No abstract available.
Hemodynamics* ; Nitroprusside*

No abstract available.
Animals ; Enalapril* ; Nicardipine* ; Nitroprusside* ; Rats* ; Skin*

Experimental renovascular hypertensive model was established by clipping left renal artery and the right side of renal artery was taken 1 week and 1 month after the operation. The renal artery ring preparations were made for contractility studies of vascular wall. The relaxing and contractile responses were recorded and compared with the data obtained from control group. The following results were obtained: 1)One week after the clipping of renal artery, the renovascular hypertensive group showed increased contractility against the various contractile agents (high K+, norepinephrine, caffeine) compared to control group. 2)One month after the clipping of renal artery, the contractile responses to various contractile agents were restored to the level of control group. 3)One week after the clipping of renal artery, the renovascular hypertensive group showed increased responsiveness to acetylcholine treatment, however did not show any remarkable changes to other relaxing agents(sodium nitroprusside, verapamil). 4)One month after the clipping of renal artery, the responses to various relaxing agents showed almost same degree of responsiveness in the renovascular hypertensive group as compared with that of control group. From the above, it is suggested that stenosis- induced renovascular hypertension might induce exaggerated vascular response at early stage in intact renal artery. And the effects may be concerned with endothelium-dependent mechanism.
Acetylcholine ; Hypertension, Renovascular* ; Nitroprusside ; Norepinephrine ; Relaxation* ; Renal Artery*

BACKGROUND: The sequence method of determining baroreflex sensitivity (BRSSEQ) has been reported to correlate poorly with the phenylephrine method of determining BRS in individuals with attenuated BRS. Inhalation anesthetics are also known to decrease BRS. We therefore assessed the effect of varying the systolic blood pressure (SBP) and R-R interval (RRI) thresholds on BRSSEQ values and compared these results with the BRS obtained by the modified Oxford technique (BRSMODOX). METHODS: The average number of valid sequences and BRSSEQ values were derived by varying the SBP threshold from 0.5 to 2.5 mmHg and the RRI threshold from 1 to 6 ms, and the relation of BRSSEQ values to BRSMODOX values using sequential administration of nitroprusside and phenylephrine was assessed in 40 healthy individuals during sevoflurane anesthesia. RESULTS: Increasing either the SBP thresholds or RRI thresholds resulted in a decrease in the number of valid sequences. As the SBP thresholds were decreased and the RRI thresholds were increased, BRSSEQ values increased. When the SBP threshold exceeded 1 mmHg, no significant correlations were observed between BRSSEQ and BRSMODOX values. Significant correlations between the two methods were observed for an SBP threshold of 0.5 mmHg and RRI thresholds of 1, 2, 3 and 4 ms. Biases between the two methods were 2.1, 2.1, 0.4, and 0.4 ms/mmHg for 0.5 mmHg and 1, 2, 3 and 4 ms. CONCLUSIONS: These findings suggest that adjusting the SBP threshold to 0.5 mmHg and the RRI threshold to 3 or 4 ms may improve BRSSEQ validity during sevoflurane anesthesia, when compared to BRSMODOX.
Anesthesia* ; Anesthetics, Inhalation ; Baroreflex* ; Bias (Epidemiology) ; Blood Pressure* ; Nitroprusside ; Phenylephrine

BACKGROUND: The goal of this study was to demonstrate the effect of esmolol to prevent reflex tachycardia occurred during sodium nitroprusside(SNP) induced hypotension. METHODS: Thirty patients were randomly assigned to the SNP group(n=15) received continuous infusion of SNP at 2.72+/-0.56 mcg/kg/min or combined SNP and esmolol(SNP-ESM) group(n=l5) received combined continuous infusion of SNP at 1.54+/-0.34 mcg/kg/min and esmolol at 200 mcg/kg/min for 1 hour to maintain a 20~25% reduction of mean arterial pressure(MAP) from baseline. Heart rate(HR) and MAP were measured at baseline, during hypotensive period(5, 10, 20, 30, 60 min) and after hypotensive period(70, 80, 90,1 20 min). RESULTS: SNP-induced hypotension resulted in significant(P<0.001) increases in heart rate during hypotensive period and MAP after the end of SNP infusion. However, infusion of SNP-ESM resulted in significant(p<0.05) reduction in heart rate and SNP requirement during hypotensive period, and rebound hypertension was not observed after the end of induced hypotension. CONCLUSIONS: SNP-ESM infusion is a safe and effective pharmacologic means and provides several advantages over single SNP that include reduction in SNP requirement, no reflex tachycardia during induced hypotension and no rebound hypertension following hypotensive period.
Heart Rate* ; Heart* ; Humans ; Hypertension ; Hypotension* ; Nitroprusside* ; Reflex ; Sodium* ; Tachycardia

