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Because infrainguinal bypasses performed on the basis of normal papaverine testing in patients with multilevel arterial occlusive disease are done below arteriographically diseased although hemodynamically normal vessels, there is concern about progression of suprainguinal disease compromising long-term success. This study has been done to assess the long-term results of such bypasses. Between 1979 and 1985, infrainguinal bypasses selected by papaverine testing were done on 92 limbs having hemodynamically normal inflow in the presence of arteriographically demonstrable aortoiliac stenoses of 15% to 70%. Long-term hemodynamic and clinical success rates were determined with criteria based on papaverine and noninvasive vascular testing. There was no significant difference in hemodynamic success at 48 months (by life-table analysis) (p = 0.98) when comparing limbs with less than 50% aortoiliac stenoses to limbs having 50% or greater stenoses. The difference between the mean degree of preoperative inflow stenoses for long-term hemodynamic successes (32.5% +/- 1.5%) and failures (34.6% +/- 3.0%) was not significant (p = 0.57). There was no significant difference (p = 0.98) in the number of subsequent inflow procedures required in limbs with preoperative aortoiliac stenoses of less than 50% (13.5%) vs. aortoiliac stenoses of 50% or greater (13.3%). Long-term results of infrainguinal bypass done below stenotic but hemodynamically normal aortoiliac vessels are not related to the amount of angiographically demonstrable inflow stenosis. Selection of patients for infrainguinal bypass on the basis of papaverine testing, irrespective of angiographic findings, eliminates unnecessary inflow procedures without detriment to long-term success.

The feasibility of studying ovarian arterial blood flow has been demonstrated, using an ultrasonic method combining real-time imaging and pulsed Doppler (the 'duplex' method). Results using a percutaneous full-bladder technique were validated by comparison with use of an ultrasound probe applied directly to the arteries at laparotomy. The ovarian arteries demonstrated qualitatively and quantitatively distinct flow patterns compared with the internal and external iliac arteries. From recorded waveforms a pulsatility index (PI) reflecting vascular impedance was calculated. The PI was found to be lower, indicating increased blood flow, in the artery supplying the ovary carrying the dominant follicle or corpus luteum. Serial studies suggest that this change occurs at an early stage of the menstrual cycle, possibly before the dominant follicle can be recognized by its size or increased hormone production. Uterine arterial flow was also detectable, more accurately abdominally than vaginally, and the changes typical of late pregnancy were already found to be present, though to a lesser degree, in the first trimester.

The present study was undertaken to examine the reflex responses of activation of cardiac sensory receptors in the conscious dog. Intracoronary (left circumflex coronary artery) injection of veratridine (0.10 micrograms/kg) reduced mean arterial pressure (-40 mmHg, P less than 0.05), heart rate (-34 beats/min, P less than 0.05), and maximum rate of rise of left ventricular pressure (LV dP/dtmax) (-419 mmHg/s, P less than 0.05). Bilateral cervical vagal cold block (BVB) eliminated the depressor and bradycardic responses of veratridine. BVB not only eliminated the negative inotropic response to veratridine but reversed it to a positive inotropic response (LV dP/dtmax increased 313 +/- 76 mmHg/s). Ganglionic blockade abolished all effects of veratridine. The bradycardia and negative inotropic effects caused by veratridine were attenuated by either atropine or metoprolol and completely eliminated by the combination of the two antagonists. Veratridine also produced a decrease in renal artery blood flow but had no effect on renal vascular resistance. In contrast, iliac blood flow was increased with veratridine, and this, combined with the depressor effect, resulted in a decrease in iliac vascular resistance (-37%), P less than 0.05). BVB abolished the changes in renal and iliac blood flow or resistance caused by veratridine. The results indicate that activation of cardiac receptors in the conscious dog elicits inhibitory reflexes to the heart and peripheral circulation that are mediated by vagal afferents. After vagotomy, veratridine elicited a reflex positive inotropic response, which may have resulted from activation of cardiac sympathetic afferent fibers.

Six hundred 'normal' volunteers have been examined, ranging in age from neonates of three days to adults of 65 years. Average compliance was measured for the aortic, iliac, and leg arterial pathways using a non-invasive atraumatic Doppler ultrasound method in non-sedated subjects. No variation of compliance with mean blood pressure was found but there was a strong dependence on age and sex. At birth, leg arteries appear to be markedly more compliant than the aorta. Relative values are reversed in the first five years, after which the aorta remains more compliant, reaching a maximum value around 10 years and then decreasing sharply towards leg values until 20 years. Beyond this age aortic compliance very slowly, and aorta, iliac, and leg arteries appear to tend towards equal compliance in the sixth decade. An explanation for the significant differences between aortic compliance in males and females from menarchy to menopause is offered and implications of these compliance variations in atherogenesis are discussed.

A new concept for determining relative blood flow in single arteries using videodensitometry to obtain contrast dilution curves has been experimentally evaluated. Flow as a fraction of cardiac output in the cerebral, renal, splanchnic, and iliac arteries was determined in 110 measurements in 11 dogs. The mean difference between measurements by electromagnetic flow probe and videodensitometric values was less than 2%, and the correlation coefficient was r = 0.96 for all data. The method is simple compared to previous videodensitometric techniques, because the dimensions of the vessel and the mean transit time of the contrast bolus can be neglected. The necessary equipment includes a stable image intensifier-television chain, a videotape recorder, a videodensitometer, and a graphic recorder. The method is now used to measure blood flow in cerebral, coronary, splanchnic, renal, and ileofemoral arteries during routine clinical angiography.

