Acute and chronic arterial and venous effects of captopril in congestive cardiac failure.

OBJECTIVE--To determine whether captopril alters peripheral venous tone in patients with congestive cardiac failure. DESIGN--Open study of patients at start of captopril treatment and three months later. SETTING--A hospital gamma camera laboratory. PATIENTS--16 Men with congestive cardiac failure in New York Heart Association class II or III, aged 57-73. INTERVENTIONS--Patients were initially given 500 micrograms sublingual glyceryl trinitrate followed by 25 mg oral captopril. The study was then repeated after three months'' captopril treatment. MAIN OUTCOME MEASURES--Previously validated non-invasive radionuclide techniques were used to measure changes in central haemodynamic variables and peripheral venous volumes in the calf. RESULTS--After 25 mg captopril there were falls in blood pressure and relative systemic vascular resistance and increases in cardiac index and left ventricular ejection fraction. This was accompanied by a 16% increase in peripheral venous volume (95% confidence interval 13.4% to 18.4%, p less than 0.01), which compared with an 11% increase after 500 micrograms glyceryl trinitrate (10% to 12%, p less than 0.01). Eleven patients were restudied after three months'' continuous treatment with captopril. The resting venous volume was higher than it had been initially, by about 10%, and increased by a further 8.4% after 25 mg captopril (5.4% to 11.4%, p less than 0.05). CONCLUSIONS--Captopril is an important venodilator. Venous and arterial dilatation are produced short term and during long term treatment.     

Nitric oxide regulates retinal vascular tone in humans

The purpose of the present study was to investigate the contribution of basal nitric oxide (NO) on retinal vascular tone in humans. In addition, we set out to elucidate the role of NO in flicker-induced retinal vasodilation in humans. Twelve healthy young subjects were studied in a three-way crossover design. Subjects received an intravenous infusion of either placebo or NG-monomethyl-L-arginine (L-NMMA; 3 or 6 mg/kg over 5 min), an inhibitor of NO synthase. Thereafter, diffuse luminance flicker was consecutively performed for 16, 32, and 64 s at a frequency of 8 Hz. The effect of L-NMMA on retinal arterial and venous diameter was assessed under resting conditions and during the hyperemic flicker response. Retinal vessel diameter was measured with a Zeiss retinal vessel analyzer. L-NMMA significantly reduced arterial diameter (3 mg/kg: -2%; 6 mg/kg: -4%, P < 0.001) and venous diameter (3 mg/kg: -5%; 6 mg/kg: -8%, P < 0.001). After placebo infusion, flicker induced a significant increase in retinal vessel diameter (P < 0.001). At a flicker duration of 64 s, arterial diameter increased by 4% and venous diameter increased by 3%. L-NMMA did not abolish these hyperemic responses but blunted venous vasodilation (P = 0.017) and arterial vasodilation (P = 0.02) in response to flicker stimulation. Our data indicate that NO contributes to basal retinal vascular tone in humans. In addition, NO appears to play a role in flicker-induced vasodilation of the human retinal vasculature.     

Maintenance of silastic–teflon shunts for intermittent haemodialysis

The occurrence of infection in the tissues surrounding external arteriovenous shunts was studied and die important relationship of pyogenic infection to clotting was confirmed. The local application of fusidic add tulle and lanolin greatly reduced the occurrence of both infection and clotting and the need for cannula replacement.Urokinase used for declotting shunts when standard procedures had failed, restored blood flow whether dotting was related to infection or to local vascular factors. This treatment is not advised when clotting is associated with a local abscess, as it may make cannula replacement necessary. Severe local vascular factors, such as metastatic calcification, Raynaud''s phenomenon, and venous stenosis, may lead to poor blood flow, so that despite clot lysis elective cannula replacement or the creation of a subcutaneous arteriovenous fistula is required.     

