腹腔注射舒芬太尼对SD大鼠气道反应性的影响

目的观察腹腔注射舒芬太尼对SD大鼠气道反应性的影响。方法将32只雄性SD大鼠按随机数字表法分为4组,正常对照为A组(n=8,腹腔注射生理盐水,3 ml);实验组,B1组(n=8,腹腔注射舒芬太尼60μg/kg,3 ml)、B2组(n=8,腹腔注射舒芬太尼90μg/kg,3 ml)和B3组(n=8,腹腔注射舒芬太尼120μg/kg,3 ml)。第1天对4组大鼠进行气道阻力和气道反应性应用非侵入性气道阻力仪测定并作为参考基线。第15天按照分组要求对4组大鼠进行腹腔注射干预措施,测定腹腔注射后1、2、3、5、10 min气道阻力(specific airway resistances,Raw)(cmH2O·s),第30天按照分组要求对4组大鼠进行腹腔注射干预措施,3 min后进行气道反应性测定。采用t检验和Fisher确切概率法对实验数据进行分析。结果实验第1天,与对照组A组比较,B1组、B2组、B3组大鼠腹腔注射前基线气道阻力(3.27±0.74比3.35±0.65、3.30±0.81比3.35±0.65、3.41±0.68比3.35±0.65)差异无统计学意义(t=0.230,P>0.05、t=0.136,P>0.05、t=0.180,P>0.05);实验第15天,与对照组A组干预后1、2、3、5、10 min的气道阻力比较,B1组在1、2 min气道阻力(4.15±1.27比3.95±0.89、4.74±1.05比3.78±0.85)差异无统计学意义(t=0.365,P>0.05、t=2.010,P>0.05),在3、5 min气道阻力(4.92±1.33比3.55±0.69、4.89±1.43比3.47±0.71)差异有统计学意义(t=2.586,P<0.05、t=2.516,P<0.05),在10 min气道阻力(3.86±1.28比3.41±0.69)差异无统计学意义(t=0.875,P>0.05);B2组在1 min气道阻力(4.77±1.15比3.95±0.89)差异无统计学意义(t=1.595,P>0.05),在2、3、5 min气道阻力(6.01±1.47比3.78±0.85、6.95±1.68比3.55±0.69、5.75±1.52比3.47±0.71)差异有统计学意义(t=3.715,P<0.05、t=5.295,P<0.05、t=3.844,P<0.05),在10 min气道阻力(3.95±1.18比3.41±0.69)差异无统计学意义(t=1.117,P>0.05);B3组在1、2、3、5 min气道阻力(5.14±1.25比3.95±0.89、7.91±1.35比3.78±0.85、8.15±1.48比3.55±0.69、7.69±1.23比3.47±0.71)差异有统计学意义(t=2.194,P<0.05、t=7.322,P<0.05、t=7.968,P<0.05、t=8.404,P<0.05),在10 min气道阻力(4.16±1.08比3.41±0.69)差异无统计学意义(t=1.655,P>0.05);实验第30天,4组大鼠腹腔注射后气道反应性阳性率为,与对照组A组(0%)比较,B1组37.5%差异无统计学意义(P>0.05)、B2组75%差异有统计学意义(P<0.05)和B3组87.5%差异有统计学意义(P<0.05)。结论腹腔注射舒芬太尼对大鼠呼吸系统的影响表现在气道阻力增加和气道反应性增高,并呈剂量依赖性。但这种变化在短时间内逐渐增加并达到高峰后,进而逐渐减弱。     

Effects of thiopental on resistance vessels in cat skeletal muscle

Barbiturates are used clinically as anaesthetics and to reduce raised intracranial pressure. One side effect is hypotension, usually ascribed to a depression of cardiac contractility, while their effects on the resistance vessels are more controversial: both vasodilation and vasoconstriction have been described. This study analyzes the effects of thiopental on basal vascular tone in the cat skeletal muscle. We found that total resistance increased by almost 20% at low (50mol/l) and decreased down to about 50% of control at high (350 mol/l) plasma concentrations of thiopental. The vasoconstriction dominated in the large arterioles (i.d. >25 m) and the vasodilation in the small arterioles (i.d. <25 m). A dosedependent inhibition of myogenic vascular reactivity (here defined as the maximum resistance increase to a transient rise in transmural pressure) coincided with the vasodilation. Autoregulation of blood flow was depressed by thiopental. During vasoconstriction there was a net transcapillary fluid absorption and during vasodilation a net fluid filtration. The fluid movements could be ascribed to variations in capillary hydrostatic pressure. If applicable to the cerebral circulation these results suggest that thiopental at high plasma concentrations might induce, instead of reduce, interstitial brain oedema.     