Sixty patients undergoing surgical reconstruction by classical or modified methods for aorto-iliac vascular disease were studied as to postoperative sexual function. Preoperative impotence was present in approximately half of the patients with abdominal aortic occlusion. Although internal iliac arterial blood flow was regarded as an important factor in sexual function, only a slight correlation was noted between circulatory insufficiency and postoperative sexual dysfunction. Preservation of both trunks or the left trunk of the hypogastric nerve led to a marked decrease in the incidence of ejaculation disturbances. We concluded preservation of the hypogastric nerve was more beneficial than maintenance of internal iliac arterial blood flow.

The rostral pons and caudal mesencephalon in 26 cats were electrically stimulated (greater than 2400 sites) while measuring arterial pressure and iliac, celiac and renal vascular resistance. Areas active in control of arterial pressure and iliac vasoconstriction were located in the marginal nucleus of the brachium conjunctivum (BCM) and in parts of the central tegmental fields (FTC) of the mesencephalon. Areas active in control of celiac and renal vasoconstriction were confined to the BCM. Areas active in control of iliac and celiac vasodilation were generally found ventral to the constrictor areas in the FTC of the mesencephalon. Stimulation of the caudal periaqueductal grey, locus caeruleus and underlying reticular formation elicited no change in any parameter measured. These findings suggest that multiple pathways for control of arterial pressure and vasoconstriction pass through or synapse in a discrete region of the dorsal rostral pons that is limited to the BCM.

We tested the hypothesis that loss of endothelium results in increased transport of lipoprotein into the arterial wall, favors accumulation of lipid, and thus predisposes to atherosclerosis. In rabbits initially fed a diet low in lipid, the aortas were de-endothlialized with an intraarterial balloon catheter; 28 days later, the animals were divided into two groups. Group I animals were continued on a diet low in lipid and sacrificed at 8, 11, 13, and 15 weeks after de-endothelialization. Group II animals were fed the same diet supplemented with 0.5% cholesterol and sacrificed at comparable intervals. Aortas of group I animals revealed proliferative fibromuscular intimal thickening in both de-endothelialized and re-endothelialized areas, with little or no fatty change in the intima. In contrast, aortas of group II animals revealed slight to marked fatty change in the intima, characterized by accumulation of oil red O-positive material with anisotropic lipid inclusions. The greatest quantity of lipid was present in intimal thickening beneath regenerated endothelium, and not in adjacent intimal thickening lacking an endothelial lining. These results do not support the hypothesis that the absence of endothelium favors accumulation of lipid and predisposes to atherosclerosis. The experiments indicate that lipid accumulates preferentially in areas of intimal thickening covered by regenerated endothelium.

In order to elucidate the fluid dynamic feature of arterial blood flow, the present flow visualization study was carried out with various transparent blood vessel models having a protuberance, a bifurcation, or branchings. The observed flow patterns could be understood in terms of occurrence of a secondary flow, named the horseshoe vortex. The mode of generation of the horseshoe vortex in a tube with a protuberance projecting into the boundary layer was explained as follows. A radial pressure gradient toward the tube wall was produced along the upstream surface of the protuberance because of the interaction between the viscous sheared flow and the wall. This pressure gradient made fluid particles turn round downward directly before the obstacle. Then they curled round on themselves and formed a bound vortex tube, the horseshoe vortex, which in turn passed round the front of the protuberance in both directions. In a tube with a Y-shaped bifurcation or rectangular side branch, the flow divider at the branching site acted in place of the protuberance to produce a vortex tube similar in pattern to the horseshoe vortex. The vortex tube extended from the high pressure region, i. e. the apex of the flow divider, to the low pressure region, i. e. the lateral margin of the branch orifice, and generated swirling secondary flows in the main and branched tubes. These results suggested that the following mechanical factors might initiate or facilitate athero- and thrombogenesis: collision of blood cells captured by the horseshoe vortex with blood vessel walls, the interaction of the walls and blood cells due to turbulence, and the occurrence of localized high wall shear stresses.

This paper provides biological illustrations of the applicability and mode of use of intravascular and perivascular absolute induction angiometers. Artifacts and limitations of the method as well as experimental precautions and calibration procedures are discussed. Tracing are presented to illustrate the capabilities of the method in recording pulsatile diameter changes in veins and arteries and to demonstrate its applicability to moving blood vessels as exemplified by the coronary arteries. Both intravascular and perivascular angiometry can detect diameter changes of a few micra in a vessel 1 cm in diameter. The intravascular angiometer is a resilient loop of fine bifilar wire which can be introduced into the blood vessel percutaneously via an angiographic catheter. A perivascular angiometer is an easily deformable loop made of a soft fine wire pair which is draped around a blood vessel and can thus be chronically implanted.

