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Biomedical subjects

M Muzi

Publications and source records attributed to M Muzi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Induction of anesthesia and tracheal intubation with sevoflurane in adults.

BACKGROUND: The speed, quality, and cost of mask induction of anesthesia and laryngeal mask airway insertion or tracheal intubation were studied in young non-premedicated volunteers given high inspired concentrations of sevoflurane (6 to 7%). METHODS: Twenty healthy persons who were 19 to 32 years old participated three times, received 6 l/min fresh gas flow, and were randomized to receive 6 to 7% sevoflurane in 66% nitrous oxide/28% oxygen by face mask until tracheal intubation (treatment 1) or until laryngeal mask airway insertion (treatment 3), or 6 to 7% sevoflurane without nitrous oxide to tracheal intubation (treatment 2). Participants exhaled to residual volume and took three vital capacity breaths of the gas mixture; thereafter ventilation was manually assisted. The time of exposure to the inhaled gas was varied for consecutive participants. It was either increased or decreased by 30-sec increments based on the failure or success of the preceding volunteer's response to laryngoscopy and intubation after a preselected exposure time. Failure was defined as poor jaw relaxation, coughing or bucking, or inadequate vocal cord relaxation. RESULTS: Loss of the lid-lash reflex in unpremedicated young volunteers was achieved in 1 min and did not differ among groups. Average time (and 95% confidence interval) for acceptable conditions for LMA insertion was achieved in 1.7 (0.7 to 2.7) min, and all participants had an immediate return of spontaneous ventilation. The time for acceptable tracheal intubating conditions after manual hyperventilation by mask was 4.7 (3.7 to 5.7) min and 6.4 (5.1 to 7.7) min in treatments 1 and 2, respectively. There were no cases of increased secretions or laryngospasm. The incidence of breath holding and expiratory stridor ("crowing") was 7.5% and 25%, respectively, during treatment 1 and 15% and 40%, respectively, during treatment 2. CONCLUSIONS: The induction of anesthesia to loss of lid reflex in young non-premedicated adults approaches the speed of intravenous induction techniques. No untoward airway responses were noted during mask induction of anesthesia with a three-breath technique. In response to intubation, no adverse airway responses, including jaw tightness, laryngospasm, and excessive coughing or bucking, occurred in participants whose duration of mask administration of sevoflurane met the appropriate times (as determined in this study).

Adult↗
PubMed1996

Site(s) mediating sympathetic activation with desflurane.

BACKGROUND: Three strategies were employed to better define the afferent site(s) at which desflurane initiates its neurocirculatory activation. METHODS: Young (aged 19-28 yr) healthy volunteers were employed in three separate studies. Monitoring included electrocardiography, radial artery blood pressure, and direct recordings of sympathetic outflow to skeletal muscle blood vessels by microneurography. In each study, anesthesia was established with 2.5 mg/kg propofol, and in studies 1 and 2 was maintained with 5.4% desflurane via a double-lumen tube. In study 1 (n = 7) a double-lumen tube was placed with the bronchial cuff just below the vocal cords to selectively give 14.5% desflurane or 2.4% isoflurane to the upper airway (via the tracheal lumen) or lower airway (via the bronchial lumen). Study 2 (n = 14) consisted of standard placement of a left side double-lumen tube to selectively increase the inspired desflurane concentration of either right or left lung to 11% while decreasing the inspired concentration in the opposite lung to 0%, thereby maintaining constant systemic concentrations of desflurane (gas chromatography). Study 3 consisted of lidocaine or placebo airway treatment before anesthetic induction and administration of 11% inspired desflurane by mask: group A-n = 9, topical and nebulized lidocaine, glossopharyngeal and superior laryngeal nerve blocks, and transtracheal administration of lidocaine; group B-n = 7, similar treatment as group A with placebo (saline); and group C-n = 8, systemic infusions of 2% lidocaine to match plasma concentrations of lidocaine in group A. RESULTS: In study 1, significant increases in heart rate, mean arterial pressure, and sympathetic neural activity (26%, 23%, and 62%, respectively) occurred when desflurane was directed to the upper airway. These responses were approximately twofold to sixfold larger when desflurane was given to the lower airway (lungs). There were no significant increases in these variables when isoflurane was administered to the upper airways, and a significant increase in heart rate occurred only when isoflurane was delivered to the lower airways. In study 2, separate right or left lung increases in desflurane did not change the blood concentration of desflurane or sympathetic neural activity but led to significant increases in heart rate (44%) and mean arterial pressure (32%). The simultaneous administration of desflurane to both lungs increased the millimolar (mM) concentration of desflurane in the blood from 1.17 to 2.39 mM and led to increases in sympathetic neural activity (750%), heart rate (90%), and mean arterial pressure (63%). In study 3, neither regional nor systemic administration of lidocaine reduced the significant neurocirculatory activation caused by the rapid increase in the inspired concentration of desflurane by mask. CONCLUSIONS: There are sites in the upper airway (larynx and above) that respond with sympathetic activation during rapid increases in desflurane concentration independent of systemic anesthetic changes. These responses, while lesser than those seen with rapid increases to the lung, may represent direct irritation of airway mucosa. Heart rate and mean arterial pressure responses to desflurane can be initiated by selectively increasing concentrations to either right or left lung without altering systemic levels of desflurane. From this it is inferred that there are sites within the lungs, separate from systemic sites, that mediate this response. Neither systemic lidocaine nor attempted blockade of upper airway sites with cranial nerve blocks combined with topical lidocaine was effective in attenuating the neurocirculatory activation associated with desflurane.

