Lower Peripheral Resistance Research Articles

Evaluation of renal allograft function by Doppler spectrum analysis. A preliminary study.

A decreased renal function is rather common after renal transplantation. The causes of this decreased function are diverse and difficult to differentiate. Yet, duplex examination, and especially quantitative Doppler spectrum analysis of the blood velocities in the renal artery, may be an effective method for differentiating between some of these causes. Forty-five renal transplant recipients were included in this preliminary study. Doppler spectra were recorded from the renal artery to the allograft. Parameters were derived from every Doppler spectrum in order to characterize each spectrum. Renal allograft function was evaluated on the basis of a number of clinical parameters. A significant correlation was found between the clinical parameters and the Doppler spectrum parameters indicative for changes in the peripheral resistance. Patients with a normal renal allograft function showed Doppler spectra with a high diastolic flow, typical of a vascular bed with a low peripheral resistance. Patients with a decreased renal allograft function caused by a stenosis in the renal artery could be distinguished by a low peak velocity and a low pulsatility index. A decreased allograft function caused by allograft rejection or cyclosporin nephrotoxicity also led to characteristic arterial flow disturbances. In these cases, the peripheral resistance was increased, and this was primarily reflected in a decrease in the diastolic blood velocity. We conclude that quantitative analysis of the blood velocities in the renal artery by Doppler spectrum analysis seems to be a useful, noninvasive diagnostic tool that discriminates between some of the causes of a decreased renal allograft function.

Evaluation of renal allograft function by Doppler spectrum analysis A preliminary study

Abstract. A decreased renal function is rather common after renal transplantation. The causes of this decreased function are diverse and difficult to differentiate. Yet, duplex examination, and especially quantitative Doppler spectrum analysis of the blood velocities in the renal artery, may be an effective method for differentiating between some of these causes. Forty-five renal transplant recipients were included in this preliminary study. Doppler spectra were recorded from the renal artery to the allograft. Parameters were derived from every Doppler spectrum in order to characterize each spectrum. Renal allograft function was evaluated on the basis of a number of clinical parameters. A significant correlation was found between the clinical parameters and the Doppler spectrum parameters indicative for changes in the peripheral resistance. Patients with a normal renal allograft function showed Doppler spectra with a high diastolic flow, typical of a vascular bed with a low peripheral resistance. Patients with a decreased renal allograft function caused by a stenosis in the renal artery could be distinguished by a low peak velocity and a low pulsatility index. A decreased allograft function caused by allograft rejection or cyclosporin nephrotoxicity also led to characteristic arterial flow disturbances. In these cases, the peripheral resistance was increased, and this was primarily reflected in a decrease in the diastolic blood velocity. We conclude that quantitative analysis of the blood velocities in the renal artery by Doppler spectrum analysis seems to be a useful, noninvasive diagnostic tool that discriminates between some of the causes of a decreased renal allograft function.

The Hemodynamics of the Aging Cardiovascular System

Our information on the hemodynamics of the aging cardiovascular system in normotensive and hypertensive subjects is mainly based on cross-sectional studies. In normotensive subjects with no indication of coronary heart disease, recent noninvasive studies seem to indicate that cardiac output at rest and during exercise does not decline with age. These results contrast with what has been found by invasive studies in unselected populations. In hypertensive subjects it is well established that the hemodynamics of young subjects at the early stage differ greatly from what is seen in elderly hypertensive subjects. In the early phase, a high resting cardiac output is typical, whereas in the elderly, cardiac output is very low and total peripheral resistance (TPR) very high. Echo studies have shown that left ventricular hypertrophy develops early in hypertension--together with increased stiffness and reduced left ventricular compliance. A subnormal stroke volume during exercise is seen early in the process of hypertension. Data from the 20-year follow-up study of the Bergen population demonstrate that in groups of young (17-29 years) versus elderly (60-69 years) patients with hypertension with the same mean arterial blood pressure, the hemodynamic mechanisms behind increased blood pressure were widely different. The increase in mean arterial blood pressure during exercise was much steeper in the older subjects than in the younger ones, and TPR was about twice as high during 150 W exercise. Cardiac index (CI) in the oldest group was approximately half of that in the youngest group. The differing hemodynamic patterns in the young and elderly might have implications for when and how to start drug treatment, and also for what type of treatment to select.

Cerebral hemodynamics in angioma patients: an intraoperative study.

