Drugs online research references
Anaesthesia. 1988 Mar;43 Suppl:37-41.
Effect of propofol on cerebrospinal fluid pressure and cerebral perfusion pressure in patients undergoing craniotomy.
Ravussin P, Guinard JP, Ralley F, Thorin D.
Service d'Anesthesiologie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
The effects of propofol on cerebrospinal fluid pressure, mean arterial pressure, cerebral perfusion pressure and heart rate were studied during induction, tracheal intubation and skin incision in 23 patients scheduled for elective craniotomy. Premedication consisted of midazolam 0.1 mg/kg intramuscularly and metoprolol 1 mg/kg orally. Measurements were made or derived at time zero and 0.5, 1, 1.5, 2 and 3 minutes after an induction dose of propofol 1.5 mg/kg. A continuous infusion of propofol was started at time zero at a rate of 100 mg/kg/minute. Fentanyl 2 micrograms/kg was added before tracheal intubation, application of the pin head holder and skin incision. Cerebrospinal fluid pressure and mean arterial pressure decreased significantly 2 minutes after propofol alone, by 32% and 10% respectively, while a cerebral perfusion pressure above 70 mmHg was maintained. Heart rate did not change. Propofol combined with moderate dose of fentanyl, obtunded the usual cerebrospinal fluid and arterial pressure responses to intubation and other noxious stimuli. Thus propofol seems to be a suitable intravenous anaesthetic agent for induction and maintenance in neuroanaesthesia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3259094&dopt=Abstract
Eur J Clin Invest. 1983 Feb;13(1):33-9.
Peripheral blood cell changes in response to acute hypoglycaemia in man.
Frier BM, Corrall RJ, Davidson NM, Webber RG, Dewar A, French EB.
Peripheral white and red blood cell changes were studied in response to acute insulin-induced hypoglycaemia in six normal, six splenectomized and five sympathectomized (tetraplegic) subjects. The normal subjects were restudied during beta (propranolol) and beta 1-selective (metoprolol) adrenergic blockade. In the normal subjects a lymphocytosis immediately followed the acute hypoglycaemic reaction (R) with a neutrophilia 2 h later. The early lymphocytosis was absent in sympathectomized subjects (P less than 0.001) and reduced under beta blockade (P less than 0.02) in normal subjects, indicating mediation via an adrenergic mechanism. The later neutrophilia from R + 60 min was not abolished by adrenergic blockade or preceding sympathectomy; the enhanced response with propranolol was associated with an elevated plasma cortisol. Haemoglobin, packed cell volume and total erythrocyte count rose maximally at R in all groups except the sympathectomized subjects in whom all parameters declined progressively from basal values. These peripheral erythrocytes changes appear to be mediated via an adrenergic mechanism which is unaffected by beta adrenergic blockade and which does not involve splenic contraction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6409622&dopt=Abstract
Am J Physiol. 1982 May;242(5):H810-7.
Reflex cardiovascular changes with veratridine in the conscious dog.
Barron KW, Bishop VS.
The present study was undertaken to examine the reflex responses of activation of cardiac sensory receptors in the conscious dog. Intracoronary (left circumflex coronary artery) injection of veratridine (0.10 micrograms/kg) reduced mean arterial pressure (-40 mmHg, P less than 0.05), heart rate (-34 beats/min, P less than 0.05), and maximum rate of rise of left ventricular pressure (LV dP/dtmax) (-419 mmHg/s, P less than 0.05). Bilateral cervical vagal cold block (BVB) eliminated the depressor and bradycardic responses of veratridine. BVB not only eliminated the negative inotropic response to veratridine but reversed it to a positive inotropic response (LV dP/dtmax increased 313 +/- 76 mmHg/s). Ganglionic blockade abolished all effects of veratridine. The bradycardia and negative inotropic effects caused by veratridine were attenuated by either atropine or metoprolol and completely eliminated by the combination of the two antagonists. Veratridine also produced a decrease in renal artery blood flow but had no effect on renal vascular resistance. In contrast, iliac blood flow was increased with veratridine, and this, combined with the depressor effect, resulted in a decrease in iliac vascular resistance (-37%), P less than 0.05). BVB abolished the changes in renal and iliac blood flow or resistance caused by veratridine. The results indicate that activation of cardiac receptors in the conscious dog elicits inhibitory reflexes to the heart and peripheral circulation that are mediated by vagal afferents. After vagotomy, veratridine elicited a reflex positive inotropic response, which may have resulted from activation of cardiac sympathetic afferent fibers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7081453&dopt=Abstract
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