Intra-arterial Pressure Research Articles

α-Adrenoceptor Blockade by Tibalosine

In a randomized double-blind protocol, 12 healthy male volunteers were studied twice at rest and during exercise after pretreatment for 1 week with placebo or 150 mg daily of the new alpha 1-adrenoceptor antagonist tibalosine. Six subjects received, on both experimental days, an intravenous infusion of saline and the other six received the opioid receptor antagonist naloxone. Combined measurements taken during rest and exercise showed tibalosine, on average, to decrease mean intraarterial pressure by 4.7 mm Hg and heart rate by 3.5 beats/min. Urinary volume and sodium excretion were transiently reduced by tibalosine as compared with placebo. Opioid antagonism by naloxone stimulated the pituitary-adrenal axis, but had no effect on the influence of tibalosine, as shown by hemodynamic, respiratory, and most humoral measurements. However, on interruption of exercise, opioid antagonism counteracted the inhibition of the plasma renin-angiotensin system by tibalosine, probably through the naloxone-induced increase in epinephrine release. In conclusion tibalosine reduced blood pressure at rest and during exercise independently of opioidergic mechanisms. This hypotensive action may be accompanied by sodium and fluid retention.

Hemodynamic study of internal carotid artery stenosis and occlusion: value of combined isotopic measurements of regional cerebral blood flow and blood volume

The assessment of the intracranial hemodynamic consequences of obstructive lesions of the carotid artery by measuring resting rCBF is inadequate because cerebral blood flow may remain constant in spite of significant drops in the intraluminal pressure due to autoregulation. Moreover, flow may be permanently decreased following cerebral infarction, even if the arterial anatomical conditions have resumed their normal state because of the decreased metabolic demand of an infarcted area. Measurement of the regional cerebral blood volume (rCBV) helps with the hemodynamic assessment of these conditions, since there is a linear and inverse relationship between intraarterial pressure and intracranial blood volume. In 24 patients exhibiting various carotid and ischemic brain lesions we studied both rCBF and rCBV. The latter is a comparative measure between hemispheres obtained by single photon emission tomography after autotransfusion of 99m Technetium labeled erythrocytes. There was no correlation between rCBF and clinical status, CT scan or arterial lesions. There was no correlation between rCBV and clinical status or CT scan. There was, however, an interesting correlation between rCBV and the severity of the arterial lesion. The rCBV was symmetrical in all patients with normal or moderately stenotic carotid arteries before and after operation. In some patients with severe unilateral stenosis or occlusion, there was a significant relative increase of rCBV in the hemisphere downstream from the lesion, which disappeared after surgery (endarterectomy or extra-intracranial bypass). In some patients with severe and bilateral carotid lesions, we noted an asymmetry in rCBV that disappeared after a unilateral operation. Other patients with similar lesions develop asymmetry only after an operation that resulted in a relative increase in rCBV in the hemisphere supplied by the non-operated artery. In conclusion analysis of these results suggests that in this series of patients, rCBV modifications were the consequence of cerebral autoregulation distal to the arterial lesions and provided satisfactory assessment of hemodynamic improvement after surgical repair.

The continuous measurement of intra-arterial pressure in the neonate: method and accuracy.

The authors describe an early set up measurement system which allows the continuous monitoring of intra-arterial pressure in newborn babies for a number of days. The novelty of the system is in the introduction of a high impedance (usually a short length of capillary tubing) between the infusion pump and the pressure transducer. A flushing device is used in conjunction with a syringe pump which allows the infusion rate to be accurately controlled and limited, and to enable a check to be made on the total amount of fluid that has been infused at any given time.