Local hemodynamics were investigated during 33 operations for cerebral arteriovenous malformation (AVM). In all cases, microvascular Doppler sonography was used to measure flow velocities and vasomotor reactivity to CO2 changes. Intravascular pressure recordings were performed in six patients. The AVM feeders had low intravascular pressure, high flow velocity, low peripheral stream resistance, and very poor vasomotor reactivity. Remote brain arteries showed no abnormalities. Doppler findings in arterial branches of AVM feeders that supplied normal brain indicated arteriolar dilation in their peripheral distribution. On removal of the angiomas, the arteries that formerly supplied them showed a return to normal intravascular pressure, whereas flow velocities dropped far below normal in these vessels. Remote arteries and branches of the former AVM feeders supplying the brain did not show any signs of impaired vasomotor reactivity following angioma removal. The results are in contrast to the normal perfusion pressure breakthrough theory.

Computer model analysis of the radial artery pressure waveform.

Simultaneous measurements of aortic and radial artery pressures are reviewed, and a model of the cardiovascular system is presented. The model is based on resonant networks for the aorta and axillo-brachial-radial arterial system. The model chosen is a simple one, in order to make interpretation of the observed relationships clear. Despite its simplicity, the model produces realistic aortic and radial artery pressure waveforms. It demonstrates that the resonant properties of the arterial wall significantly alter the pressure waveform as it is propagated from the aorta to the radial artery. Although the mean and end-diastolic radial pressures are usually accurate estimates of the corresponding aortic pressures, the systolic pressure at the radial artery is often much higher than that of the aorta due to overshoot caused by the resonant behavior of the radial artery. The radial artery dicrotic notch is predominantly dependent on the axillo-brachial-radial arterial wall properties, rather than on the aortic valve or peripheral resistance. Hence the use of the radial artery dicrotic notch as an estimate of end systole is unreliable. The rate of systolic upstroke, dP/dt, of the radial artery waveform is a function of many factors, making it difficult to interpret. The radial artery waveform usually provides accurate estimates for mean and diastolic aortic pressures; for all other measurements it is an inadequate substitute for the aortic pressure waveform. In the presence of low forearm peripheral resistance the mean radial artery pressure may significantly underestimate the mean aortic pressure, as explained by a voltage divider model.

Cardiorespiratory patterns in viral septicemia

Viral infections are known to produce hypotension and shock, but the cardiorespiratory patterns associated with viral septic shock have not been described. The clinical course of vine patients who died from overwhelming cytomegalovirus sepsis was reviewed. Viral septicemia was associated with increased cardiac index, decreased systemic vascular resistance index (SVRI), and elevated oxygen delivery. This pattern appeared during early and late stages of shock. In contrast to bacterial sepsis and endotoxemia, the pulmonary vascular resistance index (PVRI) was normal. These results indicate that overwhelming viral infection can produce shock associated with a high cardiac output, low peripheral resistance state similar to that seen with bacterial shock. Relative sparing of the pulmonary circulation in viral shock is consistent with the absence of endotoxemia in these patients.

Excessive reduction in peripheral resistance during exercise and risk of orthostatic symptoms with sustained-release nitroglycerin and diltiazem treatment of angina

Acute effects of placebo, sustained-release nitroglycerin, diltiazem capsules, and the combination of both drugs were monitored in nine stable angina patients. They were randomized to receive either placebo or 13 mg of slow-release nitroglycerin orally (double-blind). This was followed in 1 hour by 120 mg of diltiazem orally, given to all patients (unblinded). Invasive hemodynamic measurements were made before and after each treatment at supine and sitting rest, two levels of submaximal, and at maximal exercise and twice in recovery. Compared to the control test at maximal exercise, sustained-release nitroglycerin increased aerobic capacity 24%, lowered peripheral resistance −32%, and lowered systemic pressure −23%, while the respective changes with placebo were −3%, 5%, and 2%. When diltiazem was added to placebo compared to the control test, there was a 4% increase in oxygen consumption and −9% and −4% reduction in systemic resistance and systemic pressure, respectively. The addition of diltiazem to nitroglycerin was associated with a 20% increase in oxygen consumption a −42% reduction in systemic resistance and a −32% reduction in systemic pressure. Two patients who received introglycerin plus diltiazem experienced symptomatic hypotension, while one patient who received placebo plus diltiazem experienced hypotension. These side effects caused the study to be terminated prematurely. Thus, although the combination of nitroglycerin and diltiazem had a greater effect on afterload than either drug alone, the combination did not provide greater improvement in cardiac performance.

