Effects of Mivacurium in the Strips of Rat Thoracic Aortic Rings / 대한마취과학회지

BACKGROUND: The hypotensive effects of muscle relaxants has traditionally been associated with a ganglion block and histamine release. However, it was exhibited that the ability of certain analogues of the steroidal muscle relaxant directly caused relaxation of isolated vascular smooth muscles. The ability of mivacurium to elicit a direct relaxant effect on vascular smooth muscle has been studied using isolated rat thoracic aortic rings contracted with phenylephrine (PE). METHODS: Each ring of the thoracic aorta was suspended on wire supports in a 20 ml tissue bath under 2 gm of resting tension. All tissues were bathed in a Tris Tyrode solution at 37oC and 100% oxygen was supplied. RESULTS: Mivacurium 3 X 10 5 M and 10 3 M inhibited PE induced contractions of the aortic rings significantly (P < 0.05) and shifted the cumulative concentration-effect curves of PE to the right. The maximum contractile response from 81.9% to 55.0% (with PE 10 6 M) was the same as that seen with mivacurium 10 3 M pretreatment. Relaxation of aortic ring with mivacurium 10 3 M was not reversed with L-NAME pretreatment. Methylene blue reversed the relaxation of the aortic rings with mivacurium 10 3 M and shifted the cumulative concentration-effect curve of PE to the left. Indomethacine enhanced the relaxation of the aortic rings with mivacurium 10 3 M and shifted this curve to the right. Mivacurium 10 3 M inhibited the influx of extracellular Ca2+. CONCLUSIONS: The results suggest that the relaxation effects of mivacurium is related with the endothelium and at least, in part, cyclooxygenase inhibition and guanylate cyclase activation are related with this relaxation effect. Also, mivacurium inhibited extracelluar calcium influx.

Does Phenylephrine Affect Hypoxic Pulmonary Vasoconstriction and Arterial Oxygenation during One Lung Ventilation? / 대한마취과학회지

BACKGROUND: Vasoconstricting drugs such as dopamine, phenylephrine (PE) and epinephrine constrict normoxic lung vessels preferentially, thereby disproportionately increasing normoxic lung pulmonary vascular resistance (PVR) and inhibit hypoxic pulmonary vasoconstriction (HPV). In this study, we evaluated the effect of PE on HPV and arterial oxygenation. METHODS: This study was performed on 21 patients undergoing thoracotomy. After induction of anesthesia, Swan-Ganz catheter was inserted. After one lung ventilation was started, systolic blood pressure (SBP) of the patient was reduced to 100 mmHg using inhalation anesthetic agent and then the blood pressure was raised up to 140 mmHg by PE infusion. Hemodynamic variables were measured and arterial blood gas was analyzed at the start of one lung ventilation (control), SBP of 100 mmHg and SBP of 140 mmHg. RESULTS: The mean dose of PE infused was 5.9 +/- 3.8 microgram/kg. Infusion of PE did not increase pulmonary vascular resistant index (PVRI) significantly and did not reduce arterial PO2. There was no statistically significant difference in intrapulmonary shunt fraction (Qs/Qt) between the time of low and high blood pressures. CONCLUSION: Pulmonary vasomotor changes induced by PE are minimal and so should not affect the distribution of blood flow during one lung ventilation. On the basis of this result, PE appears to a reasonable vasoconstrictor to be used in patients undergoing thoracotomy.

Effects of Phenylephrine Induced Hypertension on the Cerebral Hemodynamics in Dogs / 대한마취과학회지

BACKGROUND: Induced hypertension has long been considered a potential adjunct to the management of focal cerebral ischemia. Whether induced hypertension causes an increase in cerebral blood flow(CBF), dependent on cerebral perfusion and/or an intracerebral redistribution of CBF by a vasoconstrictive effect of vasoconstrictor is controversial. In this study, effect of phenylephrine induced hypertension on the cerebral hemodynamics and mechanism of reduced ischemic area were studied. METHODS: Six mongrel dogs weighing between 13 and 18 kg were anesthetized with halothane 0.5 vo1%-N2O 1 L/min-O2 1 L/min. Ventilation was controlled to maintain PaCO2 within 35~40 mmHg. Cerebral blood flow was measured and calculated by the posterior sagittal sinus outflow method. Cerebral metabolic rate for oxygen(CMRO2) was calculated. Intracranial pressure(ICP) was also measured. Phenylephrine was infused to increase mean arterial blood pressure(MAP) to a level 30% above baseline value and MAP was held constant for 20 minutes before CBF, ICP, CMRO2 determination. These parameters were measured at 10, 20 minutes after induced hypertension. RESULTS: Induced hypertension resulted in increased MAP and decreased heart rate. There were no differences between baseline, hypertension 10 min, and hypertension 20 min in terms of PaCO2, PaO2, hematocrit and temperature. CBF was not changed after induced hypertension(39.1+/-9.7 vs 40+/-10 vs 40.2+/-10.1 ml 100g(-1) min(-1) (meanv+/-SD) at baseline, hypertension 10 min, hypertension 20 min, respectively). Cerebral metabolic rate was not changed also after induced hypertension. ICP increased after induced hypertension significantly(20.5+/-12.5 vs 26+/-15.3 vs 29.8+/-17 mmHg at baseline, hypertension 10 min, 20 min, respectively). CONCLUSIONS: Phenylephrine is a cerebral vasoconstrictor and that causes redistribution of cerebral blood flow to ischemic brain area.