane protein transporters. This study reinforces the environment concerns of the impact of low salinity in combination with anthropogenic pollutants and anticipates critical physiological conditions for the survival of the blue mussel in the northern areas.