Metabolic adaptations to exercise: A review of potential beta-adrenoceptor antagonist effects

Human skeletal muscle contains 2 muscle fiber types: slow twitch (type I) and fast twitch (type II). They have different profiles including their biochemical, metabolic, O 2 diffusion, microcirculatory and neuromotor characteristics. The slow twitch fiber represents endurance, high combustive potential and recruitment during moderate activity; in contrast, the fast twitch represents explosiveness, force, high capacity for phosphate splitting and lactate formation, but Is more fatiguable. A muscle rich in slow twitch fibers is confined to low peripheral resistance at rest and during exercise, higher exercise leg blood flow and higher maximal oxygen uptake (VO 2 max). During graded exercise lactate, has been shown to be a good marker for the metabolic and circulatory characteristics of the contracting muscle and the exercise intensity (W) eliciting a blood lactate concentration of 4 mmol/liter −1[(W OBLA) from o nset of b lood c actate a ccumulation] integrated for peripheral metabolic, neuromotor and central circulatory potentials both in health and disease. It is well known that a blood lactate level >4 mmol/liter −1 represents a major increase in sympathetic tone and is incompatible with endurance or prolonged exercise. With prolonged exercise and sympathetic regulation both circulation and metabolism adapt. Adipose tissue is stimulated and fatty acids are released. Muscle tissue lipoprotein lipase activity is enhanced; that is, there is increased utilization of blood triglycerides for local lipolysis in the capillary bed of the contracting muscle. Both mechanisms will increase fatty acid availability and Induce a “glycogensparing effect” resulting in a reduced respiratory exchange ratio. Studies have shown that both the magnitude of the initial glycogen stores and these adaptive responses will determine performance time. With age, changes take place in heart rate regulation, neuromotor control and muscle fibers. Thus VO 2 max Is decreased, but partly compensated for by a fast motor unit and fiber loss leading to a muscle more rich in slow twitch fibers—an “endurance training-like effect.” Relative endurance is also increased with age; however, lactate metabolism is still a critical feature. The OBLA concept describes capacity for both occupational and leisure-time physical activity.

An extreme form of the hyperdynamic syndrome in septic shock.

We classified 41 patients in septic shock on the basis of cardiac index (CI) after volume expansion with plasma protein solution, in order to obtain adequate filling pressures. Five had decreased CI (less than 3.5 1/min per m2), 31 had moderately increased CI (3.5 - 7.0 1/min per m2) and 5 had extreme hyperdynamic shock with CI superior to 7.0 1/min per m2. Among the patients with increased CI, those with extreme hyperdynamic state (EHS) had lower total systemic and pulmonary arteriolar resistances (370 vs 658 and 52 vs 119 dynes X s X cm-5, respectively) and a higher stroke index (67 vs 46 ml/m2), in spite of similar right atrial pressures. In this latter group, blood lactate was higher (6.5 vs 2.1 mmol/l), acidosis was more severe and coagulation disorders more pronounced; all five patients maintained an extremely high CI until death, which supervened after a brief episode of sinus bradycardia. A similar clinical course was rarely observed in the remaining moderately hyperdynamic group, in which mortality rate was significantly lower (35%). Three of five patients with EHS (compared to 2 of 31 in the moderately hyperdynamic group) had liver cirrhosis, the fourth died of fulminant meningococcemia and the fifth had prolonged polymicrobial bacteremia before adequate treatment was begun. Thus, underlying liver disease or particularly severe and uncontrolled infection seems to predispose to EHS. It is concluded that septic shock with extremely high cardiac output and excessively low peripheral resistances represents a distinct subset with more severe metabolic and coagulation disorders, an unusual hemodynamic evolution and a particularly poor prognosis.