To discover the relative importance of body core temperature versus bodyskin temperature in raising limb blood flow and heart rate, we exposed seven unanesthetized, chaired baboons (Papio anubis) to a variety of heating protocols. First, the baboons were exposed to a 40-45 degrees C environment for 0.75-1.5 h. Arterial or right atrial blood temperature (Tbl), skin temperature (Tsk), mean right iliac blood flow (MRIF), and heart rate (HR) all increased gradually during heating. On the average, HR increased from 106 to 160 beats/min and MRIF rose to 286% of control level. To separate influences of Tbl and Tsk on cardiovascular changes, we manipulated Tbl and Tsk independently via a heat exchanger incorporated into a chronic femoral arteriovenous shunt. In most baboons, the MRIF and HR response to a hot environment could be essentially duplicated by elevation of bTbl with Tsk held neutral, while elevation of Tsk with Tbl held neutral had little effect. One baboon exhibited significant response to Tsk elevation with Tbl held neutral, although subsequent manipulation of Tbl overrode this response. We conclude that the normal response to heating in baboons is mainly attributable to drives from internal temperature-sensitive mechanisms. Elevated Tsk shows large effects only in exceptional cases.

The effects of hemorrhage on arterial pressure, blood flows, and resistances in the coronary, mesenteric, renal, and iliac beds of healthy, conscious dogs and intact, tranquilized baboons were studied. Mild nonhypotensive hemorrhage (14+/-2 ml/kg) increased heart rate and mesenteric and iliac resistances slightly but significantly, and decreased renal resistance (-13+/-2%). Moderate hypotensive hemorrhage, 26+/-2 ml/kg, reduced mean arterial pressure (-23+/-2 mm Hg) and blood flows to the mesenteric (-56+/-3%), iliac (-58+/-5%), and coronary (-39+/-4%) vascular beds, and increased heart rate (+89+/-9 beats/min) and resistances in the mesenteric (+73+/-15%), iliac (+102+/-19%), and coronary (+27+/-5%) beds. In contrast to the other beds, renal flow rose 11+/-6% above control and renal resistance fell 31+/-2% below control. Renal vasodilatation with hemorrhage was also observed in five baboons. The increases in mesenteric and iliac resistances were blocked almost completely by phentolamine, while the increase in coronary resistance was only partially blocked by phentolamine. The renal dilatation was not blocked by phentolamine, propranolol, atropine, or tripelennamine, but was prevented by indomethacin, suggesting that this dilatation was mediated by a prostaglandin-like compound. Thus the peripheral vascular responses to hemorrhage involve intense vasoconstriction in the mesenteric and iliac beds. In the normal conscious dog and the intact, tranquilized primate, the renal bed does not share in the augmentation of total peripheral resistance with nonhypotensive and moderate hypotensive hemorrhage, but does with more severe hemorrhage. In fact, renal vasodilatation occurs with nonhypotensive or moderate hypotensive hemorrhage, which can be prevented by blockade of prostaglandin synthetase with indomethacin.

Physiologic studies in dogs have been performed with an intravascular flow/diameter sensor which can be introduced directly into the aorta or its branch vessels through a percutaneous radiologic catheter. These studies have focused upon attempts to devise a clinically practical means to protect the small intestine from radiation damage during therapy of abdominal and pelvic malignant tumors. The effects on superior mesenteric, renal, and lower extremity blood flows of controlled infusions of Pitressin given directly into the superior mesenteric artery or into a peripheral vein have been measured. In addition, using these regional flow measurements and arteriovenous differences in oxygen content, regional tissue oxygen extraction rates during Pitressin infusions have also been estimated. The data show that intravenous Pitressin at an infusion rate of 0.0124 U/kg/min may be almost as effective as Pitressin given directly into the superior mesenteric artery in lowering superior mesenteric blood flow (40%-70% reduction for intravenous, 50%-70% for direct arterial infusions) and intestinal oxygen extraction (20%-40% reduction for intravenous, 40%-50% for direct arterial infusions). The effects of Pitressin at similar dose rates on the kidney and the lower extremity are less reproducible, and it is possible that relatively selective radiation protection of the intestine using systemic (intravenous) infusions of Pitressin during abdominopelvic radiotherapy might be achievable.

Sexual function and internal iliac artery (IIA) patency were determined in 24 patients who had received at least two renal transplants, one in each iliac fossa, at the University of Maryland and Johns Hopkins Hospitals from 1975 to 1979. The pelvic hemodynamics of each patient were assessed with a penile/brachial blood pressure index (PBI). The rate of sexual dysfunction, as determined by questionnaires and personal interviews, was 46% (11 of 24 patients) compared with only 21% (five of 24 patients) after a single transplant. Nine of the 11 patients who were impotent had bilateral IIA occlusion and four of these nine had a PBI less than 0.70. One of the four patients regained full sexual function after a revascularization procedure, which confirmed that this impotence had a vascular etiology. Results of this study show that vascular insufficiency, but not necessarily vasculogenic impotence, was present in at least four of the 11 patients who were impotent (36%) and may have been avoidable by sparing at least one IIA during renal transplant procedures.

Doppler ultrasound was used to measure pulse wave velocity down the aorta and iliac arteries. Arterial wall compliance was calculated from pulse wave velocity in 45 apparently healthy men. Their arterial compliance fell significantly with advancing age, raised blood pressure, increased serum cholesterol and triglyceride levels, and reduced serum high density lipoprotein cholesterol levels. The correlation between compliance and age was independent of the other risk factors, and the correlation between compliance and lipid status was independent of age and blood pressure. There was no significant correlation between compliance and area under the glucose tolerance curve.