Adolescent↗
PubMed1996

Unilateral carotid sinus stimulation and muscle sympathetic nerve activity in man.

The carotid baroreflex influences sympathetic outflow to the peripheral circulation, yet this net response is the result of information received from both right and left carotid sinuses. To assess their individual contributions on sympathetic activity, direct measurements of muscle sympathetic nerve activity (SNA) from the peroneal nerve of the right leg were made during unilateral carotid sinus stimulation. A sustained neck pressure (approximately 25 +/- 2 mm Hg) was applied to right and left carotid sinuses, as well as bilaterally, for 5 s in 10 healthy subjects using a customized neck collar device partitioned to allow for stimulation of only one side of the neck. In addition to muscle SNA, blood pressures (radial artery) and R-R interval (RRI) changes were recorded. Muscle SNA was greater for left side neck pressure with respect to burst amplitude (left = 4.07 +/- 0.67 vs right = 2.48 +/- 0.46 microV; P < 0.05), normalized burst amplitude (388 +/- 63 vs 269 +/- 37 units; P < 0.05), burst ratio (0.64 +/- 0.05 vs 0.46 +/- 0.04; P < 0.05), and a SNA index of normalized amplitude and ratio (24832 +/- 3455 vs 6566 +/- 3259 units; P < 0.05). The combined values of the muscle SNA index for right and left sides (25590 +/- 4531 units) did not differ from the bilateral value (21906 +/- 3855 units; P > 0.05). These findings suggest that afferent input from the left carotid sinus may have a greater influence on efferent muscle sympathetic outflow (as measured in the right leg) and that the bilateral response may represent the summed right and left carotid inputs.

Adult↗
PubMed1995

The effects of clonidine on desflurane-mediated sympathoexcitation in humans.

This study explored the effectiveness of oral clonidine premedication in attenuating sympathetic activation, tachycardia, and hypertension triggered by desflurane. After institutional review board approval, informed consent was obtained from 15 young, healthy male volunteers. Heart rate (HR, electrocardiogram), mean arterial pressure (MAP, radial artery catheter), and central venous pressure (CVP, jugular vein) were monitored. Recordings of sympathetic nerve activity (SNA) were obtained from the peroneal nerve via percutaneously placed tungsten needles. After baseline recordings, subjects were randomized to receive either a placebo (n = 10) or 0.3 mg of clonidine (n = 9) per os (PO). One hour later, repeat recordings were obtained. Propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg) were given intravenously. Ventilation via a mask (100% O2) was used to maintain normocarbia. Two minutes after propofol administration, the desflurane vaporizer was set at 3.6% (0.5 minimum alveolar anesthetic concentration [MAC]) and increased at 1-min intervals to 7.2% and 11% (1.0 and 1.5 MAC). After 10 min, the trachea was intubated and 20 min later steady-state neurocirculatory recordings were obtained at 5.4%, during the first 5 min after advancing the vaporizer from 5.4% to 11% ("transition"), and at 11%. Resting HR, MAP, and SNA were similar between the two groups. PO clonidine reduced SNA, CVP, and MAP but did not change HR. In both groups propofol decreased SNA and MAP, and increased HR. The administration of desflurane via a mask resulted in significant increases in SNA, HR, and MAP. Clonidine reduced the HR and MAP responses by approximately 30%-40% during induction and transition periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1995

Cardiovascular responses to sevoflurane: a review.