BACKGROUND: The goal of this study was to demonstrate the effect of esmolol to prevent reflex tachycardia occurred during sodium nitroprusside(SNP) induced hypotension. METHODS: Thirty patients were randomly assigned to the SNP group(n=15) received continuous infusion of SNP at 2.72+/-0.56 mcg/kg/min or combined SNP and esmolol(SNP-ESM) group(n=l5) received combined continuous infusion of SNP at 1.54+/-0.34 mcg/kg/min and esmolol at 200 mcg/kg/min for 1 hour to maintain a 20~25% reduction of mean arterial pressure(MAP) from baseline. Heart rate(HR) and MAP were measured at baseline, during hypotensive period(5, 10, 20, 30, 60 min) and after hypotensive period(70, 80, 90,1 20 min). RESULTS: SNP-induced hypotension resulted in significant(P<0.001) increases in heart rate during hypotensive period and MAP after the end of SNP infusion. However, infusion of SNP-ESM resulted in significant(p<0.05) reduction in heart rate and SNP requirement during hypotensive period, and rebound hypertension was not observed after the end of induced hypotension. CONCLUSIONS: SNP-ESM infusion is a safe and effective pharmacologic means and provides several advantages over single SNP that include reduction in SNP requirement, no reflex tachycardia during induced hypotension and no rebound hypertension following hypotensive period.
Heart Rate* ; Heart* ; Humans ; Hypertension ; Hypotension* ; Nitroprusside* ; Reflex ; Sodium* ; Tachycardia

The effect of single dose clonidine premedication on the vapour requirement for isoflurane induced hypotension in 20 patients undergoing spine surgery was evaluated. The patients given 5 ug/kg of clonidine P.O. at 90 minutes before operation required a mean expired isoflurane concentration of 1.2+/-0.5 vol% to induce hypotension compared with 2.1+/-0.6 vol% in 0.2 mg/kg of diazepam predmedication group(P<0.05). To achieve satisfactory hypotension, six out of ten patients in diazepam premedication group and l out of 10 patients in clondine premedication group are required supplementary infusion of sodium nitroprusside. In conclusion, clonidine premedication is recommended in isoflurane induced hypotensive anesthesia.
Anesthesia* ; Clonidine* ; Diazepam ; Humans ; Hypotension ; Isoflurane* ; Nitroprusside ; Premedication* ; Spine

The aim of present study is to investigate the effects of cGMP on hyperpolarization activated inward current (If), pacemaker current of the heart, in rabbit sino-atrial node cells using the whole-cell patch clamp technique. When sodium nitroprusside (SNP, 80 muM), which is known to activate guanylyl cyclase, was added, If amplitude was increased and its activation was accelerated. However, when If was prestimulated by isopreterenol (ISO, 1 muM), SNP reversed the effect of ISO. In the absence of ISO, SNP shifted activation curve rightward. On the contrary in the presence of ISO, SNP shifted activation curve in opposite direction. 8Br-cGMP (100 muM), more potent PKG activator and worse PDE activator than cGMP, also increased basal If but did not reverse stimulatory effect of ISO. It was probable that PKG activation seemed to be involved in SNP-induced basal If increase. The fact that SNP inhibited ISO-stimulated If suggested cGMP antagonize cAMP action via the activation of PDE. This possibility was supported by experiment using 3-isobutyl-1-methylxanthine (IBMX), non-specific PDE inhibitor. SNP did not affect If when If was stimulated by 20 muM IBMX. Therefore, cGMP reversed the stimulatory effect of cAMP via cAMP breakdown by activating cGMP-stimulated PDE. These results suggest that PKG and PDE are involved in the modulation of If by cGMP: PKG may facilitate If and cGMP-stimulated PDE can counteract the stimulatory action of cAMP.
1-Methyl-3-isobutylxanthine ; Guanylate Cyclase ; Heart ; Nitroprusside ; Sinoatrial Node*