Percutaneous transluminal angioplasty: A suggested method for analysis of clinical, arteriographic, and hemodynamic factors affecting the results of treatment

Sixty-nine percutaneous transluminal angioplasties (PTAs) were performed in the iliac and the femoral arteries of 54 patients. The main factors that might affect the results were reviewed: associated diseases, severity of ischemic symptoms, location and type of lesions (stenosis or occlusion and their length), and presence of disease distal to the site dilated. The vascular status of the patients in our series was more severe than in most others. Improvement at follow-up (average 15 months) was maintained in 74% of 66 radiographically successful PTAs. Poor runoff was the only factor found to affect the outcome deleteriously. Intra-arterial pressure measurements performed during the procedure and vascular laboratory studies were most valuable in assessing immediate and long-term results. Wide variations in results of PTA published in the literature are due to differences in methods of selection, evaluation, and reporting. A plea is made for future presentations of PTA series in an analyzable and comparable way, including and correlating all relevant variables as in the model suggested by the present study.

Chronic effect of ketanserin in mild to moderate essential hypertension.

Ketanserin, an antagonist highly selective for 5-hydroxytryptamine (serotonin) type 2 (S2) receptors, was given as monotherapy in a dose of 40 mg b.i.d. to 24 subjects with mild to moderate essential hypertension. Its effects were evaluated in a placebo-controlled double-blind crossover study. The effect on blood pressure in 18 subjects was monitored by 24-hour ambulatory intra-arterial measurements. Systolic and diastolic intra-arterial pressures were significantly lowered by ketanserin both during the day and at night, whereas heart rate was unchanged. Cuff pressure readings (triplicate measurements) with the London School of Hygiene sphygmomanometer and an automatic device (12 measurements in 1 hour) in the outpatient clinic also showed a significant effect on both supine and standing pressures. No postural hypotension was noted. Ketanserin had no effect on endogenous creatinine clearance, serum cholesterol levels, and the plasma levels of norepinephrine, renin, and aldosterone. The only side effect that was significantly more common with ketanserin than with placebo treatment was an increase in body weight. Ketanserin may have a place in the treatment of mild to moderate essential hypertension.

Hemodynamic effects at rest and during exercise of long-term sodium restriction in mild essential hypertension.

During moderate sodium restriction for 9 months in 19 men (33 years) with previously untreated mild essential hypertension (EH) sodium excretion fell from 209 to 139 mmol/24 h. Concomitantly intraarterial pressure at rest sitting fell from 145/93 to 138/88 mmHg (5%) and during 100 W exercise from 168/90 to 162/86 mmHg (4%). The fall in BP was due to reduction in cardiac output (5-11% at rest and during exercise) while peripheral vascular resistance was raised (4-10%). Thus, moderate sodium restriction was not very efficient treatment in our patients with mild EH. The main hemodynamic disturbance of established EH--an increase in vascular resistance--was not normalized after 9 months of low salt diet.

Diurnal patterns of blood pressure, heart rate and vasoactive hormones in normal man.

In order to determine arterial pressure and vasoactive hormone relationships in normotensive man, we measured intra-arterial pressure continuously along with hourly venous hormone levels (renin, angiotensin II, aldosterone and catecholamines) for 24 hours in 5 healthy volunteers under standardized conditions. Mean 24-hour levels of intra-arterial pressure 106/63 +/- 5.4/4.9 mmHg were much lower than in patients with mild essential hypertension studied earlier. A common diurnal pattern was seen for plasma renin, angiotensin II, and catecholamines, with higher levels in the day time and lower levels at night. Aldosterone levels however, paralleled those of cortisol at night. Plasma norepinephrine levels showed close, positive correlations with arterial pressure in all volunteers. We conclude that the level of blood pressure as measured continuously over 24 hours is lower than might be expected from regular clinic recordings; that aldosterone regulation is contributed to by ACTH in the nocturnal hours; and that fluctuations in arterial pressure and sympathetic activity over 24 hours are closely coupled.

Alterations of myocardial blood flow associated with experimental canine left ventricular hypertrophy secondary to valvular aortic stenosis.

