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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study tested the feasibility of neodymium:YAG laser photocoagulation of selected sinus node areas to depress sinus rate responsiveness. In 14 open-chest dogs, origin of the sinus impulse (O point) was electrically mapped from the epicardium before and during isoproterenol infusion. Epicardial laser photocoagulation was applied to the O point observed during isoproterenol infusion and stepwise to remapped new O points until a 30 +/- 5% decrease in heart rate occurred. Long-term effects were assessed by Holter monitoring and electropharmacologic testing preoperatively and up to 10 weeks or 6 months. Mean (+/- SEM) percent decreases were observed at 10 weeks in the following parameters: average 24-hour heart rate, 17.4 +/- 5.0%; maximum heart rate on Holter, 30.5 +/- 3.5%; heart rate during pharmacologic autonomic blockade, 32.7 +/- 3.5%; and maximum heart rate on isoproterenol, 23.1 +/- 4.6% (all p less than 0.01). Curves with pacemaker recovery time plotted against control cycle length remained unchanged. Holter monitoring did not show excessive bradycardic episodes even after administration of propranolol. In three control dogs (sham operation), sinus node function remained unchanged. Histologic study of the irradiated area showed replacement by inflammatory cells, fibrosis, and cartilage formation with surrounding normal cells and occasional cells resembling pacemaker-like cells at the caudal end of the sinoatrial node. This study suggests that 1) map-guided graded laser photocoagulation of sinus node regions showing earliest activation during catecholamine stimulation successfully limits maximum heart rates without causing significant bradycardia, 2) the effects are long lasting, and 3) the remaining pacemaker behaves like the sinus node. Laser modification of sinus node function could become a form of nonpharmacologic heart rate control in patients with coronary artery disease undergoing surgery and in the syndrome of inappropriate sinus tachycardia.
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PMID:Modification of sinus node function by epicardial laser irradiation in dogs. 229 39

We evaluated the clinical effectiveness of esmolol, an ultra-short-acting, cardioselective beta-adrenergic receptor blocker, in controlling sinus tachycardia and increased systolic blood pressure occurring perioperatively in 30 ASA physical status II or III patients having elective, non-cardiac surgery. Esmolol 80 mg I.V. bolus (N = 15) or placebo (N = 15) followed by 12 mg/min or placebo were infused in 30 isoflurane-anesthetized patients using a randomized double-blind study design. The bolus plus infusions were given when surgical stimuli caused heart rate to exceed 95 bpm or systolic blood pressure 140 mm Hg. Esmolol significantly decreased heart rate (107 +/- 4, mean +/- SEM to 99 +/- 4, mean +/- SEM bpm) within 45 sec after starting the bolus plus infusion; the placebo had no effect, heart rate being 105 +/- 4 before and 106 +/- 3 bpm after the bolus plus infusion. Patients given esmolol continued to have heart rates significantly lower than patients given placebo injections throughout a six min infusion (Ex., at 5 min 81 +/- 3 vs 91 +/- 4 bpm). The study demonstrated no apparent effect of esmolol on blood pressure but that esmolol is effective in treating perioperative sinus tachycardia.
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PMID:Use of esmolol during anesthesia to treat tachycardia and hypertension. 167 91

Fifteen patients with toxic shock syndrome were seen in a 2-yr period at a university medical center. Five (33%) patients had severe cardiorespiratory failure and underwent hemodynamic monitoring before and during infusion of dobutamine hydrochloride (dobutamine). Three distinct hemodynamic stages were identified. Initially there was a hyperdynamic cardiovascular state with a high cardiac index (5.5 +/- 0.9 L/min X m2, mean +/- SEM), normal pulmonary artery wedge pressure (11.5 +/- 1.5 mm Hg), and low mean blood pressure (66 +/- 5 mm Hg). The second stage (decompensated) revealed myocardial dysfunction with decreased left ventricular fractional shortening. Serial two-dimensional and M-mode echocardiograms performed on two patients showed left atrial and left ventricular end-diastolic diameters at the upper limits of normal. The mean blood pressure recorded for all five patients was essentially unchanged; however, cardiac index decreased to 3.1 +/- 0.4 L/min X m2 and wedge pressure increased to 17.5 +/- 2.1 mm Hg. This decompensated stage responded to iv infusion of dobutamine by an increase in cardiac index to 5.4 +/- 0.5 L/min X m2, a decrease in wedge pressure to 11.0 +/- 2.0 mm Hg, and an increase in mean blood pressure to 100 +/- 10 mm Hg. During recovery, echocardiograms returned to normal. All five patients developed severe adult respiratory distress syndrome. All had reversible ECG findings of sinus tachycardia, diffuse loss of voltage, flattened T waves and diffuse nonspecific ST-T wave changes. Our findings suggest a reversible toxic cardiomyopathy as the cause of cardiorespiratory failure in toxic shock syndrome. Our experience suggests inotropic support with dobutamine is beneficial in selected cases.
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PMID:Cardiorespiratory failure in toxic shock syndrome: effect of dobutamine. 397 25

Dopamine, administered at a constant infusion rate of 1-2 micrograms/min into the cannulated sinus node artery of the isolated dog atrium, decreased sinus cycle length (SCL) from 630 +/- 19 to 501 +/- 22 msec (mean +/- SEM, 38 trials in 12 atria). However, on sinoatrial conduction time (SACT) estimated by a constant atrial pacing method, dopamine produced 2 types of response (shortening and lengthening) with sinus tachycardia. In 24 trials in 11 atria, the drug decreased SACT from 86 +/- 8 to 56 +/- 4 msec, and in 14 trials in 6 atria it increased SACT from 67 +/- 7 to 101 +/- 9 msec. In general, the effects of dopamine on SACT were dependent on the control levels of SCL: dopamine caused a reduction of SACT at small levels of SCL and a prolongation at large levels. At a control sinus rate of 120 beats/min, dopamine usually shortened SACT. Dopamine-induced shortening of SACT was blocked by a beta-adrenoceptor blocker, propranolol, and an uptake blocker, imipramine, but not by a dopaminergic inhibitor, sulpiride. Furthermore, dopamine-induced lengthening of SACT tended to be suppressed by propranolol, but not by sulpiride. It is concluded that the dopamine-induced changes in SACT are mediated via beta-adrenergic mechanism and partially due to a tyramine-like action.
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PMID:Effects of dopamine on sinoatrial conduction in isolated, blood-perfused dog atria. 651 92