剂量精确的大鼠无创气管滴注方法

目的建立一种滴注剂量精确的大鼠无创气管滴注方法。方法选用一次性使用静脉输液针的胶管制作套管,透射光插管法行大鼠气管插管,微量进样器平头针经由套管插入气管进行滴注。滴注液体为生理盐水,滴注剂量5～200μL,精确度为1μL。结果在体重200—350g的10只大鼠上共完成50次气管滴注操作,实验过程中和实验之后大鼠均无异常表现。结论套管微量进样器法具有无创、精确、安全的特点,可广泛应用于大鼠经气管给药或染毒的各类研究。     

Lung lymph flow during volume infusions

We investigated the effect of intravenous isotonic crystalloid solution infusion on lung lymph flow. Tracheobronchial lung lymph vessels were cannulated in 13 anesthetized dogs. The lymph flow rate was measured 1) with the lymph flowing against atmospheric pressure (QL), and 2) with the pressure at the outflow end of the lymph cannula equal to systemic venous pressure (QLV). QL and QLV were measured alternately in each lymph vessel. In one group of nine dogs, the base-line QL and QLV were 18 +/- 9 and 13 +/- 6 (SD) microliter/min, respectively (P less than 0.05). QL increased by 4.8 +/- 1.4-fold, and QLV increased by 3.5 +/- 2.1-fold during a 4-h infusion of 25 ml X kg-1 X h-1 of Ringer solution. QLV was significantly less than QL at all times. The increases in lymph flow were caused primarily by a reduction in the effective resistance of the lymph vessels with little rise in the pressure driving lymph from the lungs. Because QLV flowed against systemic venous pressure, the increase in QLV was blunted by a 3.1 +/- 2.3 cmH2O rise in venous pressure during the infusions. In the remaining four dogs, we infused Ringer solution rapidly in order to raise venous pressure to greater than 15 cmH2O. This caused QL to increase by 25 +/- 7-fold; however, QLV decreased to zero. We conclude that elevations in venous pressure which occur during volume infusions oppose lung lymph flow and lead to accumulation of excess fluid in the lungs.     

Arterial versus venous changes in vascular capacitance during nitroprusside infusion: a vascular modelling study.

The distributions of nitroprusside (NP) induced changes in vascular capacitance, arterial versus venous, are unknown. We measured canine ileal arterial and venous pressures and total (isolated loop) vascular volumes (scintigraphy), before and during NP infusion. NP sufficient to decrease perfusion pressure by 30% increased total vascular volume to 111 +/- 3% (+/- SEM) of control (p < 0.01). Increasing flow to restore perfusion pressure increased volume 4% more (p < 0.01). Assuming a two-compartment model and on the basis of the literature data, changes in venous capacitance were estimated and compared with arterial capacitance. During constant-flow perfusion, NP increased venous volume by 10.0% (vs. 18.1%, arterial). When flow was increased to restore pressure, venous volume increased by another 3.7% (vs. 2.6%, arterial). Assuming an original arterial to venous volume ratio of 133/1033, the final, constant-pressure increase in venous volume was almost 4 times the arterial increase. In conclusion, the increase in vascular volume during NP infusion was due primarily to similar-magnitude, active increases in venous and arterial capacitances (i.e., rightward shifts in pressure-volume relations). However, as venous volume is so much larger than arterial, the NP-induced increase in venous volume was greater.     

儿童重症监护病房医院感染暴发白色念珠菌血流感染4例分析

摘要 目的：探讨儿童重症监护病房白色念珠菌血流感染暴发的临床表现、危险因素、控制措施等,为预防和控制院内白色念珠菌血流感染暴发提供科学依据。方法：以2018年7月我院儿童重症监护病房发生的4例白色念珠菌血流感染暴发患儿为研究对象,分析患儿临床情况、临床特征、危险因素、暴发原因以及采取的预防控制措施。结果：4例医院感染暴发白色念珠菌血流感染患儿均存在基础疾病、有机械通气史、存在中心静脉或动脉置管、静脉或动脉置管前后均使用碘伏消毒、曾使用广谱抗生素、输血制品,白色念珠菌血流感染后最突出的临床表现均是发热。药敏方面,医院感染暴发的4例白色念珠菌感染患儿对唑类及5-氟胞嘧啶均耐药,但对两性霉素B均敏感。经拔除血管置管、减少或者避免广谱抗菌药的应用,根据药敏使用卡泊芬净及两性霉素B抗真菌等积极治疗,1例患儿放弃治疗后死亡,3例患儿顺利出院。通过Fisher确切概率法分析可知,留置中心静脉或动脉置管是儿童重症监护病房发生医院感染暴发白色念珠菌血流感染的危险因素（P<0.05）。结论：留置中心静脉或动脉置管是儿童重症监护病房发生医院感染暴发白色念珠菌血流感染的危险因素,医院感染暴发白色念珠菌血流感染患儿最突出的临床表现是发热,唑类及5-氟胞嘧啶耐药的患儿使用卡泊芬净及两性霉素B可能获得较好的治疗效果。     