Experimental renovascular hypertension or supravalvular aortic constriction results in left ventricular hypertrophy and impaired minimum coronary vascular resistance. However, these experimental models expose the coronary arteries to increased intra-arterial pressure, so that hypertensive vascular changes might be responsible for the impaired minimum coronary resistance. This study was performed to test the hypothesis that left ventricular hypertrophy in the absence of increased coronary pressure results in abnormalities of myocardial perfusion. Aortic valve stenosis was produced by plication of the noncoronary aortic cusp of 11 dogs at 6-8 weeks of age. Studies were carried out when the animals reached adulthood; mean left ventricular:body weight ratio was 7.1 +/- 0.4 as compared to 4.4 +/- 0.3 g/kg in 11 normal dogs (P less than 0.01). Under quiet resting conditions, myocardial blood flow measured with microspheres was significantly greater than normal in dogs with aortic stenosis. However, during maximum coronary vasodilation with adenosine, mean left ventricular blood flow in dogs with hypertrophy (3.29 +/- 0.39) was substantially less than in normal dogs (6.19 +/- 0.54 ml/min per g; P less than 0.01), whereas minimum coronary resistance was increased from 14.1 +/- 1.7 in normal dogs to 23.7 +/- 5.4 mmHg. min X g/ml (P less than 0.01). To examine the response of myocardial perfusion to cardiac stress, blood flow was measured during pacing at 200 and 250 beats/min. Compared with normal dogs, animals with hypertrophy had a subnormal increase in myocardial blood flow during tachycardia; this perfusion deficit was most marked in the subendocardium. These data demonstrate that left ventricular hypertrophy alone, without increased coronary artery pressure, is associated with impaired minimum coronary vascular resistance and with abnormalities of myocardial blood flow during pacing stress.

Hypertensive emergencies and urgencies: Pathophysiology and clinical aspects

A hypertensive urgency should be distinguished from a hypertensive emergency. Although the distinction may not always be obvious, certain guidelines may help the clinician determine which therapeutic approaches are most appropriate for each patient. Hypertensive emergencies include those conditions in which new or progressive severe end-organ damage is present and a delay in appropriate therapy might result in permanent damage, progression of complications, and a poor prognosis. Hypertensive urgencies include those conditions with minimal to no obvious end-organ damage in which blood pressure should be lowered expeditiously. The risk of immediate complications or organ damage is less likely to occur, and thus the immediate prognosis is better, although the ultimate prognosis, if untreated, is poor. There is a marked individual, racial, sexual, and age difference in the ability to tolerate high intraarterial pressure, as evidenced by patients' symptoms and signs of end-organ damage. Patients may have no symptoms of elevated blood pressure until significant intraarterial levels are reached. If symptoms are present, they may include headache, dizziness, blurred vision, shortness of breath (especially with exertion), chest pain, rapid pulse, palpitations, malaise and fatigue, nocturia, or pedal edema. 7,11–14 Signs of hypertensive disease vary and depend not only on the level of blood pressure but also include funduscopic changes with arteriolar narrowing, atrioventricular nicking, hemorrhages, exudates or papilledema, central nervous system changes and neurologic abnormalities, cardiac changes with gallop rhythm, cardiomegaly, tachycardia, ectopic ventricular beats, left ventricular hypertrophy or signs of congestive heart failure, pulmonary edema, and signs of renal insufficiency. 7,11–14 Although there is a definite correlation between the level of blood pressure and end-organ damage, there is no definite systolic or diastolic level of blood pressure that induces end-organ damage. Some patients may tolerate very high blood pressures with few symptoms or signs, whereas others may manifest end-organ damage at lower blood pressures. Thus, the definition of hypertensive emergency and urgency depends on the clinical assessment of the blood pressure level and clinical and laboratory assessments of end-organ damage. The absolute blood pressure in itself does not determine the seriousness of the clinical situation, the expediency of treatment, or the need for in-hospital monitoring in a critical care unit. It is important not to lower the blood pressure precipitously or to a subnormal level particularly in patients with end-organ damage. Such treatment may critically reduce blood flow and perfusion to vital organs and induce a cerebrovascular accident, myocardial ischemia, or renal failure. A smooth, gradual reduction in blood pressure is crucial to patient management with oral or parenteral antihypertensive drugs. However, in hypertensive emergencies blood pressure control should be accomplished within 1 hour, whereas with hypertensive urgencies control should be within 24 hours. Those patients who have hypertensive emergencies with malignant hypertension and end-organ damage should be admitted to a hospital intensive care unit for evaluation and treatment. These patients have a diffuse arteritis, as of a result of their hypertension, that may take 4 to 6 weeks to heal. Many patients who present with diastolic blood pressure 120 mm Hg or greater will be found to have a secondary cause of hypertension (such as renovascular hypertension) after careful evaluation. On the other hand, those patients with hypertensive urgencies as defined previously can be treated in the emergency room or outpatient department and can avoid hospital admission. Careful, immediate, and routine follow-up is important in these patients.

