Effects on heart

P-Adrenoceptors have been subdivided into P - and P2-adrenoceptors. A third subset called nontypical P-adrenoceptors or P -adrenoceptors have been described but are stiU the subject of debate. In terms of the interactions with various subsets of P-adrenoceptors, some antagonists are nonselective in that they antagonize the effects of activation of both P - and P2-adrenoceptors, whereas others are selective for either P - or P2-adrenoceptors. P - and P2-adrenoceptors coexist in almost all organs but generally, one type predominates. The focus herein is on the clinically relevant P -adrenoceptor-mediated effects on heart and on P2-adrenoceptor-mediated effects on smooth muscles of blood vessels and bronchioles, the insulin-secreting tissue of the pancreas, and skeletal muscle glycogenolysis for side effects profile (36). 

Verapamil (Table 1), the first slow channel calcium blocker synthesized to selectively inhibit the transmembrane influx of calcium ions into cells, lowers blood pressure in hypertensive patients having good organ perfusion particularly with increased renal blood flow. Sustained-release verapamil for once a day dosing is available for the treatment of hypertension. Constipation is a prominent side effect. Headache, dizziness, and edema are frequent and verapamil can sometimes cause AV conduction disturbances and AV block. Verapamil should not be used in combination with -adrenoceptor blockers because of the synergistic negative effects on heart rate and contractile force. 

True. Caffeine is a mild stimulant that in moderate dosage does little harm and provides a lift . When taken in excess it can have an adverse effect on heart rate. 

Patients with asymptomatic left ventricular systolic dysfunction and hypertension should be treated with P-blockers and ACE inhibitors. Those with heart failure secondary to left ventricular dysfunction and hypertension should be treated with drugs proven to also reduce the morbidity and mortality of heart failure, including P-blockers, ACE inhibitors, ARBs, aldosterone antagonists, and diuretics for symptom control as well as antihypertensive effect. In African-Americans with heart failure and left ventricular systolic dysfunction, combination therapy with nitrates and hydralazine not only affords a morbidity and mortality benefit, but may also be useful as antihypertensive therapy if needed.66 The dihydropyridine calcium channel blockers amlodipine or felodipine may also be used in patients with heart failure and left ventricular systolic dysfunction for uncontrolled blood pressure, although they have no effect on heart failure morbidity and mortality in these patients.49 For patients with heart failure and preserved ejection fraction, antihypertensive therapies that should be considered include P-blockers, ACE inhibitors, ARBs, calcium channel blockers (including nondihydropyridine agents), diuretics, and others as needed to control blood pressure.2,49... 

The second factor that exerts control on heart rate is the release of the catecholamines, epinephrine and norepinephrine, from the adrenal medulla. Circulating catecholamines have the same effect on heart rate as direct sympathetic stimulation, which is to increase heart rate. In fact, in the intact heart, the effect of the catecholamines serves to supplement this direct effect. In a denervated heart, circulating catecholamines serve to replace the effect of direct sympathetic stimulation. In this way, patients who have had a heart transplant may still increase their heart rate during exercise. 

In Phase I clinical trials with stable renal transplant patients, FTY720 led to a transient reduction in the number of circulating lymphocytes whilst being well-tolerated. Treatment was associated with a mild reduction in heart rate that was maximal 6 h after the first dose and returned to baseline with continuous treatment [52,53]. The mild effect on heart rate is believed to arise from SlPj and/or SlP3-mediated activation of G-protein-gated inwardly rectifying potassium (GIRK) channels in atrial myocytes [54-56]. 

Asthmatic bronchitis, effect on heart, 5 107 ASTM analysis methods, 10 508. See also American Society for Testing Materials (ASTM)... 

Bromperidol, 4 360t Brompheniramine, 4 359t Bromyrite, 4 304 Bronchitis, effect on heart, 5 107 Bronidox, 4 358t Bronopol, 4 358t Brpnsted acids, 12 190 Brpnsted-Lewis superacids, 12 191-192 Brpnsted superacids, 12 191 Bronze(s), 24 796... 

Chromous chloride hexahydrate, 6 531 Chromous sulfate heptahydrate, 6 531 Chromyl chloride, molecular formula, properties, and uses, 6 561t Chromyl compounds, 6 526, 536 Chromyl fluoride, 6 535 Chromyl perchlorate, anhydrous, 18 279 Chronic asthmatic bronchitis, effect on heart, 5 107... 

Tracheobronchitis effect on heart, 5 107 Trachoma, 74 338 Tracking resistance testing, 79 587 Traction, 3 726-727 Traction thickener, 22 65 Trade... 

