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Biomedical subjects

R F Davis

Publications and source records attributed to R F Davis.

At least 19 recordsLinked to original sources
PubMed1998

ST segment changes following retinal surgery.

STUDY OBJECTIVE: To describe the perioperative cardiac morbidity in adult patients undergoing retinal surgery using continuous Holter monitoring. DESIGN: Prospective study. SETTING: University hospital. PATIENTS: 56 patients scheduled for elective retinal surgery with local anesthesia. INTERVENTIONS: Patients were monitored continuously for 24 hours using a Holter recorder. Blood samples for creatine phosphokinase (CPK) and serum myocardial creatine phosphokinase (CPK-MB) were taken preoperatively and 24 hours postoperatively. The characteristics of myocardial ischemia were compared according to the number of risk factors for ischemic heart disease. MEASUREMENTS AND MAIN RESULTS: The overall incidence of perioperative myocardial ischemia was high: 26.7% (n = 15). These patients exhibited 41 episodes of ischemia with mean ST segment change from baseline of 2.2+/-0.7 mm. However, almost all (93.3%) ischemic episodes were silent. Patients with two risk factors or more had 77% more episodes of ischemia than patients with one risk factor (p < 0.005), and the duration of ischemia was 47+/-22.5 minutes compared with 34.8+/-27.5 minutes (p = NS). The first episode of ischemia occurred an average of 10 hours after surgery. No patient had intraoperative evidence of ischemia. Half of the ischemic episodes were associated with an increase in heart rate. No patient had evidence of acute myocardial infarction. CONCLUSION: Retinal surgery with local anesthesia is accompanied by a high incidence of postoperative myocardial ischemia. No negative outcome was correlated to the occurrence of postoperative myocardial ischemia. The significance of these findings has yet to be evaluated.

Aged↗
PubMed1998

Desflurane and isoflurane produce similar alterations in systemic and pulmonary hemodynamics and arterial oxygenation in patients undergoing one-lung ventilation during thoracotomy.

UNLABELLED: We tested the hypothesis that desflurane (DES) and isoflurane (ISO) produce similar effects on systemic and pulmonary hemodynamics and arterial oxygenation before, during, and after one-lung ventilation (OLV) in patients undergoing thoracotomy. After obtaining informed consent, anesthesia was induced with sodium thiopental or thiamylal, fentanyl, and vecuronium in 61 ASA physical status II-IV patients. Patients were randomly assigned to receive either DES (n = 30) or ISO (n = 31) in 100% O2 in separate groups. Hemodynamic data (radial and pulmonary artery [PA] catheters) were recorded, and blood gas values were obtained before and after induction; at selected intervals before, during, and after OLV; and before emergence. DES significantly (P < 0.05) increased heart rate (HR) and decreased mean arterial pressure (MAP) and cardiac output (CO). PA pressures and pulmonary vascular resistance (PVR) increased; systemic vascular resistance (SVR) was unchanged. Increases in HR and CO and decreases in MAP and SVR occurred during OLV and DES. Reductions in PaO2 (411 +/- 88 to 271 +/- 131 mm Hg 5 min after beginning OLV; mean +/- SD) and content (CaO2) and increases in shunt fraction (Qs/Qt; 0.25 +/- 0.12 to 0.40 +/- 0.19 at 5 min after beginning OLV) were also observed. ISO increased HR and PA pressures but did not alter MAP, CO, and PVR, in contrast to the findings with DES. Reductions in MAP and SVR and increases in CO and PA pressures were observed during OLV in the presence of ISO. Similar to the findings during DES, decreases in PaO2 and CaO2 and increases in Qs/Qt occurred during OLV and ISO. We conclude that DES and ISO produce very similar alterations in systemic and pulmonary hemodynamics and arterial oxygenation in patients undergoing OLV during thoracotomy. IMPLICATIONS: Desflurane and isoflurane produce similar cardiovascular and pulmonary effects before, during, and after one-lung ventilation in patients undergoing lung surgery.

