Drugs online research references
Am J Physiol. 1991 Nov;261(5 Pt 2):H1499-507.
Effects of beta-adrenergic agonists on splanchnic vascular volume and cardiac output.
Chang PI, Rutlen DL.
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.
The effect of beta-adrenergic agonists on splanchnic intravascular volume (SIV), measured with radionuclide imaging, and the subsequent influence of such volume changes on cardiac output (CO) were examined in 40 anesthetized dogs. Isoproterenol (6 micrograms/min) caused a decrease in total SIV of 12 +/- 1% (P less than 0.001). The decrease was due entirely to a decrease in splenic volume of 24 +/- 3% (P less than 0.001), since volume increased in the remainder of the splanchnic vasculature [hepatic and mesenteric volume increased 12 +/- 2% (P less than 0.001) and 11 +/- 3% (P less than 0.02), respectively]. CO increased from 1,724 +/- 187 to 3,138 +/- 321 ml/min (P less than 0.001); after subsequent splenectomy, isoproterenol caused a similar increment. Isoproterenol-associated SIV changes were not altered by carotid denervation and vagotomy or by beta 1-adrenergic inhibition with metoprolol but were abolished by nonselective beta-adrenergic inhibition with propranolol. With a larger dose of metoprolol and smaller dose of isoproterenol to minimize beta 1-adrenergic effects, the isoproterenol-associated CO increment was attenuated (P less than 0.01) by splenectomy. With the beta 2-agonist terbutaline (41 micrograms/min) after metoprolol, total SIV decreased 15 +/- 4% (P less than 0.001). After subsequent alpha-adrenergic inhibition with phenoxybenzamine, terbutaline caused no change in SIV and an attenuated (P less than 0.05) increase in CO. Thus beta-adrenergic agonist administration causes a decrease in total SIV due entirely to a decrease in splenic volume. The SIV decrement is dependent on beta 2- and alpha-adrenoceptor stimulation and appears to enhance CO only if beta 1-adrenergic effects are minimized.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1683172&dopt=Abstract
Bratisl Lek Listy. 1990 Sep;91(9):701-4.
[Systolic and diastolic intervals in patients with hypertrophic obstructive cardiomyopathy before and after withdrawal of verapamil]
[Article in Czech]
Jandik J, Kvasnicka J, Vokrouhlicky L.
Ustav patologicke fyziologie LFUK, Hradec Kralove.
Mechanocardiographic investigations were carried out in a group of eight patients with hypertrophic obstructive cardiomyopathy (HOCM) who had been implanted a DDD pacemaker which allowed efficient therapy to be administered in the combination of metoprolol in the dose of 300 mg/day and verapamil in doses of 240-480 mg/day. The investigation was repeated one week after temporary withdrawal of verapamil. The control group consisted of six patients with idiopathic third-degree-complete AV block with implanted DDD pacemakers. Over the period of 24 hours before investigation, these patients received 300 mg of metoprolol. All the patients had the same heart rate (70 bpm) and a constant PQ interval (0.18 s). Statistical analysis of the obtained data revealed the following findings: 1. There was no difference between the control group and the group of HOCM patients treated with verapamil. 2. Withdrawal of verapamil in HOCM patients resulted in a significant prolongation of the 2-0 interval and shortening of the O-c interval recorded on apexcardiogram compared to the control group. In conclusion, verapamil affects LV diastolic parameters in patients with HOCM and the changes are compatible with the beneficial effects of verapamil. These changes may however result partly from increased left atrial pressure due to atrial poisoning with verapamil.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2224552&dopt=Abstract
wanadoo.fr
SEVERITY: Beta-blocker intoxication is not frequent but can produce particularly severe or fatal conditions which must not be underestimated. Severity of beta-blocker intoxication varies from one compound to another. The more toxic drugs are propranolol, sotalol, oxprenolol, metoprolol, atenolol, acebutolol, labetalol, and carvedilol. Besides the drug type, history taking can provide a precise assessment of risk, particularly important in when elderly patients with a cardiovascular history have taken more than 20 tablets, when emergency care is provided late, and when other cardiotoxic or psychotoxic drugs have been coingested. IMPLICATIONS: The diagnosis of beta-blocker intoxication must be suspected in any case associating hypotension and bradycardia. The main cardiovascular complications are cardiogenic shock, atrio-ventricular conduction disorders, and obviously life-threatening ventricular arrhythmia with cardiac arrest. Centrally induced respiratory arrest is a rare but dreadful consequence which can occur suddenly even without hemodynamic failure. Neurologic toxicity is mainly expressed by consciousness disorders and more sporadically by seizures. Laboratory tests show variable serum potassium, lactic acidosis, hypoxia-hypercapnia resulting from hypoventilation, and rarely hypoglycemia. The ECG should be recorded early because electrocardiographic signs usually appear before clinical signs and QRS enlargement is a factor predictive of severe ventricular arrhythmia. INTENSIVE CARE: The patient must be placed in an intensive care unit for continuous multiparametric monitoring. Besides gastric evacuation and symptomatic measures, treatment essentially requires glucagon for its positive inotropic effect after high intravenous doses. If glucagon infusion is ineffective or unavailable, an alternative would be to use high doses of vasoactive agents, choosing isoproterenol or epinephrine as the first intention drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10862260&dopt=Abstract
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