Data adequacy The key study was well designed and conducted and documented a lack of effects on heart and lung parameters as well as clinical chemistry. Pharmacokinetic data were also collected. The compound was without adverse effects when tested as a component of metered-dose inhalers on patients with COPD. Animal studies covered acute, subchronic, and chronic exposure durations and addressed systemic toxicity as well as neurotoxicity, reproductive and developmental effects, cardiac sensitization, genotoxicity, and carcinogenicity. The values are supported by a study with rats in which no effects were observed during a 4-h exposure to 81,000 ppm. Adjustment of the 81,000 ppm concentration by an interspecies and intraspecies uncertainty factors of 3 each, for a total of 10, results in essentially the same value (8,100 ppm) as that from the human study. ... 

Within a programme aimed at the development of thyroid hormone analogues as potentially useful plasma cholesterol-lowering agents, the pyrida-zinone derivative SK F L-94901 (98) has been prepared and investigated in the U.K. [419-422]. Whereas naturally occurring thyroid hormones cannot be employed for this purpose because of their undesirable effect on heart rate, (98) has been found to represent a potent thyromimetic which retains hepatic activity but lacks cardiac activity. Structural modifications and QSAR studies have been carried out [422]. 

Atropine Sulfate Dose Effects on Heart Rate... 

Atropine s peripheral effects on heart rate (Fig. 63) and blood pressure (not shown) are substantial and very rapid in onset, peaking at about 30-60 minutes. In this graph, baseline heart rate is shown as zero. Maximum heart rate at the ID50 is thus about 125 (60 + 65). It remains at this level for about 3 hours and returns to normal at about 9 hours. At the ID50, minor changes in the electrocardiogram were noted in a study by Hayes et al.. These changes rapidly revert to normal as HR declines. 

When treating insomnia without depression, doxepin and amitriptyline (both tricyclic antidepressants) can be administered in low doses (25-100 mg) at bedtime. These antidepressants, however, do have troublesome anticholinergic side effects (dry mouth, constipation, blurred vision, dizziness) and adverse effects on the heart, and they can be lethal if taken in overdose. Because of their effect on heart function, these antidepressants should be avoided in patients with heart problems and administered cautiously, if at all, to those who are already receiving one of any number of newer antidepressants that inhibit the metabolism of the TCAs. 

Cardiovasciilar system - in vitro systems for potential to prolong QT interval, effects on heart and blood vessels, anaesthetised and conscious (reflexes intact) animals with effects on heart rate, blood pressure, ECG... 

Cardiovascular effects Drugs that increase cholinergic activity may have vagotonic effects on heart rates (eg, bradycardia). The potential for this action may be particularly important in patients with sick sinus syndrome or other supraventricular cardiac conduction conditions. 

Cardiovascular disease Acute administration of 2 drops of apraclonidine has had minimal effect on heart rate or blood pressure however, observe caution in treating patients with severe cardiovascular disease, including hypertension. 

Sometimes a pharmacological effect is the sum of more than one drug effect. This may call for the combination of two or more models, as shown in Fig. 4 where both tachycardia and bradycardia are implied as drug effects. In this case, the model used consisted of two equations equal to Eq. (10), but with an opposite direction of effect on heart rate and different model parameter values. 

D. Nitroglycerin can reduce preload, which in turn reduces wall tension and increases subendocardial blood flow. Nitroglycerin also reduces afterload, but this is a small effect compared to the reduction in preload. Its effects on heart rate and contractility are minimal, and if anything reflex tachycardia and increase in contractility would be detrimental effects of too much nitroglycerin. 

Answer This feature of bradycardia is typical of patients who take (3-blockers, which should be continued so they result ultimately in better anesthetic management. The drugs given could have been modified (i.e., etomidate instead of propofol, which does not raise or may cause a slower heart rate). The potent opioids in the fentanyl family all cause vagal transmitted bradycardia. The muscle relaxant vecuronium (norcuron) has no effect on heart rate and could have been replaced by pancuronium, which has a vagolytic effect and will counter bradycardia in the usual induction bolus doses. 

Tricyclic antidepressants have effects on heart rate (HR), blood pressure (BP), and three distinct measures of the electrocardiogram (EKG). The EKG parameters affected are (1) the PR interval, which represents depolarization of the aorta (2) the QRS duration, which represents intraventricular conduction time and (3) the QTc, which represents the depolarization and subsequent repolarization of the ventricles, corrected for cardiac rate. 

Pharmacological manipulation of heart function can be achieved in two ways in the semi-intact heart preparation. Flies can be fed various agents in their food followed, at some later time point, by an analysis of heart function. Alternatively, it is possible to apply the chemicals via the artificial hemolymph used to bathe the heart during the image capture. This latter method permits an assessment of acute effects on heart performance and a determination of the dose dependence of the effect (Fig. 3f). 

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