Anesthetics, Inhalation↗
PubMed1997

High spinal anesthesia does not alter experimental myocardial infarction size or ischemic preconditioning.

OBJECTIVE: The role of the central nervous system in the development of myocardial infarction and ventricular fibrillation in virgin and ischemically preconditioned myocardium was investigated. DESIGN: Infarct size and ventricular arrhythmias were assessed after regional ischemia-reperfusion. Animals were randomly assigned to four groups: (1) preconditioned, central nervous system intact; (2) nonpreconditioned, nervous system intact; (3) preconditioned, nervous system blocked; and (4) nonpreconditioned, nervous system blocked. Differences in hemodynamics and infarct size were assessed with analysis of variance, and differences in ventricular fibrillation were assessed with the Kruskal-Wallis test. SETTING: Experiments were performed in the Anesthesiology Research Laboratory at a medical center. PARTICIPANTS: Anesthetized open-chest New Zealand white rabbits were used for these studies. INTERVENTIONS: Rabbits underwent 30 minutes of coronary artery occlusion and 3 hours of reperfusion. The central nervous system was blocked with total spinal anesthesia. Ischemic preconditioning was elicited with 5 minutes of coronary artery occlusion and 10 minutes of reperfusion. Infarction was assessed with tetrazolium and expressed as a percentage of the risk zone (mean +/- SEM). MEASUREMENTS AND MAIN RESULTS: Preconditioning resulted in infarct size limitation compared with the control (8% +/- 4% v 43% +/- 5%; p < 0.001) and delayed the onset of fibrillation (15.5 minutes v 11 minutes; p = 0.001). Spinal blockade neither altered nonpreconditioned infarct size nor attenuated preconditioning (32% +/- 7% v 8% +/- 3%; p = 0.04), but it was associated with ventricular fibrillation in 24/25 rabbits as compared with 6/14 rabbits without blockade. In blocked animals, preconditioning resulted in a decreased duration of fibrillation (2.5 minutes v 12.5 minutes; p = 0.0004). However, spinal blockade eliminated the preconditioning-induced delay in fibrillation (10 minutes v 12 minutes; p = NS). CONCLUSIONS: It is concluded that (1) activation of efferent sympathetic nerves is not necessary for ischemic preconditioning; (2) preconditioning delays the onset of ventricular arrhythmias; and (3) spinal blockade exacerbates ischemia-induced ventricular arrhythmias.

Anesthesia, Spinal↗
PubMed1996

Adrenergic activation confers cardioprotection mediated by adenosine, but is not required for ischemic preconditioning.

BACKGROUND: The aim of this study was to determine whether (1) adrenergic activation is cardioprotective, (2) adrenergic cardioprotection occurs via adenosine receptor activation, and (3) ischemic preconditioning requires alpha-adrenergic activation. METHODS: Anesthetised open chest rabbits underwent 30 min coronary occlusion and 3 h reperfusion. Ischemic preconditioning was elicited with 5 min coronary occlusion and 10 min reperfusion. Activation of adrenergic receptors with endogenous norepinephrine was achieved with tyramine (0.28 mg/kg/min intravenously for 5 min). Adenosine receptors were blocked with 8-p-sulfophenyl theophylline (10 mg/kg intravenously), alpha 1-adrenergic receptors were selectively blocked with prazosin (0.1 mg/kg intravenously), and alpha-adrenergic receptors were blocked with phentolamine (4 mg/kg intravenously). RESULTS: Ischemic preconditioning reduced risk-adjusted infarct volume by 79% (P < 0.0005). This protection was attenuated by adenosine receptor blockade. Tyramine infusion resulted in a 1305% change from baseline plasma norepinephrine concentration (P < or = 0.01), and reduced infarct volume by 55% (P = 0.01). Adenosine receptor blockade abolished this protection. Blockade of alpha 1-adrenergic receptors with prazosin failed to abolish ischemic preconditioning (79 versus 89% reduction in infarct volume, without and with prazosin, respectively). Similarly, non-selective blockade of alpha-adrenergic receptors also failed to abolish ischemic preconditioning (79 versus 57% reduction without and with phentolamine, respectively). CONCLUSIONS: We conclude that the cardioprotection of ischemic preconditioning and alpha-adrenergic activation both involve adenosine, but ischemic preconditioning does not require alpha-adrenergic activation.