Neurohumoral control of gallbladder motility in healthy subjects and diabetic patients with or without autonomic neuropathy

Patients affected by diabetes mellitus are reported to have an increased incidence of gallbladder abnormalities. The pathophysiologic mechanisms for this phenomenon are unclear. In the present study ultrasonography was used to determine gallbladder emptying in response to a meal or separate cephalic or hormonal stimulation in 21 diabetic patients and 10 healthy subjects. Gallbladder emptying and refilling after a meal were similar in diabetic patients and healthy subjects. When diabetics were divided according to the presence or absence of cardiac autonomic neuropathy (AN), a significant reduction of gallbladder emptying in response to cephalic stimulation was found in diabetics with AN (P<0.01 in comparison with diabetics without AN or healthy subjects). A dose-response curve of gallbladder emptying in response cerulein, a cholecystokinin analog, at concentrations of 0.25, 1, and 4 g/kg/min was evaluated. No differences of gallbladder emptying were found in the three groups of subjects, indicating that gallbladder sensitivity to hormonal stimulation is not changed in diabetic patients with or without AN. Diabetic patients with AN have a significant reduction of gastric acid output and pancreatic polypeptide (PP) secretion in response to cephalic stimulation (P<0.05 in comparison with diabetic patients without AN or healthy subjects). Cerulein-induced PP secretion was similar in all three groups of subjects (P>0.05). This study indicates that in diabetic patients with AN, gallbladder emptying as well as gastric acid and PP secretions induced by neural stimulation are markedly reduced in comparison to diabetics without AN.     

Nerve-induced release of nitric oxide in the rabbit gastrointestinal tract as measured by in vivo microdialysis

1. Nitric oxide (NO) has been suggested as a gastrointestinal neurotransmitter, mediating the gastric receptive relaxation and the relaxation in the peristaltic reflex. The aim of the present study was to measure nerve-induced NO formation in vivo in the gastrointestinal tract.
2. Formation of the nitric oxide oxidation products nitrite and nitrate during vagal nerve stimulation were measured in the anaesthetized rabbit. Microdialysis probes were inserted into the wall of the stomach and proximal colon, and nitrite and nitrate in dialysate measured by capillary electrophoresis.
3. During bilateral vagal nerve stimulation there was an increase in nitrite and nitrate formation at the level of the stomach and in nitrite formation at the level of the colon. This increase was inhibited by intravenous administration of the NO synthase inhibitor N^ω-nitro-L-arginine methyl ester (L-NAME 30 mg kg⁻¹). Furthermore, L-NAME significantly increased nerve-induced gastric and colonic contractions, as well as spontaneous colonic contractions.
4. In summary, we present a new methodological procedure for quantification of small changes in nitric oxide formation in vivo. This study provides evidence that nitric oxide is released in the stomach and colonic wall during vagal nerve activity, at concentrations able to cause inhibition of smooth muscle contractions in vivo.

     

Demonstration of the existence of nitric oxide-independent as well as nitric oxide-dependent vasodilator mechanisms in the in situ renal circulation in near term pregnant rats

1. We have investigated the role of endogenous nitric oxide on renal vascular reactivity in late pregnancy in in situ blood perfused kidneys of α-chloralose anaesthetized Wistar-Kyoto rats. Nitric oxide synthesis inhibition was achieved by intravenous administration of N^G-nitro-L-arginine or N^G-nitro-L-arginine methyl ester.
2. Intra-arterial mean blood pressure was lower in pregnancy compared with nonpregnant controls. Following nitric oxide synthesis inhibition mean blood pressure increased in both pregnant and nonpregnant groups, but remained lower in pregnant animals.
3. Basal renal perfusion pressure was similar in pregnant and nonpregnant groups. Intravenous administration of N^G-nitro-L-arginine resulted in dose-dependent increases in renal perfusion pressure but responses were substantially depressed in pregnancy.
4. Renal vasoconstrictor responses to regional angiotensin II (AII) were decreased in pregnancy, whereas those to noradrenaline (NA) did not differ from nonpregnant controls. N^G-nitro-L-arginine (5 mg kg⁻¹) potentiated renal responses to regional AII and NA in both groups, but AII responses remained lower in pregnancy. Blunted renal AII responses in pregnancy were still evident following large doses of N^G-nitro-L-arginine methyl ester (100 mg kg⁻¹).
5. The results demonstrate that nitric oxide synthesis inhibition increases renal perfusion pressure to a lesser extent in pregnant compared with nonpregnant rats, and that reduced renal pressor responses to AII are still evident in pregnancy after nitric oxide synthesis inhibition.
6. These results suggest that although endogenous nitric oxide synthesis modulates renal vasoconstrictor responses in both pregnant and nonpregnant animals, this mechanism does not fully account for the blunted renal vasoconstrictor responses to regional AII or nitric oxide inhibitors in near term pregnant rats. The nature of this important physiological vasodilator mechanism in pregnancy remains to be elucidated.