Effect on breathing of acute pressure rise in pulmonary artery and right ventricle

We tested the hypothesis that breathing would be regulated in response to right ventricular and pulmonary arterial pressure changes when secondary events are controlled. Dogs were anesthetized, thoracotomies were performed, and cardiopulmonary bypass perfusion was established. Lungs were inflated to sustained pressures. The left diaphragmatic lobe was retrogradely cannulated and all other lobar arteries were ligated, forming a pulmonary arterial sac that drained to the oxygenator from the cannula and filled from systemic venous return by the beating right ventricle. Right atrial pressure was adjusted to produce sac flows of approximately 400 ml/min. We recorded systemic and pulmonary arterial pressures, sac flow, and the integrated diaphragm electromyogram (DEMG). Resistive loads were imposed on sac outflow by adjusting a clamp. Loaded mean pulmonary arterial pressures ranged from 27 to 70 Torr. Loading increased respiratory frequency without affecting peak DEMG amplitude. Responses did not occur after vagotomy. Effects were quantitatively modest: pressurization to approximately 50 Torr increased frequency approximately 3.4 breaths/min (22%). The magnitude of change was insufficient to explain in intact dogs the ventilatory responses that have been attributed to this reflexogenic unit.     

Diameter changes in skeletal muscle venules during arterial pressure reduction

Previous studies in skeletal muscle have shown a substantial (>100%) increase in venous vascular resistance with arterial pressure reduction to 40 mmHg, but a microcirculatory study showed no significant venular diameter changes in the horizontal direction during this procedure. To examine the possibility of venular collapse in the vertical direction, a microscope was placed horizontally to view a vertically mounted rat spinotrapezius muscle preparation. We monitored the diameters of venules (mean diameter 73. 8 +/- 37.0 microm, range 13-185 microm) oriented horizontally and vertically with a video system during acute arterial pressure reduction by hemorrhage. Our analysis showed small but significant (P < 0.0001) diameter reductions of 1.0 +/- 2.5 microm and 1.8 +/- 3. 1 microm in horizontally and vertically oriented venules, respectively, upon reduction of arterial pressure from 115.0 +/- 26. 3 to 39.8 +/- 12.3 mmHg. The venular responses were not different after red blood cell aggregation was induced by Dextran 500 infusion. We conclude that diameter changes in venules over this range of arterial pressure reduction are isotropic and would likely increase venous resistance by <10%.     

Quinton-Scribner Cannulas for Hemodialysis—Review of Four Years' Experience

Data on a study group of 52 maintenance hemodialysis patients cannulated with Quinton-Scribner cannula in a four-year period were analyzed. The average period of dialysis was 11.8 months with either a pumped coil or a pumpless Kiil artificial kidney system. One hundred and forty-five cannulations were performed. The mean arterial cannula survival was 7.8 months and the mean venous cannula survival was 7.2 months. The exceptional longevity of cannula survival occurred despite the high incidence of atherosclerotic changes at operation and the advanced mean age (47 years) of the patients. The cannula longevity may be partially related to the technique used and to meticulous surgical care given the patient before and after cannulation.Complications from cannulation included two deaths, one from septic pulmonary embolism of Staphylococcus origin, and one from acute Pseudomonas endocarditis. A total of 36 infections of cannulas were recognized, the majority being due to Staphylococcus aureus, but 28 percent being secondary to Gram-negative bacteria.     

Dynamic synchronization analysis of venous pressure-driven cardiac output in rainbow trout

