ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The effect of acidosis and alkalosis on vascular smooth muscle contractions evoked by noradrenaline was studied. Helical strips of rabbit aorta were mounted for isometric tension recording. Acidosis (pH 7.24–6.51) was obtained by either increasing the Pco2(hypercapnic) and/or lowering the HCO3-concentration (hypobicarbonatic). Acidosis shifted the noradrenaline concentration-response curve to the right in a competitive manner. The maximal developed tension was unchanged atpH 7.24–6.90 and decreased by 30% atpH 6.51. Alkalosis (pH 7.61–8.04) did not alter nor-adrenaline-evoked contractions. The results suggest that hydrogen ions during acidosis (pH < 7.40) but not during alkalosis (pH > 7.40) exert α-adrenoceptor blocking properties.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Studies to date on the influence of N2O on cerebral blood flow (CBF) and metabolism in dogs, rodents, and humans have produced conflicting results. In the present study the authors have employed techniques in the awake, freely breathing nonstressed goat that allowed the authors to 1) serially obtain rapidly frozen cerebral cortical biopsy specimens (for labile metabolite assay) and 2) measure changes in cerebral O2metabolism (CMRO2) and total and regional CBF (rCBF). Thus, with each animal utilized as its own control, the authors studied N2O effects on the above variables. Two determinations of the effects of 1 h of N2O (70% via a mask) on these variables were performed on each animal. Following introduction of N2O, PaCO2and arterial blood pressure did not change, but arterial epinephrine levels declined over the 60-min period. Total CBF increased in the first 5 min of N2O exposure, reached a maximum of 165% control at 15 min, and then decreased to 143% control at 60 min. rCBF evaluations showed that much of this CBF increase was confined to cerebral cortical structures (188–246% control at 60 min). Over the same period cortical CMRO2increased to 170% of control. No appreciable changes in the levels of high-energy phosphates or glycolytic intermediates were found at 60 min of N2O. The authors attribute the described changes solely to the presence of N2O and not to sympathoadrenal influences, altered ventilation, or anything related to the experimental preparation, and they conclude that N2O (at least in goats) is associated with a marked cerebral cortical “activation.”

