Changes In Arterial Blood Flow Research Articles

Normal developmental changes in carotid arterial blood flow measured by Doppler flowmetry in children

We examined the developmental changes in carotid arterial blood flow in a group of neonates, infants, and children using a Doppler flowmeter. The mean, maximum and minimum carotid arterial blood flow (CABF) were measured serially in 35 healthy newborns during the first 5 days of life (total 175 records), and in 62 healthy children aged 1 month to 13 years. In newborns, the mean CABF increased significantly on the second day of life, while the maximum and minimum CABFs increased significantly every day during the first 3 days of life. The mean, maximum, and minimum CABFs increased steadily and significantly in those older than 1 month but reached a plateau after 2 to 4 years of age. Our results indicate that CABF changes with age in early life, reflecting a change in cardiac contraction and carotid-cerebral circulatory system. The measurement of CABF by Doppler flowmetry may be useful for examining cardiac and carotid-cerebral circulatory disorder.

Carotid arterial blood flow in the ovine fetus as a continuous measure of cerebral blood flow.

The purpose of this study was to establish a continuous measure of cerebral blood flow in the ovine fetus with a transit time flow probe. Seven chronically catheterized fetal sheep were studied near term with placement of a 3R Transonic flow probe on the external carotid artery, just proximal to the internal maxillary artery. Blood flow changes were induced by altering maternal inspired oxygen and carbon dioxide concentrations, with cerebral and extracerebral blood flows also determined by the microsphere technique. Although absolute carotid and cerebral blood flow values were only modestly related under the present study conditions (r = 0.60, P < .05), both the percent change and the actual change in carotid arterial blood flow showed a strong linear correlation with that for cerebral blood flow (r = 0.84, P < .01, and r = 0.72, P < .02) but less so with that for extracerebral blood flow (r = 0.44 and r = 0.28). Measurements of carotid blood flow as studied with a transit time flow probe and induced blood gas changes can provide for a continuous assessment of changes in blood flow to the ovine fetal brain.

L-arginine and pancreatic islet blood flow in anesthetized rats.

The aim of the present study was to see if L-arginine, which induces insulin release and is a precursor of the endothelial-derived relaxing factor nitric oxide, affects whole pancreatic and/or islet blood flow. For this purpose, anesthetized male Sprague-Dawley rats were injected intravenously with either saline or L-arginine (25, 100 or 250 mg/kg body weight). All doses of arginine caused a slight increase in blood glucose concentration, while the highest dose (250 mg/kg body weight) also increased insulin concentration. However, no changes in either mean arterial blood pressure, whole pancreatic or islet blood flow could be discerned with any of the doses of arginine used. It is concluded that insulin release is not necessarily associated with an increased islet blood perfusion.

Pulmonary blood flow regulation: Influence of positive pressure ventilation

Positive pressure ventilation with PEEP has been reported to reduce hypoxic pulmonary vasoconstriction (HPV) and thus increase venous admixture. This effect was investigated in six chronically instrumented unanesthetized healthy sheep. The change in left pulmonary arterial blood flow (Q̇lpa, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N 2 alternately to the left (LLH) and right lung (RLH)) was evaluated during mechanical ventilation with and without PEEP of 10 cm H 2O in comparison to spontaneous breathing. In the spontaneously breathing animal and during mechanical ventilation without PEEP, Q̇lpa decreased during LLH from 30% to 16% of cardiac index, during RLH it increased to 51%. With 10 cm H 2O of PEEP, Q̇lpa showed an identical reaction to hypoxia both in the left and right lung. It is concluded that mechanical ventilation and PEEP up to 10 cm H 2O does not interfere with pulmonary blood flow regulation to hypoxia.

Evaluation of regional haemodynamics and alterations of vascular wall of the lower limbs in hypertensive subjects.