Measurement of venous function in vivo is inherently difficult. In this study, we used the Hilbert transform to examine the dynamic relationships between venous pressure and cardiac output (CO) in rainbow trout whose blood volume was continuously increased and decreased by ramp infusion and withdrawal (I/W). The dorsal aorta and ductus Cuvier were cannulated percutaneously and connected to pressure transducers; a flow probe was placed around the ventral aorta. Whole blood from a donor was then I/W via the dorsal aortic cannula at a rate of 10% of the estimated blood volume per minute, and the duration of I/W was varied from 40, 60, 80, 90, 120, 230, 240, 260, 300, and 340 s. Compliance [change in (delta) blood vol/deltavenous pressure] was 2.8 +/- 0.2 ml x mmHg-1x g-1 (N = 25 measurements; 6 fish with closed pericardium) and 2.8 +/- 0.3 ml. mmHg-1x kg-1 (N = 19 measurements, 4 fish with open pericardium). Compliance was positively correlated with the duration of I/W, indicative of cardiovascular reflex responses at longer I/W durations. In trout with closed pericardium, CO followed venous pressure oscillations with an average time lag of 4.2 +/- 1.0 s (N = 9); heart rate (HR) was inversely correlated with CO. These studies show that CO is entrained by modulation of venous pressure, not by HR. Thus, although trout have a rigid pericardium, venous pressure (vis-a-tergo), not cardiac suction (vis-a-fronte), appears to be the primary determinant of CO. Estimation of venous compliance by ramp-modulation of venous pressure is faster and less traumatic than classical capacitance measurements and appears applicable to a variety of vertebrate species, as does the Hilbert transform, which permits analysis of signals with disparate frequencies.     

The effect of pentosan polysulphate (SP54) on the fibrinolytic enzyme system. An experimental animal study

Pentosan polysulphate (SP54) causes a transient increase in blood fibrinolysis in conscious and anaesthetized rats. Postoperative "fibrinolytic shutdown" was prevented by a dose of 2 mg/kg body weight but there appeared to be no dose-response relationship with higher doses. Fibrinolysis was also measured in conscious unstressed animals using an indwelling jugular cannula. The venous response to SP54 in these animals was substantially higher than the arterial response. Experiments with an inferior vena cava model of thrombosis suggest that a single dose of 10 mg/kg pentosan polysulphate given 90 min after thrombus formation is sufficient to achieve thrombolysis. This effect was more marked if the animals were given multiple doses over 24 to 48 hours.     

Microcirculatory pathways in normal human spleen, demonstrated by scanning electron microscopy of corrosion casts

Confusion regarding microcirculatory pathways in normal human spleen has arisen due to extrapolation from pathological material and from other mammalian spleens, not to mention difficulties in tracing intricate three-dimensional routes from the study of thin sections or cut surfaces of tissue. We examined microcirculatory pathways in normal human spleens freshly obtained from organ transplant donors. A modified corrosion casting procedure was used to obtain an open view of vessels and their connections. Our results demonstrate: 1) "arteriolar-capillary bundles" within lymphatic nodules and extensive branching of arterioles in the marginal zone (MZ); 2) the marginal sinus around lymphatic nodules; 3) the peri-marginal cavernous sinus (PMCS) outside the MZ or immediately adjacent to the nodule itself; the PMCS receives flow via ellipsoid sheaths and MZ, or directly from arterial capillaries, and drains into venous sinuses; 4) fast pathways for flow into venous sinuses via ellipsoid sheaths; 5) arterial capillary terminations in the reticular meshwork of the red pulp or MZ ("open" circulation); direct connections to venous sinuses also occur ("closed" circulation), although rarely; and 6) numerous open-ended venous sinuses in the MZ, allowing a large proportion of the splenic inflow to bypass the red cell filtration sites in the reticular meshwork and at venous sinus walls.     

Effect of erythrocyte aggregation at normal human levels on functional capillary density in rat spinotrapezius muscle

Previous studies have shown that functional capillary density (FCD) is substantially reduced by erythrocyte aggregation. However, only supranormal levels of aggregability were studied. To investigate the effect of erythrocyte aggregability at the level seen in healthy humans, the FCD of selected capillary fields in rat spinotrapezius muscle was determined with high-speed video microscopy under normal (nonaggregating) conditions and after induction of erythrocyte aggregation with Dextran 500 (200 mg/kg). To examine shear rate dependence, the effect was studied both at normal and reduced arterial pressures (50 and 25 mmHg), the latter achieved by short periods of hemorrhage. In a separate study, volume flow was determined in arterioles (52.1 +/- 3.7 microm) under the same conditions. Before Dextran 500 infusion, FCD fell to 91% and 76% of control values, respectively, when arterial pressure was reduced to 50 and 25 mmHg. After Dextran 500 infusion, FCD was 96% at normal arterial pressure and fell to 79% and 37% of normal control values at 50 and 25 mmHg. All FCD values were significantly lower after dextran infusion. FCD reduction after lowering arterial pressure or dextran infusion appeared to be due to plasma skimming rather than capillary plugging. Reduction of FCD by dextran at reduced pressure was compensated by increased red blood cell flux in capillaries with red blood cell flow. We conclude that the level of aggregability seen in healthy humans is an important determinant of FCD only at reduced arterial pressure.     