In conclusion, sevoflurane appears to be similar to isoflurane and desflurane with a few exceptions. Sevoflurane was not associated with increases in heart rate in adult patients and volunteers, whereas higher MACs of isoflurane and desflurane and rapid increases in the inspired concentrations of these two anesthetics have been associated with tachycardia. Increasing concentrations of sevoflurane progressively decrease blood pressure in a manner similar to the other volatile anesthetics, and in unstimulated volunteers this decrease may be slightly less than with isoflurane at a higher MAC. Sevoflurane appears similar to isoflurane in its effect on regional blood flows, including the hepatic, renal, and cerebral circulation. In animals, sevoflurane appears to be a slightly less potent coronary vasodilator than isoflurane, and in a dog model, sevoflurane has not been associated with coronary flow redistribution ("steal"). Sevoflurane decreases myocardial contractility in a manner similar to equianesthetic concentrations of isoflurane and desflurane, and does not potentiate epinephrine-induced cardiac arrhythmias. Sevoflurane reduces baroreflex function in a manner similar to other volatile anesthetics. In several multicenter studies where patients with CAD or patients at high risk for CAD were randomized to receive either sevoflurane or isoflurane for cardiac or noncardiac surgery, the incidence of myocardial ischemia, infarction, and cardiac outcomes did not differ between treatment groups. Thus, sevoflurane has not been associated with untoward cardiovascular changes in volunteers and patients undergoing elective surgery compared with other volatile anesthetics, and it appears to offer a more stable heart rate profile than either isoflurane or desflurane.

Adult↗
PubMed1995

Effects of fentanyl on sympathetic activation associated with the administration of desflurane.

BACKGROUND: Activation of the sympathetic nervous system occurs when desflurane is inspired shortly after anesthetic induction and when the inspired concentration of desflurane is rapidly increased during steady-state periods of anesthesia. The purpose of this study was to determine the effectiveness and dose response of fentanyl pretreatment in attenuating the neurocirculatory responses to desflurane in healthy human volunteers. METHODS: After Institutional Research Review Board approval, three study groups were selected and, in random order, received either placebo (n = 10), a 2.5-micrograms.kg-1 intravenous bolus of fentanyl citrate followed by a continuous infusion of 1 microgram.kg-1.h-1 (n = 9), or a 5.0-micrograms.kg-1 intravenous bolus followed by an infusion of 2 micrograms.kg-1.h-1 (n = 11) before the administration of desflurane. Arterial (MAP) and central venous (CVP) pressures were measured directly, and heart rate (HR) was determined indirectly. Efferent muscle sympathetic nerve activity (SNA) was recorded from the peroneal nerve by microneurography. After neurocirculatory recordings at conscious unmedicated baseline and 12 min after fentanyl administration, anesthetic induction was carried out with 2.0 mg.kg-1 propofol and 0.2 mg.kg-1 vecuronium. Neurocirculatory measurements were repeated beginning 2 min after induction when desflurane was given via mask (semiclosed circle system, 61/min fresh gas flow, 100% O2) in three incremental 1-min steps (3.6%, 7.2%, and 11%). Intubation occurred 10 min after propofol administration. Twenty minutes after intubation, recordings were obtained during two steady-state periods during which end-tidal concentrations had achieved 5.4% (0.75 MAC) and 11% (1.5 MAC) desflurane for at least 10 min. Data also were obtained during the rapid increase in the inspired gas concentration from 5.4% to 11% ("transition"). RESULTS: Neurocirculatory variables did not differ between the three groups at conscious baseline, after fentanyl, and during steady-state periods of anesthesia. Propofol administration significantly reduced SNA and MAP. The MAP reduction was enhanced in the fentanyl-treated groups. After induction, the increases in SNA and MAP associated with the administration of desflurane by mask were not significantly reduced by fentanyl. The transition from 5.4% to 11% desflurane resulted in increases in SNA, HR, MAP, and fentanyl administration significantly attenuated the HR and MAP components. At the 11% steady-state measurement period, CVP was increased and MAP was decreased from conscious baseline, and these changes were not modified by fentanyl. CONCLUSIONS: The administration of desflurane was associated with increases in SNA, HR, MAP, and CVP. Maximum sympathetic activation and hemodynamic responses occurred 4-5 min after initiating desflurane during induction and 2-3 min after increasing the inspired concentration of desflurane during the "transition" period. Although fentanyl partially attenuated the hemodynamic component in a dose-dependent fashion during the "transition" period, it did not significantly diminish the response during induction.