This study was designed to analyse the relationship between arterial hypertension and changes in arterial blood flow and vascular wall damage of the lower limbs in hypertensive patients with various degrees of hypertension. Six hundred and fifty-four hypertensive patients (421 males and 233 females) aged 35 to 70 years and 88 healthy subjects (63 males and 25 females) aged 39 to 60 years were studied. Strain-gauge plethysmography of the lower limbs was used to calculate arterial calf blood flow (RF), arterial calf blood flow after post-ischaemic hyperaemia (PF), basal and minimal vascular resistances (BVR and MVR), time to reach peak flow (tPF), time until 50% reduction of peak flow (tT1/2) and total recovery time (tT). In 108 (67 males and 41 females) of the hypertensive patients, a morphological study by echo-Doppler duplex scanning of the popliteal artery was performed to measure medial-intimal thickening and popliteal lumen diameter. Our results indicate that regional haemodynamics of the lower limbs worsened in hypertensives in comparison with control subjects. In addition, the change in peripheral haemodynamics was related to the degree of hypertension. Moreover, medial--intimal thickening was significantly (P < 0.05) higher in severe hypertensives than mild hypertensives. Popliteal lumen diameter was significantly (P < 0.05) lower in severe hypertensives than moderate and mild hypertensives. In all these subjects mean blood pressure was correlated directly (r = 0.31; P < 0.001) with medial-intimal thickening and inversely (r = -0.37; P < 0.001) with popliteal lumen diameter. Multiple regression analysis indicated that mean blood pressure, age and serum cholesterol were independently correlated to medial-intimal thickening. This relationship was not influenced by the diabetic patients and smokers among the groups. Our results indicate that hypertension impairs peripheral flow and encourages the development of medial-intimal thickening.

Oxygen free radicals regulate splanchnic nitric oxide synthesis and blood flow

This study examines the hypothesis that oxygen radicals down-regulate splanchnic nitric oxide synthesis and contribute to splanchnic vasoconstriction following hemorrhage/reperfusion injury. Anesthetized rats underwent placement of flow probes around the superior mesenteric artery and abdominal aorta. Animals were bled to 30 mmHg for 30 min, reperfused without or with superoxide dismutase, an oxygen radical scavenger, 15 min before reperfusion and compared with sham-treated rats. Animals were sequentially teated with the nitric oxide synthase inhibitor NG-nitro- l-arginine methyl ester ( l-NAME) at 10 mg/kg and l-arginine, a nitric oxide precursor, at 200 mg/kg or 400 mg/kg. l-NAME increased systemic pressure and decreased superior mesenteric artery blood flow whereas l-arginine decreased arterial pressure and increased superior mesenteric artery blood flow in the sham animals. Hemorrhage/reperfusion injury attenuated the pressure and superior mesenteric artery blood flow changes following l-NAME and l-arginine dosing, which was reversed by superoxide dismutase treatment. These data suggest that oxygen free radicals regulate splanchnic nitric oxide synthesis, thus contributing to splanchnic vasoconstriction following hemorrhage/ reperfusion injury.

Relationship between Brain Blood Flow and Carotid Arterial Flow in the Sheep Fetus

The present study investigates whether changes in total brain blood flow can be reliably estimated by changes in carotid arterial blood flow in fetal and perinatal lambs. We therefore compared carotid arterial blood flow, measured with implanted transit-time ultrasound transducers, with brain blood flow, measured by radioactive microspheres in fetal lambs during normal oxygenation and during pulmonary ventilation with oxygen, with PO2 ranging from levels normal for the healthy fetus to levels normally seen postnatally. Cerebral perfusion pressure was modified over a wide range to alter brain blood flow: it was decreased by balloon occlusion of the brachiocephalic trunk and increased by a balloon occluder around the aortic isthmus. Carotid arterial blood flow and brain blood flow were closely related (r = 0.97, p < 0.0001). The relationship was not altered at different levels of oxygenation. However, measurements during higher cerebral perfusion pressures, obtained during aortic isthmus occlusion, had a negative influence on the agreement between carotid arterial blood flow and brain blood flow. When excluding values obtained by aortic isthmus occlusion, changes of 20% or more in brain blood flow could be predicted with carotid arterial blood flow within a confidence limit of 95%. Blood flow measurements in the carotid artery may be useful to estimate changes in brain perfusion.