The accelerated atherogenesis of venous grafts might be attributed to aggravated concentration polarization of low density lipoproteins: A numerical study

We hypothesize that after implantation the much elevated water filtration rate of venous grafts may cause aggravated concentration polarization of low density lipoproteins (LDLs), in turn lead to the accelerated atherogenesis of the grafts. To verify the hypothesis, we numerically simulated the transport of LDLs in various models of arterial bypasses with different grafts (veins or arteries) and geometrical configurations. The results showed that the venous grafts might endure abnormally high lipid infiltration/accumulation within the vessel wall due to severely elevated luminal surface LDL concentration. When compared to the conventional bypass models, the S-type bypass had the lowest luminal surface LDL concentration along its host artery floor, but the highest degree of risk to develop atherosclerotic lesions in its venous graft. Among the three conventional bypass models, the one with 30° anastomosis had the lowest risk to develop atherosclerosis in the venous graft. In conclusion, when compared with the bypass models with arterial grafts, the venous bypass models had rather high levels of LDL concentration polarization (c_w) in the vein grafts, especially at the early stages of implantation. This might result in high infiltration/accumulation of LDLs within the walls of the venous grafts, leading to a fast genesis/development of atherosclerosis there.     

Comparative effects of vasodilator drugs on flow distribution and venous return

Systemic vascular effects of hydralazine, prazosin, captopril, and nifedipine were studied in 115 anesthetized dogs. Blood flow (Q) and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant Q showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. At three dose levels producing comparable reductions in systemic arterial pressure (30-40% at the highest dose), these drugs had different effects on flow distribution and venous return. Hydralazine and prazosin had parallel and balanced effects on arterial resistance of the two vascular compartments, and flow distribution was unaltered. Captopril preferentially reduced arterial resistance of the compartment with a slow time constant for venous return (-26 +/- 6%, -30 +/- 6%, -50 +/- 5% at 0.02, 0.10, and 0.50 mg X kg-1 X h-1, respectively; means +/- SEM) without altering arterial resistance of the fast time-constant compartment. Blood flow to the slow time-constant compartment was increased 43 +/- 14% at the highest dose, and central blood volume was reduced 108 +/- 15 mL. In contrast, nifedipine had a balanced effect on arterial resistance with the lowest dose (0.025 mg/kg) but caused a preferential reduction in arterial resistance of the fast time-constant compartment at higher doses (-38 +/- 4% and -55 +/- 2% at 0.05 and 0.10 mg/kg, respectively). Blood flow to the slow time-constant compartment was reduced 36 +/- 5% at the highest dose of nifedipine, and central blood volume was increased 66 +/- 12 mL. Total systemic venous compliance was unaltered or slightly reduced by each of the four drugs. These results add further evidence to the hypothesis that peripheral blood flow distribution is a major determinant of venous return to the heart.     

Hindlimb unweighting affects rat vascular capacitance function

Microgravity is associated with an impaired stroke volume and, therefore, cardiac output response to orthostatic stress. We hypothesized that a decreased venous filling pressure due to increased venous compliance may be an important contributing factor in this response. We used a constant flow, constant right atrial pressure cardiopulmonary bypass procedure to measure total systemic vascular compliance (C(T)), arterial compliance (C(A)), and venous compliance (C(V)) in seven control and seven 21-day hindlimb unweighted (HLU) rats. These compliance values were calculated under baseline conditions and during an infusion of 0.2 microg*kg(-1)*min(-1) norepinephrine (NE). The change in reservoir volume, which reflects changes in unstressed vascular volume (DeltaV(0)) that occurred upon infusion of NE, was also measured. C(T) and C(V) were larger in HLU rats both at baseline and during the NE infusion (P < 0.05). Infusion of NE decreased C(T) and C(V) by ~20% in both HLU and control rats (P < 0.01). C(A) was also significantly decreased in both groups of rats by NE (P < 0.01), but values of C(A) were similar between HLU and control rats both at baseline and during the NE infusion. Additionally, the NE-induced DeltaV(0) was attenuated by 53% in HLU rats compared with control rats (P < 0.05). The larger C(V) and attenuated DeltaV(0) in HLU rats could contribute to a decreased filling pressure during orthostasis and thus may partially underlie the mechanism leading to the exaggerated fall in stroke volume and cardiac output seen in astronauts during an orthostatic stress after exposure to microgravity.     