Effect of nicotine on coronary blood-flow in man.

The effect of 4 mg nicotine administered in a chewing gum on coronary haemodynamics and oxygen transport, was studied by coronary sinus catheterization in eight healthy non-smoking men. Measurements were made of coronary sinus blood-flow (CSF) by thermodilution and arterial-coronary sinus (a-cs) O2-difference together with heart rate and intra-arterial pressure both at rest, and during, atrial pacing with and without nicotine. Nicotine increased myocardial oxygen consumption (MVO2) more than expected from the increase in the rate-pressure product. The increased MVO2 was covered only partly by increased coronary blood-flow; especially during and after pacing an increased a-cs O2-difference contributed significantly. This differed from the response when MVO2 was increased by atrial pacing alone, in which case the whole increase in MVO2 was covered by increased flow. The results suggest that nicotine affects coronary vascular resistance and blood-flow indirectly through a vasodilatory effect, by mechanisms related to the increased cardiac work, and directly through a vasoconstrictory effect. The suggested vasoconstrictor component is moderate in the non-ischaemic human heart.

Fifth Versus Fourth Korotkoff Phase

It is well known that neither the fourth Korotkoff phase (muffling of sounds) nor the fifth (disappearance of sounds) represent intraarterial diastolic pressure. I agree with Moss1 that whether or not a particular Korotkoff phase reflects true intraarterial pressure is not relevant. What both phases represent is a value for diastolic pressure as determined by the indirect auscultatory method. Clinical measurements should be referred to normal standards established with the same phase used in the determinations. The question is which is preferable. Most screening programs in adults and many in children have used the disappearance of sounds for the diastolic criterion because there was much less intraobserver variation.

Endogenous angiotensin-aldosterone-pressure relationships during sodium restriction.

The effects of moderate restriction of dietary sodium and potassium supplementation on plasma levels of renin, angiotensin II, aldosterone, and cortisol and on arterial pressure were studied in 12 patients with mild essential hypertension. To define hormone-blood pressure relationships, venous hormone levels were measured hourly and intra-arterial pressure continuously for 24 hours after 4 to 6 weeks of sodium restriction, 4 to 6 weeks of potassium supplementation, and a similar period of control diet. Our results show that compared with the control diet, moderate sodium restriction was associated with increased levels of aldosterone but no overall change in renin, angiotensin II, or cortisol levels. Further, slopes of regression lines relating log renin and log angiotensin II to aldosterone were increased, as were log cortisol/aldosterone regression lines. On the contrary, regression lines of log renin and log angiotensin II versus arterial pressure were unaltered by sodium restriction. Hormone and blood pressure relationships were not changed by the potassium supplemented diet. Although confirmatory data are needed, our findings suggest that moderate sodium restriction enhances aldosterone responsiveness to endogenous angiotensin II and adrenocorticotropic hormone without diminishing the pressor activity of endogenous angiotensin II. These results may explain in part the disappointingly small hypotensive effect of modest sodium restriction in mild essential hypertension.

Effects of angiotensin II on arterial pressure, renin and aldosterone during exercise.