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The authors studied 12 patients who required deliberate hypotension for spinal fusion operations in order to investigate the efficacy of captopril for reducing dose requirement for sodium nitroprusside (SNP). Six patients, selected at random, were pretreated with captopril, 3 mg/kg po, and the remaining six patients served as controls. All patients received a similar anesthetic technique, consisting of thiopental 3 mg/kg, pancuronium 0.1 mg/kg, morphine 0.5 mg/kg, plus nitrous oxide 70% in oxygen. SNP was used to maintain mean arterial pressure (MAP) at 50–55 mmHg during deliberate hypotension lasting 140 · 13 minutes (mean · SE). Patients who received captopril required less SNP than untreated patients both early during hypotension (1.4 · 0.5 μg · kg−1· min−1vs.4.8 · 0.8 μg·kg−1· min−1,P< 0.05), as well as late during hypotension (2.2 · 0.2 μg · kg−1· min−1vs.5.6 · 0.6 μg · kg−1· min−1,P< 0.05). Whole blood cyanide was significantly lower in the patients pretreated with captopril than the untreated controls both early in the hypotensive period (2.7 · 0.6 μmol/1vs.13 · 4 μmol/1,P< 0.05) and also late in the hypotensive period (3.7 · 0.8 μmol/1vs.30 · 10 μmol/1,P< 0.05). MAP was reduced by captopril pre-treatment both following induction of anesthesia (64 · 4 mmHg captoprilvs.80 · 4 mmHg control,P< 0.05) and during surgery before deliberate hypotension (86 · 5 mmHg captoprilvs.100 · 4 control,P< 0.05). Cardiac output did not differ significantly between the groups, either awake or after anesthetic induction. The authors conclude that captopril pretreatment significantly reduces the dose of SNP required to produce deliberate hypotension and, therefore, reduces the potential for cyanide toxicity. No adverse hemodynamic consequences of combining captopril with thiopental, N2O, or morphine anesthesia were observed.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Patients and rats with chronic renal insufficiency (CRI) anesthetized with enflurane do not have significantly greater increases in postoperative serum inorganic fluoride levels when compared with subjects with normal renal function. The authors chose to investigate whether this observation is due to decreased anesthetic metabolism, secondary to the renal disease. Thus, male Fischer 344 rats with surgically induced CRI were studied to determine the effect of severe renal impairment: first, onin vivohepatic function as measured by a serum liver enzyme profile, and second, onin vitrohepatic metabolism as indicated by microsomal anesthetic defluorination rates and cytochrome P-450 levels. Rats were operated on in two stages, 1 week apart, and assigned to one of three groups. Group 1 rats had a capsule stripping of each kidney. Group 2 rats had a capsule stripping of one kidney and then a nephrectomy of the other. Group 3 rats had the upper and lower poles of one kidney excised and then a nephrectomy of the other. There was no change in renal function in rats from Group 1 and 2. Chronic renal insufficiency in Group 3 rats was manifested by threefold elevations in serum creatinine and urea nitrogen levels and reciprocal decreases in clearances. After 89–98 days, blood was obtained for a serum liver enzyme profile and rats were killed for determination ofin vitrohepatic metabolism. There were no changes suggestive of hepatic damage. Although there was an approximate 25% decrease in hepatic cytochrome P-450 content in the Group 3 rats, there was no evidence of altered drug metabolism as indicated by the rates of defluorination of methoxyflurane, enflurane, isoflurane, or sevoflurane. Lack of unusually high fluoride levels and subsequent nephrotoxicity in subjects with CRI anesthetized with enflurane is apparently not due to decreased hepatic defluorination of the anesthetic.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The object of this study was to determine whether high doses of insulin administered preventively in combination with glucose and potassium exert a protective effect upon the myocardium. This approach should result in a preoperative accumulation of the myocardial glycogen stores with an increased anaerobic provision of energy-rich substrates (ATP) during coronary ischemia. Two comparable groups of seven dogs each, undergoing experimental extracorporeal circulation (ECC) with 90-min aortic cross-clamping were examined. Cardiac output (CO), systolic left ventricular blood pressure (pventr), left ventricular enddiastolic pressure (LVEDP), mean central venous pressure (CVP), and heart rate (HR) were recorded at left atrial (LA) pressures of 5, 10, 15, and 20 mmHg in order to construct ventricular function curves. These data were registered prior to the onset of ECC (preischemic value), after termination of ECC and after two 10-min periods of reperfusion. The first group served as control and the second group received high iv doses of insulin (total 25 U/kg) within 60 min prior to the onset of the ECC. In the control group, pventrand CO after termination of the ECC and after the first reperfusion were significantly (P< 0.05) less than the preischemic values; after the second reperfusion they reached the preischemic range. In contrast, pventrand CO in the insulin group already were within the preischemic range at the termination of the ECC. After the first and the second reperfusion, CO was even greater than the preischemic value. LVEDP changed inversely, while CVP and HR showed no significant differences. The calculated left ventricular peak power (LVPpeak) changed proportional to the change in CO, and the systemic vascular resistance (SVR) did not show any significant change. It is concluded that preventive insulin administration helps maintain myocardial cell function during ischemia. By this method an earlier restitution of a vigorous cardiac performance can be achieved, indicating increased ischemic tolerance and improved myocardial protection.