Adenosine↗
PubMed1996

Dichloroacetate reduces plasma lactate levels but does not reduce infarct size in rabbit myocardium.

Dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDHC), enhances postischemic mechanical recovery of isolated hearts. It is not known whether this is secondary to reduced infarction or preservation of contractile function in viable cardiomyocytes. This study investigated the effect of DCA on myocardial infarct size. Anesthetized open chest rabbits underwent regional coronary occlusion and reperfusion. DCA (300 mg/kg plus 150 mg/kg 1 h later) was administered intravenously either before occlusion (DCA-O; n = 8) or at reperfusion (DCA-R; n = 7). Control rabbits (n = 8) received saline vehicle. Myocardial PDHC activity was measured after administration of 300 mg/kg i.v. DCA in 10 separate rabbits. DCA reduced plasma lactate levels and increased PDHC activity by 76%, from 2.79 +/- .30 mumol/min.g-1 to 4.92 +/- .44 mumol/min.g-1 (p < .005). However, infarct size in DCA-treated animals was not significantly different from Control (60 +/- 5% DCA-O, 57 +/- 6% DCA-R, 58 +/- 7% Control). We conclude that stimulation of pyruvate dehydrogenase does not limit infarct size.

Animals↗
PubMed1996

Indigo carmine inhibits endothelium-dependent and -independent vasodilation.

To investigate the potential mechanisms by which indigo carmine produces hypertension, we tested the hypothesis that indigo carmine inhibits endothelium-dependent vasodilation and determined the possible site of the inhibition (endothelium versus smooth muscle). Using isolated rat thoracic aortic rings that were precontracted with phenylephrine, we examined vasodilatory responses to acetylcholine, histamine, and Ca2+ ionophore A23187 (in endothelium-intact rings) and sodium nitroprusside and isoproterenol (in endothelium-denuded rings) in the presence and absence of indigo carmine. In addition, the effects of methylene blue on the acetylcholine- and sodium nitroprusside-induced vasodilation were compared with those of indigo carmine. Indigo carmine (10(-6), 10(-5), and 10(-4) mol/L) significantly inhibited receptor- and non-receptor-mediated endothelium-dependent vasorelaxation. Indigo carmine (10(-4) mol/L) also inhibited endothelium-independent vasorelaxation induced by sodium nitroprusside (an activator of vascular smooth muscle soluble guanylyl cyclase), although to a lesser extent than vasodilation from acetylcholine, histamine, and Ca2+ ionophore A23187. In contrast, indigo carmine (10(-4) mol/L) had no effect on the vasodilation induced by isoproterenol (an activator of adenylyl cyclase), indicating that indigo carmine selectively inhibits nitric oxide-mediated responses. Methylene blue, a known inhibitor of soluble guanylyl cyclase, inhibited both acetylcholine- and sodium nitroprusside-induced vasorelaxation. The inhibition was also greater in the acetylcholine- than the sodium nitroprusside-induced vasodilation. These results suggest that indigo carmine, like methylene blue, may inhibit endothelium-dependent relaxation by a mechanism that involves two levels. The major action of indigo carmine appears to be at the level of nitric oxide generation and/or release from the endothelial cell. In addition, indigo carmine appears to inhibit vascular smooth muscle guanylyl cyclase. Thus, indigo carmine may elevate blood pressure by interfering with these nitric oxide-mediated vasodilatory mechanisms.

Acetylcholine↗
PubMed1995

Left-sided stellate ganglion ablation or "rate-controlled" vagal nerve stimulation decreases regional myocardial metabolic impairment during acute ischemia in dogs.