Effects of vasopressin on haemodynamics in portal hypertensive rats receiving clonidine.

The effects of clonidine, vasopressin or a combination of both substances on splanchnic and systemic haemodynamics were measured in conscious rats with portal vein stenosis. Clonidine alone significantly decreased portal pressure, portal tributary blood flow and cardiac index, but did not change arterial pressure. Vasopressin alone significantly increased arterial pressure and significantly decreased portal pressure, portal tributary blood flow and cardiac index. Changes in portal tributary blood flow, arterial pressure and cardiac index were significantly higher with vasopressin than with clonidine alone. Vasopressin infusion in rats pretreated with clonidine significantly increased arterial pressure and significantly decreased portal pressure, portal tributary blood flow and cardiac index. Changes in arterial and portal pressures and portal tributary blood flow were significantly higher with combined therapy than with clonidine alone. Changes in arterial and portal pressures and portal tributary blood flow did not differ between combined therapy and vasopressin alone. Changes in cardiac index were significantly higher with combined therapy than with clonidine or vasopressin alone. Hepatic artery blood flow was not affected by either clonidine or vasopressin but significantly declined with combined therapy. In conclusion, this study suggests that a combination of vasopressin and clonidine accentuates the portal hypotensive action of clonidine but not the action of vasopressin. Moreover, this study suggests that a combination of vasopressin and clonidine may have deleterious effects on systemic and hepatic artery vascular beds.

The exercise pressor response to sustained handgrip does not augment blood flow in the contracting forearm skeletal muscle.

Previous studies have advanced the concept that during sustained handgrip (SHG) reflex increases in blood pressure are able to partially offset increases in tissue pressure and thus effectively maintain increases in muscle blood flow during mild to moderate levels of sustained handgrip. However, this concept is based upon measurements of blood flow to the entire forearm. The aim of this study was to evaluate this concept by simultaneously measuring time-dependent changes in systemic arterial pressure and blood flow in an active muscle during the actual period of exercise. To accomplish this aim, we measured 133Xenon washout from the extensor carpi radialis longus muscle over 3 min of SHG at 15, 30 and 45% of maximal voluntary contraction (MVC). During sustained handgrip at 15% MVC, muscle blood flow increased more than 20 fold from rest to exercise (P < 0.05), even though mean arterial pressure increased by only 12 +/- 4 mmHg. This large exercise-induced hyperaemia was abolished during SHG at both 30 and 45% MVC, despite large and progressive increases in mean arterial pressure of 29 +/- 3 and 54 +/- 5 mmHg, respectively. We conclude that at levels of handgrip above 15% MVC blood pressure ceases to be an important determinant of blood flow in the active skeletal muscle. Importantly, the increases in forearm blood flow that have been reported previously with such levels of static handgrip do not appear to be directed to the most active muscle.

Duplex/colour Doppler sonography: measurement of changes in hepatic arterial haemodynamics following intra-arterial angiotensin II infusion.