Chronic central leptin infusion restores cardiac sympathetic-vagal balance and baroreflex sensitivity in diabetic rats

This study tested whether leptin restores sympathetic-vagal balance, heart rate (HR) variability, and cardiac baroreflex sensitivity (BRS) in streptozotocin (STZ)-induced diabetes. Sprague-Dawley rats were instrumented with arterial and venous catheters, and a cannula was placed in the lateral ventricle for intracerebroventricular (ICV) leptin infusion. Blood pressure (BP) and HR were monitored by telemetry. BRS and HR variability were estimated by linear regression between HR and BP responses to phenylephrine or sodium nitroprusside and autoregressive spectral analysis. Measurements were made during control period, 7 days after induction of diabetes, and 7 days after ICV leptin infusion. STZ diabetes was associated with hyperglycemia (422 +/- 17 mg/dl) and bradycardia (-79 +/- 4 beats/min). Leptin decreased glucose levels (165 +/- 16 mg/dl) and raised HR to control values (303 +/- 10 to 389 +/- 10 beats/min). Intrinsic HR (IHR) and chronotropic responses to a full-blocking dose of propranolol and atropine were reduced during diabetes (260 +/- 7 vs. 316 +/- 6, -19 +/- 2 vs. -43 +/- 6, and 39 +/- 3 vs. 68 +/- 8 beats/min), and leptin treatment restored these variables to normal (300 +/- 7, -68 +/- 10, and 71 +/- 8 beats/min). Leptin normalized BRS (bradycardia, -2.6 +/- 0.3, -1.7 +/- 0.2, and -3.0 +/- 0.5; and tachycardia, -3.2 +/- 0.4, -1.9 +/- 0.3, and -3.4 +/- 0.3 beats.min(-1).mmHg(-1) for control, diabetes, and leptin) and HR variability (23 +/- 4 to 11 +/- 1.5 ms2). Chronic glucose infusion to maintain hyperglycemia during leptin infusion did not alter the effect of leptin on IHR but abolished the improved BRS. These results show rapid impairment of autonomic nervous system control of HR after the induction of diabetes and that central nervous system actions of leptin can abolish the hyperglycemia as well as the altered IHR and BRS in STZ-induced diabetes.     

Kinetics of chylomicron triglyceride removal from plasma in rats: a comparison of the anesthetized and the unanesthetized states

The kinetics of chylomicron-TG removal were studied using an experimental method which allows measurements to be made under optimal physiological conditions. Chylomicrons, labeled with palmitic acid-(14)C, were constantly infused at a rate of 0.5 mg total lipid per min into chronically cannulated, unanesthetized, unrestrained rats which had been fasted for 18 hr. Serial blood samples were withdrawn from an arterial cannula during a 20 min infusion period and for 10 min following the infusion. Plasma lipoproteins were separated into two fractions in the ultracentrifuge, and the lipids were extracted. Radioactivity in the low-density fraction (d<1.006) was taken to represent chylomicron-TG radioactivity. Using this method we studied the influence of anesthesia on the kinetics of removal of chylomicron-TG. The following three phases of the radioactivity-time curve were plotted: (a) the increase in (14)C during infusion of chylomicrons, (b) the steady-state phase during the infusion, and (c) the decay of (14)C after chylomicron infusion was stopped. The values for the anesthetized rats failed to reach a steady-state phase during the course of the experiment. From the disappearance of (14)C following the end of the infusion, the apparent half time of removal of chylomicron-TG was estimated to be 2.8 +/- 0.37 min in unanesthetized rats, 4.5 +/- 0.37 min in rats anesthetized with sodium pentobarbital, and 4.4 +/- 0.44 min in rats anesthetized with halothane. Thus, two anesthetics with different physical properties markedly slowed the removal of chylomicron-TG from the circulation. The reduced rate may have resulted from alterations in cardiac output or distribution of blood flow induced by the anesthetic agents.