Adult↗
PubMed1995

A comparison of baroreflex sensitivity during isoflurane and desflurane anesthesia in humans.

BACKGROUND: Desflurane anesthesia has been associated with heart rate (HR) and sympathetic nerve activity (SNA) responses that differ from those during isoflurane anesthesia. Whether these differences might be due to better preservation by desflurane of the baroreceptor reflex control of HR or SNA in humans was examined. METHODS: Baroreflex sensitivity was assessed in 18 volunteers anesthetized with either desflurane or isoflurane. Measurements of HR, blood pressure (BP), and efferent SNA (percutaneous recordings from the peroneal nerve) were made, and baroreflex sensitivity was evaluated at conscious baseline and during 0.5, 1.0, and 1.5 MAC anesthesia. Baroreflex responses were triggered by bolus intravenous injections of nitroprusside (100 micrograms) and phenylephrine (150 micrograms). The linear portions of the baroreflex curves relating HR to mean arterial pressure and relating SNA to diastolic pressure were determined to obtain cardiac and sympathetic baroslopes, respectively. RESULTS: Cardiac (HR) baroslopes were equally diminished at increasing MAC of both anesthetics. Sympathetic baroslopes were preserved at 0.5 MAC isoflurane but diminished at 0.5 MAC desflurane. Higher MAC produced equal depression of sympathetic baroslopes with both anesthetics. CONCLUSIONS: Increasing MAC of desflurane and isoflurane anesthesia results in similar and progressive decreases in BP but dissimilar SNA and HR responses. These differences are not explained by disparate effects of these anesthetics on the baroreceptor reflex control of SNA or HR.

Adult↗
PubMed1995

Neurocirculatory responses to sevoflurane in humans. A comparison to desflurane.

BACKGROUND: Sevoflurane and desflurane are new volatile anesthetics with low blood solubilities that confer properties of rapid anesthetic induction and emergence. Desflurane has been associated with neurocirculatory excitation after the rapid increase in inspired concentrations. The current study evaluated and compared the sympathetic and hemodynamic responses associated with the administration of sevoflurane to those associated with administration of desflurane in humans. METHODS: After Institutional Review Board approval, 21 healthy, young (19-32 yr) volunteers were randomly selected for participation. Arterial and central venous pressures were measured directly, and heart rate, forearm blood flow, and plasma norepinephrine concentrations were determined indirectly. Efferent muscle sympathetic nerve activity was recorded by microneurography. After neurocirculatory recordings at conscious baseline, measurements were repeated beginning 2 min after 2 mg/kg propofol while the anesthetic was increased incrementally by mask over a 10-min period at 1%, 2%, and 3% sevoflurane (n = 12) or 3%, 6%, and 9% desflurane (n = 9). Responses to intubation were recorded and, 20 min later, recordings were evaluated during steady-state periods of 0.41, 0.83, and 1.24 MAC. Data also were obtained after steady-state 0.83 MAC measurements when the inspired gas concentration was rapidly increased to either 3% sevoflurane or 9% desflurane ("transition" to 1.24 MAC). RESULTS: Neurocirculatory variables did not differ between the two groups at conscious baseline. During the period of administration via mask and during the "transition" period, the significant increases in sympathetic nerve activity, heart rate, mean arterial pressure, and central venous pressure associated with desflurane were not observed with sevoflurane. Ten minutes after induction, mean arterial pressure and heart rate responses to intubation did not differ between groups. With increasing anesthetic concentration, there were progressive and similar decreases in mean arterial pressure in both groups and no changes in heart rate. Central venous pressure, sympathetic nerve activity, and plasma norepinephrine increased with the greater minimum alveolar concentration multiple of desflurane but not with that of sevoflurane. CONCLUSIONS: The neurocirculatory excitation seen with rapid increases in desflurane did not occur with sevoflurane. At steady-state, increasing the concentration of sevoflurane was associated with lower sympathetic nerve activity and central venous pressure and similar mean arterial pressure and heart rate with that of desflurane.