The present study was performed to determine the immediate (hours) and long-term (28-day) effects of angioplasty-balloon dilatation on arterial wall diameter, histology, response to vasoconstrictors, and passive mechanics. Dilated left iliac arteries of New Zealand rabbits were compared to control, right iliac arteries. In the immediate studies, dilation increased arteriographic diameter by 32%, denuded the endothelium, stretched and may have lysed smooth muscle cells, decreased arterial wall thickness, and increased passive stress and incremental elastic modulus. The dilated arteries failed to contract to norepinephrine or potassium chloride. In contrast, 28 days after dilation, arteriographic diameter had returned to normal, an intimal thickening had formed, passive stress and the incremental elastic modulus had decreased to below normal, and the arteries contracted, but to only 53% to 67% of control. Angioplasty had no long-term effect on arterial sensitivity (EC50) to potassium chloride or serotonin but did produce a decreased sensitivity (6X) to norepinephrine. These studies demonstrate that the effects of dilatation of the normal artery are partially reversible, suggest that restenosis after angioplasty is more likely to be due to intimal proliferation than increased arterial stiffness, and suggest that vasospasm of arteries after long-term recovery from the dilation is more likely to be mediated by serotonin than by norepinephrine.

The effects of smooth muscle activation on the pressure dependence of arterial wall characteristic impedance were studied with isolated segments of canine iliac and carotid arteries. Measurements of external diameter and transmural pressure were made before and after activation of the arterial smooth muscle (SM) by norepinephrine (NE) in concentrations of 0.5 and 5 mug/ml and used to compute values of characteristic impedance (Z0). In the absence of SM tone, values of Z0 for both arterial sites increased monotonically with transmural pressure. For the larger [NE], values of ZO exhibited a minimum at pressures of the order of 125 mmHg and increased for both larger and smaller values of pressure, For the smaller [NE], values of Z0 showed a similar pressure dependence but with a broader minimum. It is concluded that the previously demonstrated constancy of vascular impedance with changes in arterial pressure is at least the result of the presence of a tonic level of SM activation in conduit arteries.

Temporary hypertensive increases in blood pressure, or variations in blood pressure when there was an already existing hypertension, in which the blood pressure either moved within the limits of hypertensive blood pressure values or temporarily returned to normal, occurred in 129 men ages 23-85, in whom repeated measurements of the blood pressure and pulse wave rate (PWG) were carried out in the aorta and iliac artery in the course of a longitudinal study over years. Both categories--temporary and chronic hypertensives--showed significant differences in the height of the PWG increase per 10 mm Hg (delta-c-p). The delta-c-p value for the chronic hypertensives (n equals 43) was 0.73 plus or minus 0.35 m/sec, that of the temporary hypertensives 0.56 plus or minus 0.24 m/sec (p smaller than or equal to 0.01). The mean value for both groups was 0.62 plus or minus 0.29 m/sec. Delta-c-p increased with age (0.54 m/sec yields 45th year; 0.60 m/sec from 46-55 years; 0.61 m/sec from 55-65 years; 0.67 m/sec at 66 and over). The increase of delta-c-p with age is caused by the increase in chronic hypertension. Delta-c-p was constant over a mean pressure range of 90-190 mm Hg in temporary and chronic hypertensives, irrespective of the amount of the (individual) mean difference in pressure, but it was distinctly greater in chronic than in temporary hypertensives. On lowering pressure, the delta-c-p was also greater in chronic than in temporary hypertensives. When normal pressures were attained, temporary hypertensives showed no differences from the PWG of normotensive of the same age. The differences between temporary and chronic hypertensives are explained by the different relations in the structure of the wall of the aorta, but especially because the function of the muscular layer was better maintained in temporary hypertensives. The raising of the PWG in temporary hypertensives is probably caused by the increased tension in the wall alone. Whether, in addition to the increased incorporation of collagen and a rarification of the smooth muscle, the thickness to radius ratio also increases above that usual for the age group in chronic hypertension is still not clear, but it is not essential for the explanation of the greater increase in the delta-c-p. The longitudinal delta-c-p values obtained in individual subjects confirms the transverse delta-c-p findings, with regard to size and age group, which were obtained by comparisation of cross sections of groups of normotive and hypertensive subjects.

Ultrasonic pulsed-Doppler signals from deep-lying vessels in the normal abdomen and pelvis are described. The signal characteristics combine to produce a Doppler "signature" that is specific for each vessel. The clinical potential of this method of deep flow detection is considered in relation to three areas of Doppler signal analysis: first, qualitative indication of the presence, direction, or absence of flow in a structure; second, more quantitative description of time velocity waveforms and Doppler spectral content; and third, the estimation of absolute volume flow. Limitations of these methods for the abdominal signals obtained are discussed.

The interaction of carotid chemoreceptor and pulmonary inflation reflex control of peripheral and coronary vasoactivity and myocardial contractility was examined in conscious dogs. Stimulation of carotid chemoreceptors resulted in an increase in rate and depth of respiration, an increase in myocardial contractility, and more intense vasoconstriction in the iliac than in the mesenteric, renal, or cerebral beds. The coronary bed responded primarily with vasodilation. The increase in rate and depth of respiration stimulated pulmonary inflation reflexes, which in turn were partially responsible for the coronary vasodilation, but also attenuated the positive inotropic response and even reversed the initial peripheral vasoconstriction to a period of significant vasodilation.