This study was designed to see whether during ischemia a metabolic advantage results with left-sided ablation of the stellate ganglion (SGA), an available clinical technique. Its effects on hemodynamics and regional metabolism during myocardial ischemia were compared with those of electrical stimulation of the left vagus nerve (VS), a nonclinical technique, and those of a control condition (ischemia without intervention). The left anterior descending coronary artery (LADa) of 30 dogs was constricted to reduce blood flow by 50% and then 75% from that before constriction and after autonomic intervention (baseline). Electrocardiogram, left-ventricular (LV) first-time derivative (dP/dt), and systemic, LADa, and LV end-diastolic pressures were continuously recorded. Before and during each constriction, cardiac output and regional myocardial blood flow (by microspheres), blood gas tensions, pH, hemoglobin O2 saturation, lactate, glucose, sodium, and potassium concentrations were measured. During ischemia, SGA and VS each decreased heart rate, myocardial contractility (dP/dt), and filling pressures, the decrease in each variable being greater with VS. Also during ischemia, myocardial O2 delivery and consumption decreased to the same extent in the ischemic zone with VS, but the O2 delivery/consumption ratio was higher only with SGA. In addition, ischemic lactate production was lower with SGA and VS than with no autonomic intervention. It is concluded that left-sided SGA or VS to a heart rate of 80 to 90 beats per minute similarly mitigated metabolic impairment during myocardial ischemia. Although the study was only designed to compare modification of ischemia by two different techniques, the results suggest that ischemic zone O2 delivery/consumption ratio and hemodynamic stability were better with SGA.

Animals↗
PubMed1995

Long-term changes in psychological symptomatology associated with HIV serostatus among male injecting drug users.

OBJECTIVE: To examine long-term changes in psychological symptomatology from 6 to 24 months after notification of HIV serostatus among male injecting drug users (IDU). DESIGN: Self-report and interview data were collected at 6-month intervals as part of a longitudinal study monitoring HIV infection and risk-associated behaviors among IDU. SETTING: A community-based methadone-maintenance clinic. PARTICIPANTS: Ninety-seven male IDU (81 HIV-seronegative, 16 HIV-seropositive), including both methadone-maintained and out-of-treatment IDU. MAIN OUTCOME MEASURES: Analyses of long-term changes in psychological symptomatology associated with HIV serostatus among male IDU. RESULTS: Analyses of long-term changes in psychological symptomatology between groups revealed no significantly greater levels of overall psychological distress or significant elevations on subscales of the Symptom Checklist-90 for HIV-seropositive compared with HIV-seronegative male IDU. Also, no significantly higher scores on the Beck Depression Inventory or the psychiatric composite score of the Addiction Severity Index were observed between groups. CONCLUSIONS: Our results suggest that HIV-seropositive male IDU do not express greater levels of psychological symptomatology from 6 to 24 months following notification of seropositivity compared with HIV-seronegative male IDU. Several explanations for these findings are considered. Future work should examine why male IDU do not report significant and long-term elevations in symptoms post-notification of HIV seropositivity. Also, studies of changes in psychological symptomatology as a function of HIV serostatus among female IDU need to be conducted to assess implications for treatment interventions among this underserved population.

Adult↗
PubMed1995

Fluorescent vs. radioactive microsphere measurement of regional myocardial blood flow.