To evaluate the effect of isotonic exercise on the response to angiotensin II, angiotensin II in saline solution was infused intravenously (7.5 ng X kg-1 X min-1) in seven normal sodium replete male volunteers before, during and after a graded uninterrupted exercise test on the bicycle ergometer until exhaustion. The subjects performed a similar exercise test on another day under randomized conditions when saline solution only was infused. At rest in recumbency angiotensin II infusion increased plasma angiotensin II from 17 to 162 pg X ml-1 (P less than 0.001). When the tests with and without angiotensin II are compared, the difference in plasma angiotensin II throughout the experiment ranged from 86 to 145 pg X ml-1. The difference in mean intra-arterial pressure averaged 17 mmHg at recumbent rest, 12 mmHg in the sitting position, 9 mmHg at 10% of peak work rate and declined progressively throughout the exercise test to become non-significant at the higher levels of activity. Plasma renin activity rose with increasing levels of activity but angiotensin II significantly reduced the increase. Plasma aldosterone, only measured at rest and at peak exercise, was higher during angiotensin II infusion; the difference in plasma aldosterone was significant at rest, but not at peak exercise. In conclusion, the exercise-induced elevation of angiotensin II does not appear to be an important factor in the increase of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

PREVALENCE OF HYPOXAEMIC CHRONIC OBSTRUCTIVE LUNG DISEASE WITH REFERENCE TO LONG-TERM OXYGEN THERAPY

Of the Sheffield population aged 45 years or more, an estimated 0·3% (confidence interval 0·06%-0·5%) had intra-arterial oxygen pressures 7·3 kPa and forced expiratory volumes <50% of predicted values (ie, had hypoxaemic chronic obstructive lung disease). According to both the USA Medicare criteria for reimbursement and the UK Department of Health and Social Security draft guidelines for prescribing long-term oxygen, 603 (confidence interval 134-1072) subjects in Sheffield would be eligible to have oxygen supplied by concentrator, and 60 000 (confidence interval 13 000-107 000) in England and Wales. This is considerably higher than the number now prescribed long-term oxygen by general practitioners. In less than a quarter of the cases was there hypercapnia (PaCO 2 ≽6·1 kPa). The majority of those most severely affected were current smokers, and one-quarter were receiving no medication. General practitioners are unlikely to be able to assess accurately a patient's need for long-term oxygen treatment without specialised advice and measurement.

Differential intraarterial pressure recordings from different arteries in the rat

Intraarterial pressures were recorded from five different sites in pentobarbital anesthetized rats. Simultaneous recordings were made from the brachial artery, carotid artery, femoral artery, tail artery, and a small end-branch of the superior mesenteric artery under basal conditions and under vasoconstrictor and vasodilator influences to find out whether similar mean arterial pressures (MAP) can be recorded from the various sites. It was found that MAP of proximal arteries (brachial and carotid) is higher than the MAP recorded from more distal arteries (mesenteric, tail, and femoral). A pressure difference of 5–6 mm Hg was found to exist from the level of the carotid artery to that of the femoral artery during all experimental conditions. Our results indicate that the same artery should always be used to compare MAP between different rats. Moreover, calculations of arterial resistance (MAP/BF) of most vascular beds in the rat, using MAP values obtained from the tail or the femoral artery, as are commonly done in physiologic or pharmacologie studies, can result in slightly lower resistance values than the true resistance. To obtain true arterial resistance of any vascular bed, one has to use MAP recorded at the particular vascular bed for the calculation of resistance.

Osler's Maneuver and Pseudohypertension

We describe a simple bedside procedure (which we call "Osler's maneuver") that differentiates patients with true hypertension from those whose blood pressure is spuriously elevated because of excessive sclerosis of the large arteries ("pseudohypertension"). The maneuver is performed by assessing the palpability of the pulseless radial or brachial artery distal to a point of occlusion of the artery manually or by cuff pressure. We classified 24 elderly hypertensive patients as either Osler-positive (n = 13) or Osler-negative (n = 11), and measured their intraarterial pressure, arterial compliance, and systemic hemodynamics. Patients with pseudohypertension (Osler-positive) had falsely elevated blood-pressure readings, with a difference of 10 to 54 mm Hg between cuff and intraarterial pressure. Arterial compliance was lower in Osler-positive subjects and correlated with the difference between cuff and intraarterial pressures, indicating that the stiffer the artery, the more pronounced the degree of pseudohypertension. Pseudohypertension is common in the elderly and becomes more severe as arterial compliance decreases and sclerosis of large arteries progresses.