This study documents the changes in selected regional hemodynamics occurring in response to large doses of intravenous morphine. It was performed in normal conscious dogs. Their cardiovascular systems was unaltered by the presence of other drugs or recent surgery. The animals had been surgically prepared previously by implantation of chronic indwelling electromagnetic and Doppler ultrasonic flow probes on the aorta and the cranial mesenteric, renal and iliac arteries and placement of aortic catheters. Morphine, 1 mg/kg, produced mesenteric vascular dilation (30 per cent maximum decrease in resistance), renal vascular dilation (11 per cent maximum decrease in resistance) and nonsignificant changes in iliac vascular resistance. Morphine, 3 mg/kg, resulted in a similar amount of renal dilation (maximum 12 per cent decrease in resistance) but constricted the mesenteric vasculature (maximum 120 per cent increase in resistance) and the iliac vasculature (68 per cent maximum increase in resistance). These changes were observed despite the lack of sustained major changes in cardiac output, blood pressure, total peripheral resistance, or heart rate. It is therefore concluded that morphine has only minimal effects on systemic hemodynamics, but has significant effects when the alterations it produces in regional hemodynamics are considered. Such alterations may be physiologically significant when perfusion to these individual organs is a concern. The minimal systemic effects of high dose morphine is a phenomenon, for the most part, common to both dogs and humans. Whether similar regional hemodynamics changes as these occur in humans cannot be determined at this time since continuous flow monitoring techniques have, as yet, not been applied to humans.

Specific hemodynamic factors have been shown to be associated with atherosclerotic plaque localization at the human carotid bifurcation. Flow field characteristics may also determine plaque distribution in the abdominal aorta. We therefore characterized flow patterns in a glass model abdominal aorta that included its major branches under conditions of steady flow. Outflow resistances of the celiac, superior mesenteric, renal, inferior mesenteric, and iliac arteries were varied to produce flow distributions consistent with rest, the postprandial state, and vigorous lower limb exercise. Flow patterns were visualized with three colors of dye injected simultaneously through capillary tubes at selected locations and recorded as still photographs and by cinephotography on videotapes. Under resting conditions a large region of flow separation and stagnation occurred at the posterior wall of the aorta directly opposite the orifices of the superior and inferior mesenteric arteries. Similar separation regions were observed during the simulated postprandial state but diminished markedly when distal outflow was increased to levels consistent with exercise. In the highly susceptible infrarenal aortic segment, beginning about 2 cm below the renal artery orifices, multiple secondary flow patterns with three to four counterrotating vortex formations were observed under both resting and postprandial conditions but disappeared in the exercise state. Secondary flow patterns were not noted in the suprarenal abdominal aorta, which is usually relatively spared. Such features have been related to plaque localization elsewhere, and the disappearance of these patterns with increased flow velocity during exercise is consistent with the previously noted protective effect of unidirectional laminar high-flow states. The beneficial effects of physical fitness programs may be related in part to these hemodynamic modifications.

1. Experiments were done on anaesthetized cats to study the effect of electrical stimulation of afferent renal nerves on the circulatory system and on the release of renin from the kidney. 2. Stimulation of afferent renal nerves over a wide range of parameters consistently elicited an increase in arterial pressure and heart rate. This response was still present in paralysed animals and was not accompanied by changes in respiration or in sympathetic autonomic activity usually associated with painful stimulation. Mesenteric and iliac vasoconstriction was observed concomitantly with the increase in arterial pressure. 3. Release of renin from the contralateral innervated kidney was not significantly changed by stimulation of afferent renal nerves. 4. The existence of renal vascular mechanoreceptors was investigated by altering renal circulation. Stenosis of the renal artery or a marked reduction in renal perfusion pressure elicited an increase in arterial pressure while stenosis of the renal vein elicited a decrease in arterial pressure. These responses, however, were not affected by denervation of the kidney and were therefore interpreted as not being due to neural mechanisms. 5. The precise nature, location and physiological role of renal receptors involved in the cardiovascular responses observed during electrical stimulation of afferent renal nerves remain to be determined.

Four pregnant and four castrated ewes were chronically instrumented for the measurement of external iliac blood flow to test the hypothesis that pregnancy alters alpha-adrenergic sensitivity in a major regional circulation. Complete dose-response curves were generated to methoxamine, phenylephrine, and norepinephrine. Pregnancy was associated with no change in methoxamine sensitivity, an increase in phenylephrine sensitivity, and a decrease in norepinephrine sensitivity. These differential changes in drug sensitivity suggest (1) the alpha 1-receptor population is functionally similar between the two groups of animals, (2) uptake 1 is inhibited, and (3) either catechol-O-methyltransferase activity is increased or the alpha 2- or beta-receptor population changes in this circulation during pregnancy. These data illustrate the complexity of the change in the adrenergic system during pregnancy.

