Heart rate effects

Khat produces sympathomimetic effects, increasing heart rate and blood pressure. When khat is chewed, the increases are gradual, maximizing at about 2 hours and lasting for 4 hours. However, tolerance develops to blood pressure and heart rate effects in habitual users. Mydriasis and increases in respiration also occur. Cathinone induces thermogenesis in brown adipose tissue, which is mediated by jS-adrenergic receptors (Tariq et al. 1989). 

Vivian JA, Kishioka S, Butelman ER, Broadbear J, Lee KO, Woods JH. (1998). Analgesic, respiratory, and heart rate effects of cannabinoid and opioid agonists in rhesus monkeys antagonist effects of SR 141716A. J Pharmacol Exp Ther. 286(2) 697-703. 

Clapman, R. M. Cain, C. A. Absence of heart-rate effects... 

After determination of the heart rate effect and the lethal effect, the rats are sacrificed for determinations of brain tissue concentrations. The whole brain is removed and tissue anesthetic concentration is determined by gas chromatography. 

The vagus nerve acts to decelerate heart rate via a cholinergic input to the sinoatrial node, and atropine blocks this action, leading to an increase in heart rate. Effects are noted at doses as low as 0.6 mg per 70 kg of body weight, and the maximum increase of 35 to 50 beats per min is achieved at doses of 2 to 3 mg per 70 kg of body weight. Heart rate begins to increase within 15 min of an IM injection, peaks at 60 to 90 min, and can persist for 4 hr (Penetar, 1990 Penetar, Haegerstrom-Portnoy, Jones, 1988). 

Heart rate effects similar to those reported for verapamil have been reported to occur after the intravenous administration of diltiazem to human patients and in dogs administered verapamil, diltiazem, and 2-substituted aminoindenes (52, 95, 140, 165) ... 

Syringa vulgaris Malaria Verbascoside Heart rate effect Decrease of heart rate. [51]... 

A drug that blocks the heart rate effect of a slow IV infusion of phenylephrine is... 

Bui, L.T., D.T. Nguyen, and P.J. Ambrose. 2006. Blood pressure and heart rate effects following a single dose of bitter orange. Ann. Phannacother. 40(l) 53-57. 

SAGAWA In the earlier study the excised preparation showed a heart rate between 120 and 140 and we really couldn t see any clear-cut effect of the heart rate on the maximum elastance value when we paced the heart at faster rates. Recently it has become possible to study the heart rate effect between 60 and 120 cpm, and yes, there was a clear-cut effect there roughly a 20-30% increase in end systolic elastance. Above 120 cpm the increase became very small all the way to 180 cpm, probably an extra 10% increase. Above 180 cpm, statistical analysis shows an increase, although it is very small. 

Nitrous oxide produces respiratory depression (38,39). It has been shown to produce a direct myocardial depressant effect in dogs (40) and in humans breathing a 40% N2O/60% oxygen mixture (41) however, this may be offset by the activation of the sympathetic nervous system (42). The combination of nitrous oxide and opioids can produce decreases in myocardial contractiHty, heart rate, and blood pressure (43). 

Desflurane is less potent than the other fluorinated anesthetics having MAC values of 5.7 to 8.9% in animals (76,85), and 6% to 7.25% in surgical patients. The respiratory effects are similar to isoflurane. Heart rate is somewhat increased and blood pressure decreased with increasing concentrations. Cardiac output remains fairly stable. Desflurane does not sensitize the myocardium to epinephrine relative to isoflurane (86). EEG effects are similar to isoflurane and muscle relaxation is satisfactory (87). Desflurane is not metabolized to any significant extent (88,89) as levels of fluoride ion in the semm and urine are not increased even after prolonged exposure. Desflurane appears to offer advantages over sevoflurane and other inhaled anesthetics because of its limited solubiHty in blood and other tissues. It is the least metabolized of current agents. 

Midazolam and diazepam decrease arterial pressure without a change ia heart rate. Like thiopeatoae, midazolam is a respiratory depressant. Advantages of midazolam are its amnestic effect, coupled with less postoperative depression (102). A reversal agent for the benzodiazepiaes has also become available. Flumazenil [78755-81-4] C25H24FN2O2, (5) displaces the beazodiazepiaes from their receptor but has Httie demoastrable activity of its owa (103,104). 

The Class I agents decrease excitability, slow conduction velocity, inhibit diastoHc depolarization (decrease automaticity), and prolong the refractory period of cardiac tissues (1,2). These agents have anticholinergic effects that may contribute to the observed electrophysiologic effects. Heart rates may become faster by increasing phase 4 diastoHc depolarization in SA and AV nodal cells. This results from inhibition of the action of vagaHy released acetylcholine [S1-84-3] which, allows sympathetically released norepinephrine [51-41-2] (NE) to act on these stmctures (1,2). 

Isoproterenol. Isoproterenol hydrochloride is an nonselective P-adrenoceptor agonist that is chemically related to NE. It mimics the effects of stimulation of the sympathetic innervation to the heart which are mediated by NE. It increases heart rate by increasing automaticity of the SA and AV nodes by increasing the rate of phase 4 diastoHc depolarization. It is used in the treatment of acute heart block and supraventricular bradyarrhythmias, although use of atropine is safer for bradyarrhythmias foUowing MI (86). 

P-Adrenoceptor Blockers. There is no satisfactory mechanism to explain the antihypertensive activity of P-adrenoceptor blockers (see Table 1) in humans particularly after chronic treatment (228,231—233). Reductions in heart rate correlate well with decreases in blood pressure and this may be an important mechanism. Other proposed mechanisms include reduction in PRA, reduction in cardiac output, and a central action. However, pindolol produces an antihypertensive effect without lowering PRA. In long-term treatment, the cardiac output is restored despite the decrease in arterial blood pressure and total peripheral resistance. Atenolol (Table 1), which does not penetrate into the brain is an efficacious antihypertensive agent. In short-term treatment, the blood flow to most organs (except the brain) is reduced and the total peripheral resistance may increase. 

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. 

Nicorandil. Nicorandil is a potassium channel opener that can lower blood pressure 21, 20, and 29 mm Hg after single oral doses of 10, 20, and 30 mg, respectively (250). There are no significant changes ia heart rate. Headache is the primary side effect. Nicorandil has potent coronary vasodilator effects. It causes sustained vasodilation of arteriolar resistance and venous capacitance blood vessels, thus reduciag cardiac preload and aftedoad. 

Cromakalim. Cromakalim has along half-life (254). Cromakalim at an oral dose of 1.5 mg ia humans significantly lowers blood pressure 19/12 mm Hg (systohc/diastoHc pressure). It iacreases reaal blood flow, PRA, and heart rate. Cromakalim has bronchodilating activity that is beneficial for hypertensive asthmatic patients. Because of some undesirable effects seen ia cardiac papillary muscles of animals oa long-term treatmeat, future clinical trials are to be carried out usiag the active enantiomer, lemakalim (BRL 38227). 

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