Body composition and its relation to systemic haemodynamics, fluid volume partitions and energy utilization in rats with bilateral ventromedial hypothalamic lesions.

Body composition and its relationship with intra-arterial pressure, fluid volume partitions and oxygen consumption were studied in male rats four months following ventromedial hypothalamic (VMH) destruction during the static phase of the development of obesity. Compared with sham-operated controls, rats with VMH lesions had a greater body weight which was related to an increased body lipid content and an elevated arterial pressure and total peripheral resistance. Fluid volume distribution was normal and total body oxygen consumption (per unit of body weight) was reduced. Bilateral destruction of the ventromedial hypothalamus was confirmed in each of the rats studied and no relationship could be demonstrated between the lesion size and the magnitude of haemodynamic changes. It is concluded that the increased arterial pressure observed in obese VMH lesioned rats was directly related to an elevated total body lipid content.

INVASIVE V. NON-INVASIVE MEASUREMENT OF ARTERIAL PRESSURE: Comparison of Two Automatic Methods and Simultaneously Measured Direct Intra-Arterial Pressure

Two indirect arterial pressure monitors, the Finapres and the Accutorr, were investigated and compared with the direct measurement of intra-arterial pressure. Pressures in patients in a variety of circulatory states were measured and analysed in relation to two types of random error: first, the "intra-individual standard error" (within one session of measurement) and second, the "inter-individual standard error" (between sessions). (This distinction is important, since in routine monitoring of arterial pressure one is usually dealing with the first type of error only.) This study showed that sudden changes in pressure were closely followed by the Finapres. A pressure reading of the Accutorr takes about 15-20 s, meaning that, within this period, variations will not be observed. The accuracy or reproducibility of each method, as expressed in intra-individual variance, diminished in the order Intra-Arterial-Line, Finapres, Accutorr. The inter-individual variation decreased in the order Intra-Arterial-Line, Accutorr, Finapres. Most of the inter-individual variance of the Finapres is probably real because of the more peripheral position of its cuff. A correlation between malfunctioning of the Finapres and vasoconstriction or hypothermia of the finger could not be demonstrated.

The effect of nicardipine on blood pressure, its variability and reflex cardiac control.

Eight untreated patients with essential hypertension (average casual blood pressure 180/110 +/- 27/12 mm Hg) were studied following control, acute (a single oral dose of 30 mg nicardipine hydrochloride), and chronic (2 months nicardipine oral therapy) treatment periods. During the 2 month treatment period, ambulatory mean intra-arterial (IABP), measured when the patients were awake, fell from 165/105 +/- 6/12 (control) to 150/96 +/- 14/12 mm Hg (P less than 0.05), but heart rate remained unchanged (84 +/- 12 control vs 80 +/- 9 beats min-1). There was an absolute reduction in blood pressure in response to tilting, the Valsalva manoeuvre, and exercise handgrip, but the percent increase in pressure following nicardipine was not significantly different from that in the control period. There was no change in baroreflex sensitivity after either acute or chronic treatment, but the set point of the reflex was reset to a lower pressure following chronic therapy. Both single and multiple doses of nicardipine significantly reduced intra-arterial pressure. Chronic therapy was associated with return of the heart rate to control values, which was due to resetting of the baroreflex control mechanism.

Relationship between plasma renin activity and physical fitness in normal subjects.

The relationship between plasma renin activity (PRA) at rest and physical fitness was studied in 40 normal young subjects on a liberal sodium intake. Plasma renin activity was measured in arterial blood withdrawn at the end of a 30-min period of rest in recumbency, while physical fitness was expressed by the highest oxygen uptake achieved during an uninterrupted graded exercise test performed in the sitting position on an electromagnetically braked ergometer bicycle (peak VO2). Log PRA correlated significantly and inversely with peak VO2 adjusted for body weight (r = -0.34; P less than 0.05) in single regression analysis. Using multiple regression and adjusted peak VO2, age, urinary sodium excretion and mean intra-arterial pressure as independent variables, no combination of two or more independent variables yielded significant partial correlation coefficients with log PRA. This correlation suggests that PRA at rest is inversely related to the subject's physical fitness.