     

Adenosine for the management of patients with tachycardias--a new protocol

We developed a new protocol for diagnosis and treatment of patientswith sustained tachycardias (heart rate > 150 beats. min^–1).The patients first underwent vagal manoeuvres; if those remainedunsuccessful, i.v. adenosine in increasing doses of 6, 12, and18 mg was administered until sinus rhythm (SR) or transientatrioventricular (AV) block, unmasking the underlying rhythm,was recorded. In the latter and in the non-responding casesother antiarrhythmics were applied. Ninety-three episodes of tachycardia in 46 patients were treatedaccording to this protocol. Six episodes (6%) were terminatedby carotid massage, 64 of the remaining 87 episodes (74%) respondedto adenosine with return to SR. Conversion to SR occurred moreoften in episodes with narrow- than in wide-complex tachycardia(81 vs 59%, P<005). To achieve SR, the mean adenosine dosewas lower in narrow- than in wide-complex tachycardia (13±8vs 21 ± 10 mg; P<0.01). The duration of asystole afteradenosine did not differ between these two groups, whereas theduration of arrhythmia after adenosine differed significantly(8.5 ± 5.8 vs 18.6 ± 22.9 s; P<0.05). Sideeffects of adenosine such as flush, dyspnoea, and chest paindid not seem to be dose dependent and occurred in about 20%. According to our protocol, in more than 75% SR was achievedin patients with sustained tachycardias after vagal manoeuvresand adenosine.     

N—苯基马来酰亚胺／苯乙烯／丙烯腈共聚合体系的研究

测定了６０℃下Ｎ－苯基马来酰亚胺在苯溶剂中分别与苯乙烯,丙类腈共聚的二元竞聚率,并据此估算其三元共聚物组成,研究表明,实验值和计算值较为接近,如果适当控制混合单体比例和反应条件,可望得到组成较均一的共聚物。     

Effect of Oral Administration of Dotarizine on Cerebrovasculature Subjected to Constriction Followed by Dilatation in Rabbits

In the study presented the effect of Dotarizine on blood flow velocity in cerebral arteries - in middle cerebral artery (MCA), and basilar artery (BA)- was investigated and compared utilising transcranial Doppler sonography during normoventilation, 15 min hyperventilation with subsequent 3 min anoxia in anaesthetized rabbits. In the Dotarizine treated group (12 rabbits) 25 mg/kg of Dotarizine dissolved in 0,25% agar was administered orally for five days twice daily. In the control group (9 rabbits) animals were fed with agar of the same concentration. The results revealed that decrease of flow velocity caused by hyperventilation and increase during anoxia were less pronounced in the Dotarizine treated group than in control group of animals. A difference between changes of flow velocity in MCA and BA during anoxia was found and the different reactivity of both vessels was established.     

CO2 and indomethacin vasoreactivity in patients with head injury

Summary The purpose of this study was to compare the effect of hyper-ventilation and indomethacin on cerebral circulation, metabolism and pressures in patients with acute severe head injury in order to see if indomethacin may act supplementary to hyperventilation. Fourteen severely head injured patients entered the study. Intracranial pressure (ICP), mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored continuously. Within the first four days after the trauma the CO₂ and indomethacin vasoreactivities were studied by measurements of cerebral blood flow (CBF) (Cerebrograph 10a, intravenous¹³³Xe technique) and arterio-venous difference of oxygen (AVdO₂). Ischaemia was evaluated from changes in CBF, saturation of oxygen in the jugular bulb (SvjO₂), lactate and lactate/oxygen index (LOI). Data are presented as medians and ranges, results are significant unless otherwise indicated. Before intervention ICP was well controlled (14.8 (9–24) mmHg) and basic CBF level was 39.1 (21.6–75.0) ml/100 g/min). The arterio-venous oxygen differences were generally decreased (AVdO₂ = 4.3 (1.8–8.1) ml/100 ml) indicating moderate luxury perfusion. Levels of CMRO₂ were decreased (1.54 (0.7–3.2) ml/100 g/min) as well.Duringhyperventilation (APaCO₂ = 0.88 (0.62–1.55) kPa) CBF decreased with 11.8 (–33.4–29.7) %/kPa and ICP decreased with 3.8 (0–10) mmHg. AVdO₂ increased 34.0 (4.0–139.2) %/kPa, MABP was unchanged, CMRO₂ and CPP increased (CPP = 3.9 (–10–20) mmHg). AVD (lactate) and LOI were unchanged. No correlations between CBF responses to hypocapnia and outcomes were observed.An i.v. bolus dose ofindomethacin (30 mg) decreased CBF 14.7 (–16.7–57.4) % and ICP decreased 4.3 (–1–17) mmHg. AVdO₂ increased 27.8 (–40.0–66.7)%, MABP (MABP = 4.9 (–2–21) mmHg) and CPP (CPP = 8.7 (3–29) mmHg) increased while CMRO₂ was unchanged. No changes in AVd (lactate) and LOI indicating cerebral ischaemia were found.Compared to hyperventilation (changes per 1 kPa, at PaCO₂ level = 4.05 kPa) the changes in MABP, CPP and CBF were significantly greater after indomethacin, while the changes in AVdO₂, ICP, SvjO₂, and LOI were of the same order of magnitude.Nocorrelation between relative reactivities to indomethacin and CO₂, evaluated from changes in CBF and AVdO₂, or between the decrease in ICP after the two procedures were found. Thus, some patients reacted to indomethacin but not to hyperventilation, and vice versa.These results suggest that indomethacin and hyperventilation might act independently, or in a complementary fashion in the treatment of patients with severe head injury.