To define the relationship between compliance mismatch and the development of neointimal hyperplasia, one 3 cm segment of common iliac artery was externally banded in seven dogs, thereby fixing the arterial diameter at end diastole. To quantify compliance, end-diastole diameter and its change with pulse pressure were measured by induction angiometry. This technique uses intravascular soft trifilar wire probes introduced through distally placed polytetrafluoroethylene sidearms. Compliance was checked in the banded and contralateral undissected unbanded control iliac arteries at 3 and 6 months, at which times the vessels were fixed by perfusion, excised, and examined histologically. Sustained (6-month) compliance mismatch was successfully induced within the banded segments (p less than 0.0001), and no compliance mismatch was seen in the control segments (p = 0.357). The intima of all banded vessels was virtually indistinguishable from that in controls grossly and histologically. Mild focal intimal thickening, less than 3 cell layers thick involving less than 5% of the vessel circumference, was typically seen in both banded and control vessels (range 6.57 +/- 6.80 micron to 38.86 +/- 57.16 micron). In marked contrast, at the sites of the polytetrafluoroethylene-to-femoral artery anastomosis, near-occlusive neointimal hyperplasia (1714 +/- 415.47 micron) was seen in all animals. Residual lumen area in the banded and control vessels was only minimally abnormal (range 98.65% +/- 2.18% to 99.96% +/- 0.08%). These data indicate that compliance mismatch alone is an insufficient stimulus for the development of neointimal hyperplasia in the canine model.

A duplex-system echographic study, with simultaneous visualization of the vessel proper and its doppler flow rate curves, was carried out in 35 women with normal biphasic menstrual cycles. A typical flow rate curve was demonstrated for each of the vessels. The assessment of numeric pulsation index values showed its significant reduction in the ovarian artery where the ovary contains a mature follicle or a luteal body. The results obtained have been analysed in morphofunctional terms. A conclusion is made that a more accurate prediction of the ovulation and assessment of the microcirculatory ovarian bed in various diseases is possible.

Hypertonic saline treatment of hemorrhagic shock (HS) results in increased systemic blood pressure, cardiac output, and splanchnic blood flow. To determine whether this elevation in blood pressure and flow would augment blood loss from injured intra-abdominal vessels and thus enhance mortality rate, "controlled" HS was induced by bleeding of 20 ml/kg from an arterial cannula that was immediately occluded after hemorrhage, and "uncontrolled" HS was induced by incision of three major radicals of the ileocolic artery leading to continuous intra-abdominal blood loss. Seventy rats were divided into eight groups: Group I (n = 5) underwent carotid artery and jugular vein cannulation and was observed for 3 hr; in Group II (n = 10) "controlled" HS was induced by arterial hemorrhage of 20 ml/kg; in Group III (n = 7) "controlled" HS was treated by 5 ml/kg NaCl 0.9%; in Group IV (n = 8) "controlled" HS was treated by 5 ml/kg NaCl 7.5%; in Group V (n = 4) midline laparotomy and identification of the ileocolic artery was performed; in Group VI (n = 9) "uncontrolled" HS was induced by incision of three major branches of the ileocolic artery; in Group VII (n = 9) "uncontrolled" HS was treated by 5 ml/kg NaCl 0.9%, and in Group VIII (n = 18) "uncontrolled" HS was treated by 5 ml/kg NaCl 7.5%. In untreated "controlled" HS (Group II), mean arterial pressure (MAP) fell to 35 torr followed by a spontaneous rise to 62 torr (p less than 0.001) after 3 hr with a survival of 80% of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)

A mathematical model was developed for the characterization of quasistatic nonlinear viscoelastic behaviour of large arteries with activated smooth muscle. Arteries were considered to belong to the class of viscoelastic materials with fading memory and the first order term of the integral polynomial constitutive equations of Pipkin and Rogers satisfying the nonlinear superposition principle was modified to handle responses to increasing and decreasing loads independently. The two creep functions contained by the obtained one dimensional constitutive equation were determined experimentally from the series of creep and recovery tests of increasing amplitude performed on isolated canine iliac arteries following the activation of the vascular smooth muscle by normal dose of norepinephrine in vitro. Utilizing the constitutive equation of the arterial wall and the tabulated values of creep functions successive stress-strain hysteresis loops of various constant stress rates were simulated by digital computer. The computed hysteresis loops demonstrated the main characteristics, such as the weak and asymmetric rate-sensitivity of the experimentally observed hysteresis of arteries qualitatively well, thus allowing certain conclusions on the mechanism of quasistatic viscoelastic behaviour of vascular smooth muscle.

The cardiovascular responses evoked through the nasopharyngeal reflex by the inhalation of formaldehyde vapour were studied in conscious rabbits after bilateral electrolytic lesions of the ventrolateral medulla coinciding with the A1 group of catecholamine cells. Arterial blood pressure was measured in the central ear artery, heart rate was determined from the arterial pressure trace, and iliac blood flow was determined using a Doppler ultrasonic flow meter placed around the lower abdominal aorta. There were no significant changes in the heart rate, blood pressure and iliac conductance responses elicited through the nasopharyngeal reflexes of sham operated animals in which electrodes were inserted without the passage of current. The blood pressure changes produced by inhalation of formaldehyde in control rabbits were not significantly altered in animals with ventrolateral medullary lesions. However, the magnitude of the bradycardia and of the fall in iliac conductance evoked by the inhalation of formaldehyde were approximately halved 4 h and 1 day after the lesions but were fully restored at 2 weeks. These experiments suggest that the A1 group of catecholamine neurones help mediate the bradycardia and vasoconstriction elicited through nasopharyngeal reflexes in terrestial animals exposed to noxious vapours.