Angiotensin II (AT-II) has been used to target regionally-administered cytotoxic microspheres in patients with intrahepatic tumours. The optimisation of vasoconstrictor targeting requires a knowledge of the blood flow changes induced by agents such as AT-II. We therefore assessed duplex/colour Doppler sonography (DCDS) as a means of evaluating the effects of AT-II infusion on hepatic arterial blood flow (HABF) and arterial resistance in patients with intrahepatic tumours. HABF was measured continuously in nine patients using DCDS before, during and after an infusion of AT-II (15 micrograms in 3 ml of saline over 90 s) via a hepatic artery catheter. In seven patients with less than 30% hepatic replacement by tumour, the baseline level of HABF was 331 +/- 85 ml min-1 (mean +/- s.d.), and this was reduced by 75-80% within 30 s of the start of AT-II infusion. HABF recovered rapidly from the end of the infusion, and increased by up to 20% above the baseline for approximately 2 min. In two patients with greater than 50% hepatic replacement, HABF showed no reduction but rose continuously from the start of AT-II infusion, increasing by a factor of 2-2.5 after 3-4 min. Arterial resistance showed reciprocal changes in all cases. We conclude that DCDS is effective in assessing the temporal changes in hepatic arterial blood flow caused by AT-II. In order to optimise tumour targeting, the injection of microspheres loaded with cytotoxic drugs should be completed before the end of the AT-II infusion. The targeting advantage of AT-II in patients with a high percentage hepatic replacement by tumour should be re-assessed.

Hepatic arterial haemodynamics changes following intra-arterial angiotensin II infusion: Duplex/colour Doppler sonography

Previous studies have shown that the delivery of cytotoxic microspheres to liver tumours may be improved by manipulating the tumour to normal liver blood flow ratio using angiotensin II (AT-II). The optimization of this targeting requires the assessment of the temporal blood flow changes induced by agents such as AT-II. Duplex/colour Doppler sonography (DCDS) was evaluated as a means of studying the effects of AT-II infusion on hepatic arterial blood flow (HABF) and arterial resistance in patients with colorectal liver metastases. HABF was measured continuously in six patients with colorectal liver metastases using DCDS before, during and after an infusion of AT-II (15 micrograms in 3 ml of saline over 90 s) via a hepatic artery catheter. The baseline level of HABF was 320 +/- 87 ml/min (mean +/- S.D.), and this was reduced by 70-76% within 30 s of the start of AT-II infusion. HABF recovered rapidly from the end of the infusion, and increased by up to 20% above the baseline for approximately 2 min. Arterial resistance showed reciprocal changes in all cases. These changes were both quantitatively and qualitatively similar to intra-operative measurements previously performed in the same patients using a standard intra-operative flowmeter. The degree of concordance obtained from the intra- and post-operative measurements confirms the effectiveness of DCDS in assessing the temporal changes in hepatic arterial blood flow caused by AT-II. Prior to the start of therapy, the evaluation of vasoconstrictor agents should be carried out in individual patients to predict response, in order to establish the optimal phase for the injection of cytotoxic microspheres.

Cortical bone microperfusion: response to ischemia and changes in major arterial blood flow.

In order to investigate the effects of short-term ischemia on cortical bone microperfusion, an isolated porcine tibia diaphyseal preparation based on intact nutrient vessels was developed. Laser Doppler flowmetry (LDF) was utilized to assess continuously the cortical microcirculation and the response to short-term ischemia. The femoral artery was isolated and clamped to develop the condition of bone ischemia. On release of the clamp, reactive hyperemia was documented in all animals. Using a roller pump connected to a segment of femoral artery, the same preparation was utilized to investigate the effect of a changing femoral artery flow on the cortical microcirculation. A positive correlation between LDF output and change in arterial inflow (r = 0.64) was defined. This model has the potential for studying the effect of ischemia on bone cell viability.

Splanchnic blood flow response to intraaortic balloon pump assist of hemorrhagic shock

Hemorrhagic shock results in marked changes in splanchnic arterial blood flow. We studied the effects of intraaortic balloon pump assist (IABP) upon splanchnic blood flow during sustained hemorrhagic shock and following volume resuscitation. Hemorrhagic shock was induced (mean blood pressure = 30 mm Hg) for 120 min in 20 dogs. Controls ( n = 11) underwent resuscitation with shed blood and lactated Ringers solution only. In the study group ( n = 9), IABP was begun after 60 min of hemorrhagic shock and continued throughout a 90-min period after resuscitation. Hemodynamic parameters were assessed and splanchnic blood flow was estimated (radioactive microsphere technique) at baseline, through 120 min of sustained hypotension, and during the resuscitation period. Splanchnic blood flow was significantly reduced in both the control and the IABP groups during the period of hemorrhagic shock. Interestingly, the IABP group was found to have a return to preshock splanchnic viscera perfusion without the hyperemic reperfusion phenomenon seen in control animals resuscitated with shed blood and Ringers lactate alone. IABP assist of hemorrhagic shock appears to improve vasomotor control of splanchnic blood flow in this experimental preparation of shock. This may result in less reperfusion injury to the splanchnic viscera during the resuscitation of severe hemorrhagic shock.