BACKGROUND:This study was designed to determine whether remifentanil or sodium nitroprusside (SNP) with sevoflurane anesthesia can induce safe deliberate hypotension (DH) to a target mean arterial pressure (MAP) of 55-65 mmHg in patients with controlled hypertension. METHODS:Thirty patients with controlled hypertension and who were scheduled for posterior lumbar interbody fusion were randomly assigned to receive remifentanil (n = 15, group R) or SNP (n = 15, group S).All the patients received a balanced anesthetic technique including 1.5-2 vol% sevoflurane.Group R received remifentanil by target-controlled infusion.The infusion was initiated with a target concentration at 4 ng/ml and this was adjusted every 1 min by 1 ng/ml to maintain the MAP to the target level of 55-65 mmHg.In group S, the infusion of SNP was initiated at 1 ug/kg/min and this was increased by 0.5 ug/kg/min.Cerebral oximetry was done and the cardiac index was measured with esophageal Doppler. RESULTS:DH was achieved at a MAP = 60 mmHg within 5.7 min for group R and 3.7 min for group S.The intraoperative blood loss was lower in Group R than that in Group S (304 +/- 103 vs 650 +/- 141 ml, P < 0.05).The frequency of added ephedrine injection to control the MAP and discontinuation of the study drug due to a MAP < 60 mmHg were higher in group S than in group R (46% vs 13%, P < 0.05 and 62% vs 20%, P < 0.05, respectively). CONCLUSIONS:Compared to SNP, remifentanil with sevoflurane anesthesia induced safer DH for patients with controlled hypertension.
Anesthesia ; Arterial Pressure ; Ephedrine ; Humans ; Hypertension ; Hypotension ; Methyl Ethers ; Nitroprusside ; Oximetry ; Piperidines ; Sodium

PURPOSE: This study was done to determine whether maturatin alters endothelium- dependent responses in pulmonary arteries. METHODS: Vascular rings of pulmonary arteries, with and without endothelium, taken from rabbits of 3 and 30 days of age were suspended in organ chambers filled with Krebs-Henseleit solution, bubbled with 95% O2-5% CO2 and maintained at 37degrees C. Immediately after mounting, the rings were stretched progressively until a maximal response to KCl was achieved. The rings were incubated with indomethacin and allowed to equilibrate before contraction and relaxation study. RESULTS: When the endothelium was intact in arterial rings from 3-day-old rabbits, acetylcholine (ACH) (10-6 M) relaxed preconstricted rings with histamine (5x10-6 M) (98.1 4.7% relaxation, mean SD). In rings without endothelium, KCl (10-2 to 9x10-2 M) and histamine (5x10-8 to 10-5 M) caused concentration-dependent contractions. When normalized to maximal contractions achieved to each agonist, the concentration-effect curves to KCl and histamine in rings without endothelium were similar to both ages. Rings with endothelium showed a progressive shift to the right of the concentration- effect curve to histamine. Relaxation to sodium nitroprusside were unaffected by age. In preconstricted ring, ACH (10-8 to 5x10-6 M) caused relaxations in rings with endothelium which were greater at 30-day compared to 3-day-old rabbits. CONCLUSION: These study demonstrates that endothelium-dependent relaxation increase with age, possibly due to changes in the release and/or effect of endothelium-derived relaxing factor (EDRF or nitric oxide) from pulmonary arteries during the neonatal period.
Acetylcholine ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Histamine ; Humans ; Indomethacin ; Infant, Newborn* ; Nitroprusside ; Pulmonary Artery* ; Rabbits ; Relaxation*