Skeletal muscle capillary supply in a fish that lacks respiratory pigments

The relationship between capillary density and mitochondrial volume density has been investigated for the slow trunk muscle of the haemoglobinless ‘Icefish’, Chaenocephalus aceratus Lönnberg. In general, for teleost slow muscles capillary densities, NA(c,f), are positively correlated with mitichondrial volume densities, Vv(mit,f). However, the capillary density for the slow trunk muscle of the Icefish is low (544 ± 24 capillaries/mm 2) when compared with teleosts of similar mitochondrial volume densities (0.34 ± 0.01). For example, for slow muscle fibres in Saithe ( Pollachius virens) Vv(mit,f) is 0.35 ± 0.02 but the capillary density is 4507 capillaries/mm 2. Estimates of capillary surface and volume densities for the Icefish (198 and 0.035 cm −1, respectively) are in the range reported in the literature for other teleost species. Thus, for C. aceratus NA(c,f) provides a relatively poor index of the functional properties of the peripheral exchange vessels. Mean capillary cross-sectional area for C. aceratus (64 ± 7 μm 2) was two to three times greater than that found in most teleost species. The low peripheral resistance reported for the Icefish, C. aceratus is therefore the result of the presence of large bore capillaries, the resulting high flow rates also allowing the maintenance of favourably hgih capillary - tissue P O 2 gradients.

Blood flow measurements in the fetal descending aorta: technique and clinics.

A combination of two-dimensional and realtime pulsed-Doppler ultrasound provides a noninvasive method of measuring human fetal blood flow without side effects. By not altering the physiological conditions of the fetus, it minimizes external stimuli that might affect blood flow. However, due to the inaccessibility of the vessels under investigation, errors from the ultrasound technique arise and these are still being assessed. Studies of fetal blood flow suggest that the fetal circulation has a low peripheral resistance and that the increase in blood flow found with increasing gestational age is due predominantly to the increase in the actual dimensions of the fetal vasculature. Investigations in abnormal pregnancies, such as small-for-dates and those with cardiac arrhythmias have shown that the fetal cardiovascular system is capable of compensating efficiently to maintain normal physiological conditions, but only within the limits defined by the Frank Starling mechanism.

Increased cardiac output and lowered peripheral resistance during metoprolol treatment.

Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.

Hemodynamic effects of cecal ligation sepsis in dogs

Cecal ligation sepsis was studied in eight pentobarbital-anesthetized dogs with hemodynamic measurements at baseline, 2 days after cecal ligation, and following Ringer's lactate resuscitation. Microsphere techniques were used to measure peripheral arteriovenous (A-V) shunting and distribution of cardiac output. Cecal ligation sepsis was manifested by pyrexia, leukocytosis, decreased blood pressure, and purulent peritonitis. Although cardiac index (CI) increased in two, decreased in four, and was unchanged in two dogs, femoral artery blood flow (FAQ) decreased in all animals (125 to 84 ml/min, P < 0.01). Hindlimb A-V O 2 difference increased while O 2 consumption and A-V shunting did not change. Distribution of cardiac output increased significantly to the kidneys (163%, P < 0.01) and liver (1168%, P < 0.01), but was unchanged to skin, pancreas, and skeletal muscle. Intrarenal distribution of blood flow did not change despite increased total renal blood flow during sepsis. Ringer's lactate resuscitation (20 ml/kg) during sepsis increased CI, while FAQ and A-V O 2 differences returned to baseline values. Hindlimb A-V shunting remained low and unchanged. In contrast to the effects of local inflammation in canine septic hindlimbs, there does not appear to be a specific vasodilator released during cecal ligation sepsis which causes increased peripheral blood flow and elevated A-V shunting. Cecal ligation in dogs, however, does not mimic the disproportionately low peripheral resistance and reduced O 2 extraction seen in hyperdynamic human sepsis. These results should, therefore, be interpreted with caution.

Arterial blood pressure and the flow in the calf at rest and during reactive hyperemia.

The influence of a handgrip-induced rise in arterial blood pressure on the blood flow in the calf at rest and on the maximal flow during reactive hyperemia after 5-minute arterial occlusion was studied in 7 healthy subjects. Isometric contractions of the forearm muscles (handgrip) with 20% of the maximal voluntary contraction during 3 minutes caused a significant increase in mean blood pressure of 19% (SEM 3%; p less than 0.05). No significant increase in the mean blood flow at rest was found. The maximal blood flow during reactive hyperemia was increased by 42% (SEM, 5%; p less than 0.05). The lowest peripheral resistance during reactive hyperemia was decreased by 15% (SEM 6%; p less than 0.05).

Effect of angiotensin-II blockade on systemic and hepatic haemodynamics and on the renin-angiotensin-aldosterone system in cirrhosis with ascites.