Time course of hypoxic pulmonary vasoconstriction after endotoxin infusion in unanesthetized sheep

Endotoxin [lipopolysaccharide (LPS)] has been reported to reduce hypoxic pulmonary vasoconstriction and thus increases venous admixture. The time course of this failure of pulmonary blood flow regulation was investigated in six chronically instrumented unanesthetized sheep after infusion of Escherichia coli LPS (1 microgram/kg). The change in left pulmonary arterial blood flow (LPBF, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N2 alternately to the left and right lungs) was compared before and at various time intervals after the administration of LPS. During baseline conditions, LPBF was 33% of total cardiac output and decreased to 15% when the left lung was ventilated with a hypoxic gas mixture. One hour after endotoxin infusion, LPBF remained at 33% of total cardiac output yet only decreased to 28% during the hypoxic challenge. The response to one-lung hypoxia was still significantly depressed 10 h post-LPS administration. It is concluded that hypoxic pulmonary vasoconstriction is almost completely abolished for a prolonged time period after a small dose of LPS.

Central nervous control of hepatic circulation

This study was undertaken to assess the role of the hypothalamus and medulla oblongata in regulation of liver circulation in anesthetized dogs. Blood pressure, flow in hepatic artery and portal vein, and shifts of blood volume in the liver were recorded. Stimulation of the anterior hypothalamus produced changes in arterial pressure which were followed by passive changes in hepatic arterial blood flow; changes in hepatic artery resistance were rather small. Stimulation of the medial and posterior hypothalamus increased hepatic arterial resistance by 65–170%. Liver portal blood flow during stimulation of most of the hypothalamic sites decreased, hepatic portal pressure rose and vascular portal venous resistance increased 2.5–3-times. Three areas only (sympatho-inhibitory area, paraventricular and lateral hypothalamic nuclei) when stimulated produced dilatation of hepatic portal and splanchnic vascular beds, thus increasing portal blood flow. All cases of stimulation led to the decrease of blood volume in the liver by 10–36%. Stimulation of medullary structures (n. tractus solitarii, reticular nn.) caused similar changes in hepatic circulation, however the amplitude of reaction was 1.5–6-times smaller than upon hypothalamic stimulation. Central impulses to the hepatic vessels are transmitted by sympathetic adrenergic nerve fibers through vascular α-adrenoreceptors. It is concluded that the hypothalamic level of the central nervous system, unlike the bulbar one, exerts considerable, differentiated, well coordinated and to some extent specific influences on hepatic circulation.

Renal Versus Hindquarter Hemodynamic Responses to Vasopressin in Conscious Rats

Experiments were performed on conscious rats to (a) compare the responsiveness of the renal and hindquarter vascular beds to infusions of exogenous arginine vasopressin (AVP), and (b) determine whether either bed demonstrates V2-vasopressinergic vasodilation when the vasoconstrictor properties of AVP are blocked. Rats were chronically instrumented with pulsed Doppler flow probes on either the left renal artery or the distal abdominal aorta as well as with femoral arterial and venous catheters. One series of experiments examined the vascular responses of these two beds to exogenous AVP infused intravenously (i.v.) at 0.2, 2.0, or 5.0 ng/min. The lowest infusion rate was associated with no detectable changes in mean arterial blood pressure (MAP), heart rate (HR), renal or hindquarter blood flow (RBF or HQBF), or vascular resistance in these beds. In contrast, the higher infusion rates caused a marked increase in MAP, a decrease in HR, and a reduction in HQBF; RBF was unaffected, however. A second series of experiments tested for the presence of a V2-vasodilatory influence during infusion of AVP at 5 ng/min by selectively blocking V1-vasopressinergic receptors or both V1- and V2-receptor types. Little evidence for V2-mediated vasodilation was found in either vascular bed, however. We conclude that although the renal vasculature appears relatively insensitive to exogenous AVP, this insensitivity probably is not due to vasodilation mediated by activation of V2-receptors.

