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

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

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 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*

OBJECTIVETo study the function of zinc in preventing human sperm from being damaged by sodium nitroprusside (SNP), an external NO donor.

METHODSAnalyses were made of the function of zinc in protecting sperm from being influenced by SNP in such aspects as sperm motility, head-tail connection and the breakage of sperm DNA chain by using phase-contrast microscope and single cell gel electrophoresis (SCGE).

RESULTSSperm motility was obviously inhibited by SNP. The percentage of comet cells increased significantly but the stability of sperm head-tail connection decreased. Zinc could promote sperm motility, protect the DNA chain and prevent the sperm head-tail connection from breaking.

CONCLUSIONZinc can protect sperm from being damaged by NO. Its mechanism may be related to the mercaptol group of sperm chromatin.

Adult ; DNA Damage ; Humans ; Male ; Nitric Oxide ; toxicity ; Nitroprusside ; toxicity ; Spermatozoa ; drug effects ; Zinc ; pharmacology

Delayed type cerebral vasoconstriction (DCV) following aneurysmal subarachnoid hemorrhage is an important cause of permanent neurological injury and death. The mechanism of DCV remains unknown. Recently many investigators have used a new treatment for DCV involving the use of intraventricular sodium nitroprusside. We report upon a clinical case where a relatively large amount of sodium nitroprusside was intrathecally delivered by intraventricular catheter for the treatment for DCV.
Catheters ; Humans ; Nitroprusside* ; Research Personnel ; Sodium* ; Subarachnoid Hemorrhage ; Vasoconstriction ; Vasospasm, Intracranial*