Interstitial compliance, defined as the ratio between changes in interstitial fluid volume (delta IFV) and interstitial fluid pressure (delta IFP), has been measured for rat skin. IFP has been measured with sharpened glass capillaries connected to a servocontrolled counterpressure system, while IFV has been determined as the extravascular distribution space for 51Cr-EDTA. The measurements were performed at hydration and dehydration of various duration. Compliance was 0.162 ml/g dry tissue per mmHg in dehydration, corresponding to 5.4 ml/100 g wet tissue per mmHg. The volume-pressure curve was similar at 2-4 and 24-28h of dehydration. Up to 20% increase in IFV compliance was similar to that in dehydration, but thereafter increased severalfold upon further increase in IFV. Even at sixfold increase in IFV, IFP did not rise by more than 1 to 2 mmHg. Control IFV in skin amounts to 40 ml/100 g wet tissue and IFV will therefore change by 14% when IFP changes by 1 mmHg from the control level. This change in IFV will cause interstitial fluid colloid osmotic pressure to increase or decrease by somewhat more than 1 mmHg in dehydration or hydration respectively from a normal control level of about 9 mmHg. With further increase in IFV secondary to increased capillary filtration, the interstitial edmaprevention will depend on washout and/or dilution of interstitial proteins since IFP did not increase by more than 1 to 2 mmHg.

Eighty patients underwent percutaneous transluminal dilatation and recanalisation of atheromatous lesions of the arteries of the lower extremities in the University Hospital of Maastricht in the period of 1980 to 1984. Out of 80 attempted procedures of the iliac and femoro-popliteal tract 71 (89%) were technically possible and were considered initially successful. In all cases of iliac artery lesions a retrograde arteriogram was performed prior to PTA. Intra-arterial pressure measurements at rest and after hyperemia were used for exact assessment of the hemodynamic significance of the stenosis before and after PTA. A follow-up of all patients successfully treated by angioplasty was performed. The early hemodynamic success rate of PTA for iliac lesions was 90 per cent and for femoral-popliteal segment 83 per cent. There was no morbidity or mortality. The cumulative 3-year patency rate for both segments was 74 per cent.

Nonpregnant and pregnant sheep at 110 to 140 days' gestation were chronically instrumented for measurement of mean arterial pressure, heart rate, cardiac output, common internal iliac artery blood flow, and middle uterine artery blood flow. Systemic and regional vascular resistances were calculated from pressure/flow data. Either isoxsuprine, 10 microgram/kg/min, or terbutaline, 0.40 microgram/kg/min, was infused continuously for a period of one hour. The above-mentioned parameters were monitored during control, infusion, and postinfusion periods. The findings show that: (a) isoxsuprine had greater effects on the mean arterial pressure, heart rate, and cardiac output than did terbutaline; (b) both agents had minimal effects on the common internal iliac artery blood flow of pregnant ewes, but isoxsuprine decreased the middle uterine artery blood flow significantly; and (c) with isoxsuprine, a marked vasodilatation occurred in the common internal iliac vascular bed of nonpregnant ewes, in contrast to the insignificant changes in the pregnant ewes. The conclusions drawn were that: (1) the more pronounced effects of isoxsuprine are most probably related to a greater beta 1 stimulation; (2) contiguous regional vascular beds respond differently to pharmacologic stimuli; and (3) the state of a given vascular bed during the resting state determines its response to vasoactive agents.

To examine the effects of sustained (48-hour) hypoxemia on fetal and maternal adrenocorticotropic hormone concentrations and on maternal progesterone, uterine blood flow was reduced in eight sheep at day 128 of pregnancy by means of an adjustable Teflon clamp placed around the maternal common internal iliac artery. Control measurements were made in four animals in which the vascular clamp was not adjusted. Fetal PaO2 fell from 20.6 +/- 1.1 mm Hg (mean +/- SEM) to 16.6 +/- 0.6 mm Hg within 1 hour after application of the clamp and remained suppressed during 48 hours. There was a transient acidemia at 1 to 2 hours that had corrected by 8 hours. Fetal adrenocorticotropic hormone levels rose from 24 +/- 6 to 1320 +/- 205 pg/ml at 2 hours but decreased by 16 hours. Measured by high-pressure liquid chromatography, more than 95% of immunoreactivity corresponded to adrenocorticotropic hormone1-39. Fetal cortisol levels rose by 6 hours and remained elevated through 48 hours. Maternal adrenocorticotropic hormone, cortisol, and progesterone levels were unchanged during the study period. We conclude that fetal hypoxemia-acidemia after restriction of uterine blood flow provokes fetal adrenocorticotropic hormone release, but the elevation in adrenocorticotropic hormone is not sustained. However, the level of fetal cortisol rises progressively, consistent with fetal adrenal activation.