Transvaginal Doppler Ultrasonography in Early Pregnancy: Blood Flow Development in the Umbilical Cord

The umbilical arterial and venous blood flow of 60 pregnancies between the sixth and fifteenth week of gestation was investigated using Doppler ultrasound technology. Although fetal heart activity was detected from the fifth week, umbilical arterial blood flow was not identified until the sixth week, and venous flow was not seen until the seventh week. The characteristics of the Doppler velocity waveform changed significantly as gestation progressed. Initially, the waveform showed a short flat systolic component without diastolic flow. Systole gradually increased in duration and peaked. The diastolic component increased and became continuous at 14 weeks. After the fourteenth week, the velocity waveform did not differ greatly from those of later gestation. Arterial blood flow changes evidenced by a serial decline in the pulsatility index presumably reflects decreasing resistance of the embryonic and fetal placental vessels associated with maturation of the fetoplacental unit.

Quantitation of the hepatic arterial buffer response to graded changes in portal blood flow

Hepatic arterial blood flow changes inversely in response to altered portal blood flow. The hepatic arterial capacity to buffer portal flow changes was studied over a wide range of portal flow with arterial pressure held steady (the active buffer response) or uncontrolled. The active component of the buffer response led to nearly full dilation of the hepatic artery at low portal flows as shown by inability to dilate further in response to adenosine infusion; at high portal flows the hepatic artery was nearly fully constricted as shown by lack of further constriction to norepinephrine. With pressure uncontrolled, active and passive effects combined to produce an increased compensation with similar efficiency (44% ± 4%) over the full range of portal blood flows. Thus, although the active component of the hepatic arterial buffer response becomes less efficient at very high and low portal flows, the combination of active and passive effects leads to a larger buffer capacity which is equally efficient over a wide range of portal blood flow changes.

Effect of acute changes in renal arterial blood flow on urine oxygen tension in dogs

The relationships between urine oxygen tension (PuO2), PaO2, and acute changes in renal arterial blood flow (RBF) were studied in 19 anesthetized dogs. Indwelling sensors that measure continuously PO2 were inserted into the femoral artery and the ureter. RBF was measured by an electromagnetic flowmeter placed over the renal artery. PuO2 increased significantly from 36 to 72 torr during a stepwise increase in PaO2 from 70 to 180 torr. RBF was decreased in a stepwise fashion from a baseline value of 5.51 to 4.16, 2.13, and finally to .20 ml/kg.min by aortic constriction. PuO2 decreased significantly from a baseline value of 72 torr to 66, 57, and finally to 23 torr. The correlation coefficient between RBF and PuO2 was .84, which was significantly higher than that between RBF and femoral arterial pressure or that between RBF and urinary flow rate. This study demonstrates that PuO2 is a sensitive indicator of acute RBF changes in normal, healthy dogs.

Duplex Scanning for Assessment of Mesenteric Ischemia

The accurate diagnosis of mesenteric arterial occlusive disease has in the past required invasive examination, primarily arteriography. Recent innovations in duplex ultrasound scan technology have for the first time provided a method for the noninvasive assessment of the splanchnic circulation in man. Mesenteric duplex scanning has been used successfully to measure postprandial changes in celiac and superior mesenteric arterial blood flow as well as changes in visceral flow produced by other pharmacologic stimuli.