OBJECTIVES: This study compared simultaneous regional myocardial blood flow (RMBF) measurements using fluorescent microspheres (FM) and radiolabeled microspheres (RM). The utility of an internal standard during processing was also examined. METHODS: Paired FM and RM were injected into the left atrium of 9 anaesthetised rabbits. RMBF was altered by use of either regional ischaemia or (-)-N6-(2-phenylisopropyl)-adenosine. Radioactivity of blood reference and tissue samples was quantitated using standard methods. Samples were then digested with potassium hydroxide and microspheres recovered by vacuum filtration, with an additional label of FM as the internal standard. FM labels were extracted using Carbitol acetate and quantitated using fluorescence spectroscopy. Agreement between the fluorescent and radioactive methods was assessed using both orthogonal regression and difference-against-mean analyses. RESULTS: Using recovery-uncorrected data, the slope of the orthogonal regression of RM and FM-determined RMBF was not statistically different from 1, but the intercept was statistically different from 0 [-0.03(0.01), P = 0.005] and the mean RMBF by each method differed from one another [1.24(0.08) vs. 1.17(0.08) ml.min-1.g-1, P = 0.0002]. The mean +/- 2 s.d. of the differences of RMBF (RM minus FM) was +0.07 +/- 0.30 ml.min-1.g-1. Although recovery of FM from tissue averaged 97.6(1.2)%, use of the internal standard to correct for losses substantially improved the agreement between RM and FM-determined RMBF: the orthogonal regression slope was not statistically different from 1, the intercept was not statistically different from 0, and the means of the flows were not different. The mean +/- 2 s.d. of the differences of RMBF was -0.01 +/- 0.22 ml.min-1.g-1. The internal standard also improved RMBF estimates from samples with simulated large spillage during processing. CONCLUSION: Fluorescent microspheres are an equivalent alternative to radiolabeled microspheres for the estimation of RMBF. Although the overall recovery of microspheres using this technique was high, use of an internal standard is recommended for correction of random losses.

Animals↗
PubMed1994

Mitral insufficiency after pericardiectomy for constrictive pericarditis.

We report the case of a 24-year-old man in whom a clinical syndrome developed while he was on active military duty in Saudi Arabia that was subsequently diagnosed as constrictive pericarditis. Phrenic nerve to phrenic nerve pericardiectomy and posterior pericardial release successfully relieved the ventricular constriction with a resultant increase in the cardiac index from 1.9 to 3.8 L.min-1.m-2. Transesophageal echocardiographic monitoring during the operation disclosed trace mitral regurgitation before median sternotomy. The severity of the regurgitation noticeably increased to the moderate level immediately after pericardial resection. This echocardiographic finding had improved 1 week later, but the regurgitation still was greater than baseline. Mitral valve function had returned to baseline by 4 weeks after the operation. Possible mechanisms of this evolving pattern of perioperative mitral valve dysfunction are discussed.

Adult↗
PubMed1994

Anaesthetics alter the magnitude of infarct limitation by ischaemic preconditioning.

OBJECTIVE: The aim was to determine whether three commonly used animal anaesthetics alter the magnitude of infarct limitation achieved with ischaemic preconditioning. METHODS: Eighty four anaesthetised non-preconditioned and preconditioned open chest rabbits underwent a 30 min coronary occlusion followed by 3 h reperfusion. Ischaemic preconditioning was achieved with 5 min coronary occlusion beginning 15 min before the 30 min coronary occlusion. The anaesthetics studied were: pentobarbitone (30 mg.kg-1 intravenously +30-50 mg.kg-1.h-1 intravenously), isoflurane (1.5-2.5% end expiratory), and ketamine/xylazine (cocktail of 67 mg ketamine and 6.7 mg xylazine.ml-1, 1 ml.kg-1 intramuscularly +0.3-1.3 ml.kg-1.h-1 intramuscularly). Area at risk was delineated with ZnCdS particles and infarction assessed with tetrazolium. RESULTS: There were no significant differences in area at risk, heart rate, arterial pressure, and temperature between non-preconditioned and preconditioned hearts. Although infarct size was not significantly different among non-preconditioned hearts for each anaesthetic regimen (p = NS), the magnitude of infarct limitation with preconditioning varied with the anaesthetic employed (decrease in infarct size from control values of 81%, 44%, and 33% for pentobarbitone, isoflurane and ketamine/xylazine, respectively, p = 0.0145 for comparison of the three magnitudes, two factor ANOVA). CONCLUSION: Anaesthetic regimens affect the degree of infarct size limitation seen with ischaemic preconditioning.

Anesthetics↗
PubMed1994

"Normothermic range" temperature affects myocardial infarct size.