Anesthetics↗
PubMed1995

Ruptured aneurysm of the superficial femoral artery.

OBJECTIVE: True isolated "arteriosclerotic" aneurysms of the superficial femoral artery are rare. One case of isolated superficial femoral artery aneurysm and review of literature is reported. DESIGN: Case report and review of the literature. SETTING: Hospitalized care. PATIENT: An 80-year old man presenting with rupture of superficial femoral artery aneurysm was observed and treated with graft interposition, which resulted in limb salvage. INTERVENTION: Removal of the aneurysm and replacing of the arterial aneurysmatic segment by interposition of a polytetrafluoroethylene prosthetic graft. MEASURES: Patency of the graft with no evidence of ischemic or embolic complication assessed with a follow-up period of 6 months. RESULTS: From the review of the literature we collected 21 isolated true arteriosclerotic superficial femoral artery aneurysms in 17 patients. These aneurysms may be discovered after the onset of complications such as rupture (33%) or thrombosis and limb ischemia (19%). Other aneurysms are frequently concomitant (69%), mostly represented by abdominal aortic aneurysms (40%). CONCLUSIONS: Ruptured arteriosclerotic aneurysm of the superficial femoral artery is very uncommon and the treatment of choice is based on replacing of the aneurysmal segment with a prosthetic graft interposition or proximal and distal artery ligation and bypass. Early diagnosis and surgical reconstruction is recommended for patients with aneurysms of the superficial femoral artery that are 2.5 cm or greater in maximum diameter and for complicated aneurysms of any size.

Aged↗
PubMed1994

Sympathetic activation with desflurane in humans.

Although the blood pressure lowering effects of desflurane and isoflurane were similar at equi-MAC, we noted a different pattern of response during intervals of rapidly increasing the inspired concentration of desflurane, when substantial increases in SNA, HR, and MAP occurred. Because of the lower potency of desflurane compared to isoflurane, higher concentrations of desflurane are necessary to establish an adequate surgical plane of anesthesia. Although clinically relevant concentrations of isoflurane did not trigger sympathetic activation, isoflurane triggered responses at an inspired concentration (approximately 5%) nearly equal to that of desflurane. The present research demonstrates that the initial exposure to desflurane in clinically relevant concentrations following anesthetic induction and the deepening of anesthesia with higher concentrations of desflurane can be profoundly sympatho-excitatory. Considerable caution should be taken when administering desflurane to patients who may be placed at risk by these responses.

Adult↗
PubMed1994

Propofol and autonomic reflex function in humans.

The effects of continuous infusions of propofol on baroreceptor reflex regulation of cardiac rate and peripheral sympathetic nerve activity were evaluated in seven healthy, normotensive, young (19-26 yr), male volunteers. Heart rate, radial artery pressure, and continuous recordings of efferent sympathetic vasoconstrictor outflow (from the peroneal nerve) were monitored. Baroreceptor perturbations were produced by bolus intravenous injections of nitroprusside (100 micrograms) followed 60 s later by phenylephrine (150 micrograms). These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 micrograms.kg-1 x min-1) at least 25 min after subjects were paralyzed (vecuronium), had tracheas intubated, and were ventilated (30% O2:70% N2) to maintain normocarbia. Additional data were collected during hypercarbic conditions and during a lower infusion rate of propofol (100 micrograms.kg-1 x min-1) combined with 70% nitrous oxide. Propofol infusions significantly lowered sympathetic nerve activity (SNA) and blood pressure (BP) and increased heart rate (HR). Cardiac baroreceptor sensitivity determined during nitroprusside was reduced 60% during propofol infusions and was only subtly improved during simultaneous N2O administration. In contrast, reflex sensitivity during phenylephrine was not changed from awake values during each of the three experimental conditions. Reflex regulation of SNA was nearly abolished during normocarbic conditions under propofol anesthesia but restored to conscious levels during hypercarbia and during N2O administration. These data indicate that propofol markedly attenuates reflex responses to hypotension, but that reflex sympathetic responses are better maintained in hypercarbic conditions and when lower doses of propofol are used in conjunction with N2O.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Reproducibility of Doppler ultrasonography in the study of hepatic blood flow].