We have studied the effect of angiotensin-II blockade with saralasin on the cardiovascular and hepatic hemodynamics and on the renin-angiotensin-aldosterone system in fourteen patients with cirrhosis and ascites. Control measurements showed that most of the patients had a low mean arterial pressure, high plasma volume, normal or high cardiac index, low peripheral resistance and high plasma renin activity and aldosterone concentration. The wedged hepatic venous pressure was increased in each patient and the estimated hepatic blood flow was normal in most of them. Overall, saralasin induced a significant reduction of the mean arterial pressure, cardiac index and peripheral resistance. The decrease of the peripheral resistance was greater than that of the cardiac index. Six of the patients developed a marked reduction of the mean arterial pressure with low doses of saralasin (1--2.5 microgram/kg/min), and they had significantly higher plasma renin activity and lower mean arterial pressure than the remaining eight patients who showed a slight or no hypotensive response in spite of infusing saralasin up to a dose of 10 micrograms/kg/min. Overall, the decrease of the mean arterial pressure correlated directly with the baseline values of plasma renin activity. Angiotensin-II blockade induced a significant reduction of the wedged hepatic venous pressure. The hepatic blood flow did not show any significant change. The decrease of the wedged hepatic venous pressure was directly related to the reduction of the mean arterial pressure and also to the control plasma renin activity. Our study indicates that in most patients with cirrhosis, ascites and high plasma renin activity, arterial pressure is maintained by the effect of endogenous angiotensin II on the peripheral vasculature, and we suggest that a pre-existing arterial hypotension secondary to an arteriolar vasodilatation is the cause of renin release in these patients. Our results also show that angiotensin-II blockade is accompanied by a reduction of the post-sinusoidal hepatic vascular resistance.

Obesity and Essential Hypertension

Systemic hemodynamics, intravascular volume, and plasma renin activity were determined in 135 lean, mildly obese, or distinctly overweight subjects who were normotensive or had borderline or established essential hypertension. Cardiac output (but not index) was higher and peripheral resistance lower in obese than in lean subjects, except in borderline hypertension. intravascular volume was increased in obese patients, and more so when corrected for body height; correction for body weight led to relative volume contraction. Intravascular volume correlated directly with cardiac output in the entire population, as well as in the subgroups. Intravascular volume correlated inversely with total peripheral resistance in all subjects and in each subgroup. Both correlations remained significant when an approximation was used to correct influences of obesity on total blood volume. Sodium excretion was higher in obese than in lean subjects. Thus, despite the expanded intravascular volume in obesity, the pathophysiologic relationship between systemic hemodynamics and intravascular volumes remains unchanged. Relatively low peripheral resistance in obesity may decrease the risk of systemic vascular disease. Nevertheless, since circulating volume is increased, the greater venous return adds an additional load to a left ventricle that is already burdened by a high afterload caused by arterial hypertension. (<i>Arch Intern Med</i>141:81-85, 1981)

Plasma catecholamines following low and high doses of ouabain in anesthetized dogs with or without cervical vagotomy.

Circulating catecholamine (CA) levels in the aortic blood did not change significantly in anesthetized dogs during a period of 60 min following the rapid intravenous injection of ouabain at a dose of 10 microgram/kg, but they did increase significantly after administration of a dose of 75 microgram/kg. After bilateral cervical vagotomy, the high dose of ouabain caused a greater and earlier elevation in circulating CA levels than in intact animals along with an increased cardiac index and a lower peripheral resistance. These findings suggest the existence of a vagal inhibitory mechanism upon liberation of CA following the administration of ouabain. Although ventricular arrhythmias did occur before the increase in circulating CA, preinjection CA levels were significantly higher in animals presenting ventricular fibrillation, suggesting that a high background adrenergic tone facilitates the production of ventricular arrhythmias by ouabain. Moreover, ventricular tachycardia occurred earlier in vagotomized dogs, in which the immediate elevation of circulating CA could have been a precipitating factor for this type of arrhythmia.

Haemodynamics of hypertension in pregnancy assessed by M-mode echocardiography.