OBJECTIVES: This study tested the hypothesis that small changes in temperature above the hypothermic range may alter myocardial infarct size after acute coronary occlusion-reperfusion. A secondary hypothesis, that a correlation between temperature and infarct size may be independent of an associated change of heart rate, was also evaluated. METHODS: Eighteen pentobarbitone-anaesthetised, open chest rabbits underwent 30 min coronary artery occlusion and 3 h reperfusion at blood temperatures ranging from 35-42 degrees C, achieved and maintained using surface methods (not paced, group NP). In a second group of 11 animals, heart rate was held constant across the same range of temperatures (paced, group P), before and throughout coronary artery occlusion-reperfusion. Infarct sizes were assessed by the tetrazolium method. RESULTS: Target temperature was effectively controlled over the duration of the experimental protocol to within +/- 0.25 degrees C. Area at risk did not vary with temperature. Infarct size, normalised to area at risk, was correlated with temperature in both groups (infarct size = 7.9 x temp-250.0, r = 0.75, p = 0.0003, group NP; infarct size = 11.7 x temp-404.5, r = 0.88, p = 0.0004, group P). There was no significant difference between the slopes of these two lines (p = 0.18), indicating that the positive correlation between infarct size and temperature is not related to changes of heart rate. CONCLUSION: Temperatures in the range of 35-42 degrees C affect myocardial infarct size significantly, independent of heart rate.

Animals↗
PubMed1994

Cardioprotection provided by adenosine receptor activation is abolished by blockade of the KATP channel.

Adenosine agonists and openers of the ATP-sensitive potassium (KATP) channel have been reported to limit infarct size (IS). We tested the hypothesis that these phenomena are interdependent. Anesthetized swine underwent 60 min of coronary artery occlusion and 90 min of reperfusion. Preconditioning was elicited by two cycles comprising 10 min of occlusion and 10 min of reperfusion (n = 7 swine). An intracoronary infusion of adenosine (Ado; n = 10) or (-)-N6-(2-phenylisopropyl)-adenosine (R-PIA; n = 7) replaced preconditioning ischemia. KATP channels were blocked with sodium 5-hydroxydecanoate (5-HD) in the absence (n = 6) or presence (n = 8) of R-PIA. Control pigs (n = 7) received saline vehicle. IS was assessed with tetrazolium and normalized as percentage of area at risk. Preconditioning resulted in a reduced IS compared with Control (3.9 +/- 1.8 vs. 43.5 +/- 6.9%, respectively; P < 0.0005). Ado and R-PIA also reduced IS [21.1 +/- 6.8 (P < 0.01) and 11.2 +/- 7.4% (P < 0.005), respectively]. 5-HD alone did not alter IS, but it abolished R-PIA-induced cardioprotection (IS 5-HD + R-PIA = 48.6 +/- 13.2%). Thus Ado A1-receptor agonists mimicked the cardioprotection of ischemic preconditioning. The Ado-induced limitation of IS was abolished by blockade of the KATP channel. We conclude that both Ado A1 receptors and KATP channels may be involved in ischemic preconditioning.

Adenosine↗
PubMed1994

Midazolam produces vasodilation by mixed endothelium-dependent and -independent mechanisms.