The reproducibility of hepatic blood flow measurement with pulsed Doppler US was assessed in 6 healthy volunteers. All subjects underwent two different study sessions and were examined by three different operators after overnight fasting. Each operator was blind to his measurements. Hepatic arterial and portal venous blood flow and hepatic arterial maximum velocity were measured; resistive index (RI), pulsatility index (PI) and hepatic perfusion index (HPI) were calculated. Each measurement was repeated three times per session. The data from repeated measurements were analyzed with the analysis of variance (ANOVA) method to assess the intra- and intersubject variations for each variable. The Scheffe test was used to evaluate intra- and interobserver variations. Significant differences among the 6 examined subjects were found for all the variables measured, except for hepatic arterial maximum velocity. The same subject exhibited significant differences in mean velocity of the main portal vein trunk and of its right branch, in maximum hepatic arterial velocity, RI, portal vein section area and blood flow. No significant interobserver variation was observed in the same session and no intraobserver variation detected for all the measurements performed in different sessions. Thus, we conclude that pulsed Doppler US is a repeatable method for measuring hepatic blood flow and may therefore be useful to detect changes in hepatic perfusion.

Analysis of Variance↗
PubMed1994

Color Doppler flow imaging of renal disease. Value of a new intravenous contrast agent: SH U 508 A (Levovist).

This study was aimed at assessing the diagnostic value of a new intravenous contrast agent SH U 508 A (Levovist) in improving color Doppler detection of renal mass vascularity. The study included 30 patients with renal masses: 22 adenocarcinomas, 1 sarcoma, 1 leiomyosarcoma, 1 urothelioma, 1 hemorrhagic cyst and 4 angiomyolipomas. The vascularization of the renal masses was investigated by means of color Doppler US, before and after the intravenous injection of SH U 508 A (Levovist), on the basis of blood flow patterns within and around the lesions. At precontrast scanning, low color Doppler signal at the periphery or within the lesions was observed in 13/30 patients only. After contrast administration, the signal-to-noise ratio increased, which allowed the visualization of tumor vessels in 26/30 patients. In 4/30 patients only no major enhancement of tumor vessels was observed. Our experience suggests that SH U 508 A (Levovist) improves color Doppler sensitivity in depicting the tumor vessels which were missed at baseline exams and in evaluating renal vein and inferior vena cava involvement.

Color↗
PubMed1993

Sympathetic hyperactivity during desflurane anesthesia in healthy volunteers. A comparison with isoflurane.