1. Echocardiographic haemodynamic and left ventricular parameters were determined in twenty-one normontensives and thirty-six hypertensives during the last trimester of pregnancy. 2. Equivalent blood pressure control was obtained in hypertensives with bet rest only, oxprenolol or methyldopa, but remained above normotensive levels. 3. Cardiac output was elevated in the last trimester of pregnancy in normotensivves and hypertensives. 4. Left ventricular mass was increased in normal pregnancy, but displayed an exaggerated increase in hypertensives. 5. Total peripheral resistance was inappropriately elevated in hypertensive pregnancy, but was normalized in the oxprenolol-treated group. 6. There was no reduction in heart rate or cardiac output in the beta-adrenoreceptor blocker-treated group. This feature, in combination with lowered peripheral resistance, may contribute to the improvement in foetal outcome observed in maternal hypertension of pregnancy treated with oxprenolol.

Increase in the calculated resistance of anatomically fixed stenosis in vitro in association with decrease in distal resistance.

The effects of changes in distal resistance on stenotic resistance were studied in vitro. Physiological saline was passed through the left carotid artery obtained from the dog, flexible rubber tubing, or through solid polyethylene tubing with a constant perfusion pressure or with a constant flow rate. Various stenotic resistances were established using a screw type constrictor and the distal resistance was varied by allowing physiological saline to pass through either a 23 gauge hypodermic needle (high peripheral resistance) or 23 and 20 gauge needles (low peripheral resistance ). For arteries with anatomically fixed stenosis, the calculated resistance was increased in association with reduction of the distal resistance. The stenotic resistance in the flexible rubber tubing changed in the same manner as that of the carotid artery, while the solid polyethylene tubing showed no significant stenotic resistance changes due to altering the distal resistance. These findings suggest that the stenotic resistance change of the artery correlates with the elasticity of the vessel wall and also indicate that resistance values were of little usefulness for evaluating the effects of vasodilating stimuli on the vessel segment with a significant stenosis.

The effect on the splanchnic blood flow and cardiac output of various carbon dioxide concentrations during fluroxene (Fluoromar) anaesthesia. An animal study.

Seven dogs premedicated with pethidine 10 mg/kg body weight, were anaesthetized with mebumal natrium 25 mg/kg body weight i.v. and gallamoni jodidum 80 mg, together with O2‐N2O in a ratio of 1 to 1. Thereafter four dogs were constantly hyperventilated and three constantly hypoventilated under stepwise increasing anaesthesia with fluoromar® (= fluroxene), up to 6% inspiratory concentration. A change was made between the groups at this fluoromar concentration, from hyper‐ to hypoventilation and vice versa, after which the fluoromar concentration was reduced stepwise to 0% inspiratory. During the course of this anaesthesia, the related values for flow, pressure and resistance in the systemic and splanchnic circulations were measured at fluoromar concentrations: 0–1 1/2–3‐6‐6‐3‐1 1/2‐0%.The relative changes in the systemic circulation during increasing concentrations of fluoromar are independent of hypo‐ or hypercapnia, while the absolute magnitudes of the measured parameters are strongly dependent on the CO2 tensions. The hypercapnic dogs had the highest cardiac output, stroke volume and most rapid pulse, as well as the lowest peripheral resistance. The same group of dogs had the lowest liver blood flow and the greatest splanchnic resistance. The mean pressures in the aorta, right atrium and portal vein were not different between the groups.A straight line dependence at 6% fluoromar, was demonstrated between cardiac index and Paco2: cardiac index (1‐min‐1‐m‐2) = 1.22 + 0.23 ± Paco2 (kPa), ((cardiac index (1‐min‐1‐m‐2) = 1.22 + 0.03 ± Paco2 (mmHg)), and peripheral resistance and Pao2: peripheral resistance (kPa 1‐1 min) = 12.85—0.5 ± Paco2 (kPa), ((peripheral resistance (dyn‐sec‐cm‐5 ± 10‐3) = 7.72‐0.04 ± Paco2 (mmHg)). The pressure in the portal vein appears to rise and the liver flow to fall with rising carbon dioxide tension, but the relationship is not significant.In the latter half of the investigation only small changes were demonstrated which could be related to the falling concentration of fluoromar. These were slight rises in the mean pressure of the aorta and cardiac frequency, similar for both groups. In addition, a slight rise in the peripheral resistance and splanchnic resistance were observed in the hypocapnic group. No changes were seen in the cardiac output and liver flow in any of the groups during falling fluoromar concentrations. The absolute magnitude of the measured parameters in relation to the CO2 tension reflects the conditions in the first half of the investigation, but the difference between the groups is less pronounced. This was partly due to the smaller difference in Paco2 between the groups in this part of the investigation and partly due to the time and experimental course.