Aortic rings were obtained from rat thoracic aorta and studied in vitro with and without functionally intact endothelium to determine whether "the mechanism" requires endothelium [or endothelium-derived relaxing factor (EDRF)]. In aortic rings precontracted with either phenylephrine (PE, 3 x 10(-8)-3 x 10(-7) mol/L) or KCl (40 mmol/L), midazolam produced concentration-dependent relaxation, with and without endothelium. Rings without endothelium demonstrated significantly less relaxation than those with endothelium regardless of whether they were precontracted with PE or KCl. With intact endothelium, midazolam produced greater relaxation in PE-contracted aortic rings than in KCl-contracted aortic rings; the midazolam concentration producing 50% relaxation from the contracted state (RC50) was 8.8 +/- 3.6 x 10(-7) mol/L for PE-contracted rings and 3.3 +/- 1.1 x 10(-6) mol/L for KCl-contracted rings (P < 0.05). In aortic rings with intact endothelium pretreated with NG-monomethyl-L-arginine (L-NMMA, 10(-4) mol/L), an inhibitor of nitric oxide (NO) synthesis, midazolam produced relaxation of similar magnitude to that seen in the denuded aortic rings except at the highest concentration (1 x 10(-5) mol/L). Pretreatment with the cyclooxygenase inhibitor, indomethacin (2.5 x 10(-5) mol/L), did not change the midazolam-induced relaxation in rings with intact endothelium as compared to untreated control aortic rings. In contrast to the intact endothelium state, when endothelium was removed, midazolam produced greater relaxation in the KCl-contracted aortic rings than in PE-contracted rings (RC50, 1.2 +/- 0.3 x 10(-5) mol/L vs 2.3 +/- 0.4 x 10(-5) mol/L, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Propofol produces endothelium-independent vasodilation and may act as a Ca2+ channel blocker.

The mechanism of vasodilation induced by propofol was investigated using isolated rat thoracic aortic rings. Aortic rings were precontracted with potassium chloride (KCl) (40 mM) or phenylephrine (PE) (3 x 10(-8) to 3 x 10(-7) M) in the presence and absence of intact endothelium. Propofol produced similar concentration-dependent relaxation in aortic rings with and without endothelium regardless of whether they were precontracted with KCl or PE. The relaxation response to propofol was significantly greater in KCl-contracted aortic rings than in PE-contracted aortic rings. The propofol concentration producing 50% relaxation from the contracted state (RC50) was lower in aortic rings contracted with KCl than with PE, both with (5 +/- 0.6 x 10(-5) M vs 8.3 +/- 5.7 x 10(-4) M, P < 0.001) and without intact endothelium (3.9 +/- 0.5 x 10(-5) M vs 7.2 +/- 3.8 x 10(-4) M, P < 0.001). Propofol inhibited the Ca(2+)-induced contractions of aortic rings exposed to Ca(2+)-free media and depolarized with KCl (40 mM, 100 mM) in a dose-dependent manner. These effects are similar to those produced by verapamil. Propofol (5 x 10(-5) M) had minimal effect on the intracellular Ca2+ release elicited by PE (10(-5) M). We conclude that vasodilation produced by propofol is not endothelium-dependent but is likely due to blockade of voltage-gated influx of extracellular Ca2+.

Animals↗
PubMed1991

Fusion of the occiput to the upper cervical spine. A review of 37 cases.

This is the first report of a large series of patients undergoing preoperative traction to reduce spinomedullary compression from cranial settling. In all cases, an attempt was made to reduce the malalignment with Gardner-Wells or halo traction before posterior fusion. One patient required an anterior retropharyngeal decompression of the odontoid performed as a one-stage procedure at the time of the posterior operation, and two required subsequent anterior transoral-transpharyngeal resection of the odontoid. From 1974 to 1989, 37 patients underwent posterior occipital cervical arthrodesis. All cases presented with neurologic deficit, and most had signs of brain stem compression, such as L'hermitte's sign or Ondine's curse. The most common cause of basilar impression was rheumatoid arthritis, neoplastic destruction, previously failed C1-C2 fusion, or Down's syndrome. Mean postoperative follow-up was 2 years and 10 months; the patients with less than 2 years' follow-up were followed until successful fusion. Eight of 9 patients with L'hermitte's sign or Ondine's curse and 10 of 12 patients with intractable occipital pain were relieved of their symptoms after reduction and triple-wire stabilization-fusion. Eighteen of 25 patients with long tract signs improved after surgery. Interestingly, 14 (93.3%) of 15 patients with myelopathy improved when successful preoperative reduction of their deformity occurred, whereas only 4 (40%) of 10 patients with fixed basilar impression improved (chi 2 = 8.57, P = .014). Symptoms such as Ondine's curse, L'hermitte's sign, intractable occipital headache, and myelopathy are usually relieved by skeletal traction and posterior fusion without need of an additional transmucosal anterior procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