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Univariate descriptors such as the mean frequency and spectral edge frequency have been proposed for intraoperative representation of the EEG. Such univariate descriptors of the EEG are accurate only when the EEG behaves as a unimodal distribution of frequencies that change slowly with time. EEGs were recorded from 64 patients undergoing anesthetic inductions and 30 patients undergoing cardiopulmonary bypass to determine the characteristics of the observed distribution of frequencies. Multimodal EEG activity was observed in 64% of these cases, including 83% of those patients undergoing cardiopulmonary bypass. The differences between the two peaks averaged 7.6 Hz, and the average ratio of the power of the peaks to the intervening valley was 2.5:1 and 1.9:1. Calculations of mean frequency and spectral edge frequency failed to adequately reflect the complexity of the EEG in these cases. Burst-suppression activity was observed in 26% of cases during cardiopulmonary bypass, and averaging over time destroyed the characteristic pattern. Thus, univariate descriptors of the EEG appear inadequate to describe the behavior of EEG during anesthesia in a large percentage of cases.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The hemodynamic effects of verapamil pretreatmentversusno pretreatment were evaluated in five acutely hyperkalemic dogs. Using ECG evidence for severe hyperkalemia, the halothane-anesthetized dogs were rendered acutely hyperkalemic to similar plasma levels of K+(K+= 8.2 · 0.8 mEq/1 verapamil plus hyperkalemia, K+= 9.4 · 0.2 mEq/1 hyperkalemic controls). The verapamil–hyperkalemic group had significantly lower cardiac indexes (CI) (CI = 1.3 · 0.5 1 · min−1· m−2verapamil plus hyperkalemiavs.CI = 3.0 · 0.2 1 · min−1· m−2hyperkalemic controls) and lower mean arterial pressures (MAP = 60 · 13 mmHg verapamil plus hyperkalemiavs.MAP = 96 · 7 mmHg hyperkalemic controls). Calcium therapy for hyperkalemia that returned CI to control levels in hyperkalemic controls only partially reversed the severe hemodynamic depression and did not improve the AV block seen during hyperkalemia in the presence of the calcium entry blocker verapamil. Surprisingly, the total mEq of KC±l infused at the same rate into verapamil-pretreated dogs to result in similar high serum potassium levels was only one-third that required in dogs not pretreated with verapamil (1.6 · 0.3 mEq/kg KCl in verapamil–hyperkalemia groupvs.5.0 · 0.7 mEq/kg KCl in hyperkalemic controls). The authors conclude 1) verapamil renders hyperkalemia likely after much less intravenous K+administration; 2) the hemodynamic depression seen during acute hyperkalemia in halothane-anesthetized dogs is much more severe in the presence of verapamil; 3) calcium therapy is only partially effective in reversing the hemodynamic depression caused by hyperkalemia in the presence of the Ca++entry blocker verapamil; 4) Ca++in the dosage studied was not therapeutic for second-degree A-V block seen in the acutely hyperkalemic dog pretreated with verapamil and anesthetized with halothane.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6–9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia.Principal responses were as follows: mean arterial pressure (MAP) was 193 · 4 mmHg awake and decreased to 114 · 3 mmHg and 135 · 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 · 3 mmHg and to 69 · 3 mmHg and 96 · 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 · 1.3 ng · ml−1· h−1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents. Cardiac output was normal in awake rats and blood pressure elevation was due to increased peripheral resistance. Both anesthetic agents decreased cardiac output and myocardial blood flow and increased brain blood flow. The authors conclude that the cardiovascular and hormonal responses to halothane and enflurane anesthesia in renovascular hypertensive rats are different than the responses seen in normotensive rats. Such alterations may explain the differences seen in regional blood flow to various organs.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Fifteen patients undergoing thoracotomy were given 0.25 or 0.50 mg morphine intrathecally (L2–L3 or L3–L4) for an analgetic and pharmacokinetic study. Administration of morphine at the end of the operation resulted in a highly variable duration of analgesia ranging from 1–20.5 and 1–40 h for the 0.25 and 0.50 mg groups, respectively. Calculation of cumulative consumption pattern of additional analgesics given im indicated a dose-related analgesia lasting around 12 h. Morphine concentrations in the CSF were high and dose dependent. Thus, at 1 h, CSF concentrations (means · SEM) were 4,228 · 361 ng/ml and 10,447 · 1,538 ng/ml for the 0.25-and 0.50-mg groups, respectively. The plasma concentrations generally were very low,i.e., under 1 ng/ml.For the 0.50 and 0.25 mg groups, the terminal elimination half-life in CSF was 175 · 9 min and 196 · 13 min, respectively: the volume of CSF distribution was 0.88 · 0.16 ml · kg−1and 1.06 · 0.17 ml · kg−1, respectively; and the clearance from CSF was 2.81 · 0.41 μl · kg−1· min−1and 3.41 · 0.55 μl · kg−1· min−1, respectively (means · SEM).The study indicates that the significant pharmacokinetic parameter related to the long duration of analgesia after intrathecal morphine administration probably is the high CSF concentrations found, since the rate of elimination from CSF is similar to what is reported for morphine in plasma. Furthermore, modulation of nociceptive input in the thoracic region also may be achieved by lumbar administration, but a slower onset should be anticipated.

ISSN:0003-3022    

出版商:OVID    

年代:1984

数据来源: OVID