The effects of nitrendipine, 8 micrograms/kg/minute, were evaluated in six conscious dogs through measurements of arterial pressure and blood flow in the ascending aorta (cardiac output), mesenteric, renal, and iliac arteries before and after induction of chronic perinephritic hypertension. Before hypertension was induced, nitrendipine reduced mean arterial pressure 19 +/- 2.3% (from 95 +/- 3.2 mm Hg), decreased total peripheral resistance (60 +/- 2.6%), and increased cardiac output (108 +/- 10.5%). These values returned to baseline within 15 to 30 minutes. Nitrendipine caused the greatest increase in blood flow in the iliac bed (98 +/- 9.9%), an intermediate increase in the mesenteric bed (37 +/- 3.7%), and the least increase in the renal bed (7 +/- 2.2%). Two to six weeks after induction of hypertension, administration of nitrendipine elicited significant (p less than 0.01) decreases in mean arterial pressure (32 +/- 2.5% from 151 +/- 4.8 mm Hg) and total peripheral resistance (67 +/- 1.3%) compared with its administration in normotensive dogs, while the increase in cardiac output was not significantly changed (111 +/- 10.9%). These changes in arterial pressure and vascular resistances also were prolonged (i.e., hemodynamics returned to baseline after 75-90 minutes). The increase in iliac (99 +/- 16.8%) and renal (9 +/- 6.1%) blood flows after nitrendipine administration in hypertensive dogs was similar to that found in the normotensive dogs, but mesenteric blood flow doubled (84 +/- 8.4%). Thus, in conscious, hypertensive dogs, nitrendipine administration appears to markedly decrease arterial pressure and total peripheral and regional resistances, which also require more time to return to baseline, but appears to increase blood flow by a greater amount only in the mesenteric bed.

To investigate the impact of fentanyl on the carotid chemoreceptor reflex, nine mongrel dogs were permanently monitored with electromagnetic flow transducers around the right common iliac artery and with heparin-filled catheters in the descending aorta and in one of the main carotid arteries with the tip just proximal to the carotid sinus. Carotid chemoreceptor activation (CCRA) produced by consecutive injections of nicotine (0.2-0.4 micrograms/kg) through the carotid catheter elicited bradycardia, expressed as an increase in cardiac cycle length by 140% +/- 18%, and a 252% +/- 16% increase in mean iliac arterial vascular resistance. These responses were markedly attenuated by fentanyl in a dose-dependent fashion: cardiac cycle length increased only by 50% +/- 7% (P less than 0.01) with 4 micrograms/kg and by 19% +/- 6% (P less than 0.01) with 8 micrograms/kg of intravenous fentanyl. These changes were paralleled by significantly (P less than 0.01) lesser increases in mean iliac arterial resistance (122% +/- 9% and 50% +/- 5%). It is concluded that fentanyl impairs the integrity of the carotid chemoreceptor reflex.

The relationship between lymph flow, lymph node arterial and venous perfusion pressure and lymph node resistance have been studied in an in vivo isolated canine iliac lymph node perfused through an afferent lymphatic with heparinized canine plasma. The relationship between the rate of perfusion and perfusion pressure across the node was linear but the calculated resistance of the node decreased as the rate of perfusion increased. In nine dogs the mean resistance to lymph flows less than 0.1 ml/min was 180 mmHg/ml min, but 68 mmHg/ml min to rates of perfusion above 1.0 ml/min. An increase of venous pressure in the veins draining the node increased the node's resistance by 8.6 mmHg/ml min for each 10 mmHg increase of venous pressure. The effect on node resistance of an increase of venous pressure was greater at low rates of perfusion. A decrease of arterial pressure in the arteries supplying the node reduced the node's resistance by 2 mmHg/ml min for each 10 mmHg decrease of arterial pressure. Increases of arterial pressure had an opposite effect of a similar magnitude. The effect on node resistance of a change of arterial pressure in either direction was greater at low rates of perfusion.

Numerous schemes have been used for measuring hemodynamic properties of deeply lying arteries; however, all have their limitations. This paper describes a new relatively nontraumatic intravenous approach that uses a catheter in connection with a pulsed ultrasonic Doppler velocity meter (PUDVM) and an echo track. The catheter was initially tested in a hydraulic model system for calibration of velocity and flow parameters. Lately, the catheter has permittted measurements of local instantaneous blood velocity, flow, and wall motion characteristics in adult Beagle dogs in the abdominal aorta and iliac artery. Evaluation studies have been conducted to compare the catheter-tip recordings with an independent method for measuring blood flow and wall motion. Coupling of this catheter-tip device with the PUDVM and echo track provides chronic measurements of hemodynamic parameters in these deep vessels which were virtually impossible to obtain previously. This technique may prove useful in monitoring vessel pathology longitudinally as well as in basic experimental situations requiring flow and arterial wall mechanical properties.

A variety of devices has been used for measuring flow properties of deep-lying arteries, but many have limitations. This paper describes a relatively nontraumatic intravenous approach which uses a catheter in connection with a pulsed ultrasonic Doppler velocity meter (PUDVM) and an ultrasound echo track. The venous ultrasound catheter (VUC) has permitted measurements of local instantaneols blood velocity, flow, and wall motion in the abdominal aorta and iliac arteries of beagle dogs; evaluation studies have been conducted to compare the VUC recordings with an independent method for measuring blood flow and wall motion. Coupling of this catheter-tip device with the PUDVM and echo track provides chronic measurements of hemodynamic parameters in these deep vessels which were virtually impossible to obtain previously. This technique may prove useful in monitoring vessel pathology longitudinally as well as in basic experimental situations requiring flow and arterial wall mechanical properties.