To 100 patients who underwent various operations under general anesthesia, Effortil and methoxamine were given in order to assess and to compare their effects on blood pressure and pulse rate. The drugs were administered intravenously in 6 to 10 mg doses when the systolic pressure fell to 80 mmHg. or lower during the operation. The results obtained are as follows: 1. Excellent pressor effect was obtained with Effortil in 84% of 50 patients while in 72% with methoxamine. 2. Both drugs were equally effectve in elevating both systolic and diastolic pressures. 3. The effect of Effortil on pulse rate was much less than that of methoxamine which moderately reduced the pulse rate, especially in the early phase. 4. No untoward effects of either Effortil or methoxamine were observed in this study.
Anesthesia, General ; Blood Pressure ; Etilefrine* ; Heart Rate ; Humans ; Methoxamine

The bradycardiac and presor to intravenous and intraventricular methoxamine were examined in urethane-anesthetized rabbits 1) Intravenous methoxamine produced bradycardiac pressor responses. Atropine (2 mg/kg, i,v.) weakened but not abloished the bradycardiac effect. 2) The bradycardiac effect elicited by intravenous methoxamine was not affected by int-ravenous prazosin, rehimbiine, guanethidine and propranolol, butt was attenuated by intra venous chlorisondamine reserpine. 3) The pressor effect elioited by intravenous methoxamine was weakened by prazosin, but was scarcely affected, rather potentiated, by intraTenous yohimblne, guanethidine, chlorisondamine, propranolol and resperpine. 4) Intraventricular methoxamine produced pressor and bradycardiac responses. 5) The bradycardiac effect elicited by intraventricular methoxamine was net affected by intravenous atropine, prasosin and yohimbine. This was attenuated by intravenous guane- thidine, chlorisondamine, propranolol and reserpine, and by intraventricular atropine prazosin and propranolol, respectively. 6) The pressor effect elicited by intraventricular methoxamine was attenuated by intra- ventricular and intravenous prazosin. This was not affected by intravenous atropine, gua-nethidine, chlorisondamine, propranolol, reserpine and yohimbine, and by intraventricular atropine, prasosin and Propranolol, respectivelr. 7) From these results it was inferred that bradycardiac effect elicited by methoxamine was not an action through the mediation of aleph 1-adrenoceptors but was a result from non-specific actions on some brain receptors.
Atropine ; Brain ; Chlorisondamine ; Guanethidine ; Methoxamine* ; Negotiating ; Prazosin ; Propranolol ; Rabbits* ; Reserpine ; Yohimbine

BACKGROUND: Hemodilution may increase cerebral blood flow (CBF) but the mechanism(s) remain controversal. Autoregulation is easily modified or disturbed by several conditions. The aim of this study was to evaluate the effects of isovolemic hemodilution on the autoregulation of cerebral blood flow in a rabbit model. METHODS: Stepwise hemodilution was accomplished by incrementally removing whole blood from the animals in amounts of 8-12 ml and replacing this with an equal volume of 6% hetastarch in saline. This procedure was continued until the target content values of approximately Hct -18% were achieved. To evaluate the influence of pressure changes on CBF, mean arterial pressure (MAP) was increased from a baseline pressure (approximately 78 mmHg) to 145 mmHg by infusing methoxamine, and cerebral blood flow was measured at each MAP level using the hydrogen clearence method after MAP had been stabilized for 15 min. RESULTS: Stepwise hespen replacement caused a sudden drop of Hct from 37.4% to 18.5% and a simultaneously a significant increase in local CBF of 161% in the hemodilution group. Hemodilution significantly reduced CaO2 in the hemodilution group (9.45 +/- 1.7 ml O2/dl) versus the control group (18.34 +/- 1.3 ml O2/dl). However, despite these decrease in CaO2, calculated cerebral oxygen delivery (DO2) was as well maintained in the hemodilution group (22.47 +/- 7.28 ml O2/100 gm/min) as in the control group (24.14 +/- 8.67 ml O2/100 gm/min). MAP increases from 78 mmHg to 145 mmHg produced a significant increase in CBF from 122.4 +/- 32.8 ml/100 gm/min to 170.9 +/- 23.7 ml/100 gm/min in control group (39.6%) and from 218.4 +/- 75.6 ml/100 gm/min to 268.4 +/- 106.5 ml/100 gm/min in the hemodilution group (44.6%) (P<0.001). These CBF increases were not significantly different in the two groups. CONCLUSIONS: The present study demonstrates that in the normal brain the decrease in CaO2 caused by hemodilution is well compensated for by an increase CBF, and that oxygen transport to the brain is also well maintained during at a Hct value of 20%. Although the present study did not show the tight CBF control within the MAP range from 78 mmHg to 145 mmHg, hemodilution did not alter the response of the cerebral circulation to increased MAP.
Animals ; Arterial Pressure ; Brain ; Hemodilution* ; Homeostasis* ; Hydrogen ; Hydroxyethyl Starch Derivatives ; Methoxamine ; Oxygen

Vasopressor effects of epinephrine, norepinephrine, ephedrine, phenylephrine, methoxamine and of mephentermine were compared in resrpinized dogs with or without nitrous oxide-oxygen-halothane anesthesia. The results are as follows: (1) Epinephrine and norepinephrine were shown to have the most potent pressor effect in reserpinized and nitrous oxide-oxygen-halothane-anesthetized dogs. Phenylephrine, methoxamine, mephen-termine and ephedrine were less potent in decreasing order. (2) Decrease in mean arterial pressure was less marked in dogs reserpinized and anesthetized with nitrous oxide-oxygen-halothane than in reserpinized but unanesthetized dogs. (3) It revealed that nitrous oxide-oxygen-halothane anesthesia potentiated the vasopressor effects of the sympathomimetic amines studied. Nitrous oxide-oxygen-halothane anesthesia is implicated to exert an sympathomimetic effect.
Anesthesia* ; Animals ; Arterial Pressure ; Dogs* ; Ephedrine ; Epinephrine ; Mephentermine ; Methoxamine ; Norepinephrine ; Phenylephrine ; Sympathomimetics*