BACKGROUND: Desflurane has been reported to produce more tachycardia and hypertension on induction than isoflurane. The present study employed microneurography to determine whether these cardiovascular effects were related to sympathetic outflow. METHODS: In 14 healthy, young (age 20-31 yr) volunteers, arterial pressure was measured from the radial artery, forearm blood flow was derived by strain gauge plethysmography, and sympathetic nerve activity (SNA) directed to skeletal muscle blood vessels was recorded from a tungsten needle placed percutaneously into the peroneal nerve. Heart rate, blood pressure, muscle SNA, respiration, tidal volume, end-tidal carbon dioxide, and desflurane or isoflurane concentrations (infrared spectroscopy) were continuously monitored before and during anesthesia. Two minutes after administering thiopental (5 mg/kg) and vecuronium (0.2 mg/kg), desflurane (n = 7) or isoflurane (n = 7) was titrated gradually to the inspired gas over several minutes to 1.5 MAC. RESULTS: The initiation of desflurane anesthesia resulted in significant changes that included a 2.5-fold increase in SNA, hypertension (peak mean arterial pressure 114 +/- 3 mmHg), tachycardia (peak heart rate 102 +/- 6 beats/min), facial flushing, and tearing. Moderate upper airway obstruction developed in three subjects approximately 4 min after initiating desflurane, despite neuromuscular blockade. These responses were not observed in subjects receiving isoflurane. After tracheal intubation, the anesthetic concentration was maintained at 0.5 MAC for 30 min. Steady-state measurements of hemodynamics and SNA were obtained. Similar steady-state measurements were obtained 15 min after establishing 1.0 and 1.5 MAC. Both anesthetics produced a progressive reduction in blood pressure and forearm vascular resistance, and muscle SNA gradually increased. In subjects receiving desflurane, heart rate remained unchanged until the 1.5-MAC level was reached, at which time tachycardia (a 10-beat/min increase) was noted. The transition from 1.0 to 1.5 MAC desflurane resulted in significant heart rate increases (> 30 beats/min), hypertension (> 30 mmHg), and a doubling of SNA that persisted for several minutes. These responses did not occur in the isoflurane group. CONCLUSIONS: Titration of desflurane following thiopental induction and increasing the concentration of desflurane from 1.0 to 1.5 MAC result in sympatho-excitation, hypertension and tachycardia in healthy, young volunteers. Until methods are determined to attenuate these responses, desflurane should be administered with great caution to patients who may be placed at risk by these responses.

Adult↗
PubMed1992

Pneumonia complicating abdominal sepsis: an experimental model of hematogenous contamination of the lung.

Pulmonary infection complicating intra-abdominal sepsis is a major clinical problem. An experimental model for intra-abdominal sepsis was created with implantation of gelatin capsules, containing 3 x 10(8) cfu E. coli strain no. 2554, in the peritoneal cavity of 20 rats (10 animals received and 10 did not receive antibiotic therapy with ceftriaxone) in order to verify the role of the primary site of infection in the pathogenesis of pneumonia. Ten rats were sacrificed to determine the relative pulmonary weight and 10 were submitted to simple laparotomy and insertion of a germ-free capsule (sham-operated group). In this group of animals there was only one death (10%). All the rats that received antibiotic therapy survived until sacrifice while all the rats that did not receive ceftriaxone died, 7 within the 2nd and 3 on the 6th postoperative day. Pneumonia and peritonitis developed only in the animals that did not receive ceftriaxone. Bacteriological findings of material obtained from peritoneal and pleural cavities revealed the same strain of E. coli used for the experiment, suggesting that bacteria involved in the pleuro-pulmonary infections may originate in the primary site of infection and that antibiotic therapy started at the moment of contamination, can prevent this major complication.

Abdomen↗
PubMed1992

Sympathetic responses to induction of anesthesia in humans with propofol or etomidate.

Anesthetic induction with propofol commonly results in hypotension. This study explored potential mechanisms contributing to hypotension by recording cardiovascular responses including sympathetic neural activity from patients during induction of anesthesia with propofol (2.5 mg.kg-1 plus 200 micrograms.kg-1.min-1) or, for comparison, etomidate (0.3 mg.kg-1 plus 15 micrograms.kg-1.min-1). Twenty-five consenting, nonpremedicated, ASA physical status 1 and 2, surgical patients were evaluated. Measurements of R-R intervals (ECG), blood pressure (radial artery), forearm vascular resistance (plethysmography), and efferent muscle sympathetic nerve activity ([MSNA] microneurography: peroneal nerve) were obtained at rest and during induction of anesthesia. In addition, a sequential bolus of nitroprusside (100 micrograms) followed by phenylephrine (150 micrograms) was used to obtain data to quantitate the baroreflex regulation of cardiac function (R-R interval) and sympathetic outflow (MSNA) in the awake and anesthetized states. Etomidate induction preserved MSNA, forearm vascular resistance, and blood pressure, whereas propofol reduced MSNA by 76 +/- 5% (mean +/- SEM), leading to a reduction in forearm vascular resistance and a significant hypotension. Both cardiac and sympathetic baroslopes were maintained with etomidate but were significantly reduced with propofol, especially in response to hypotension. These findings suggest that propofol-induced hypotension is mediated by an inhibition of the sympathetic nervous system and impairment of baroreflex regulatory mechanisms. Etomidate, conversely, maintains hemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes.

Adult↗