Comparison of direct and indirect blood pressure measurement in anesthetized dogs.

This study was conducted to determine whether blood pressures and pulse rate could be determined accurately by indirect measurements from the front and hind legs of 15- to 40-kg dogs anesthetized with isoflurane. Indirect measurements from each animal were compared to direct measurements obtained from a catheter placed into the abdominal aorta via the femoral artery at four ranges of systolic pressure. When systolic pressure was above 80 mm Hg, indirect measurements were either the same as direct measurements or slightly lower. However, when systolic pressures were below 80 mm Hg, indirect systolic pressure measurements were 6 to 15% higher than direct measurements. Larger differences in diastolic pressures were found, which resulted in differences in mean pressure. The most accurate measurements were found when the cuff width-to-limb circumference ratio was between 0.4 and 0.6 and when systolic pressure was between 80 and 100 mm Hg.     

The role of adrenergic innervation in distributing systemic and coronary fractions of left ventricular output under increased pressure in the ascending aorta

The significance of neurogenic influences upon the distribution of systemic and coronary fraction during rise of aortic pressure by step occlusion of ascending aorta was studied in anesthetized cats. Under elevation of aortic pressure up to 60 mm Hg the increase in systemic fraction and less pronounced rise of coronary fraction were observed. When aortic pressure elevation was more than 60 mm Hg commensurable increase of both fractions occurred. Under beta-adrenoreceptor blockade elevation of aortic pressure more than 60 mm Hg evoked the significant increase in systemic fraction and reduction in coronary fraction.     

Coronary venous pressure and flow: effects of vagal stimulation, aortic occlusion, and vasodilators

Coronary venous pressure and coronary sinus flow in the canine heart were compared with intramyocardial, intraventricular, aortic, and coronary artery pressures. Stimulation of the thoracic vagus augmented coronary venous pressure, mean venous flow per systole, and coronary venous systolic resistance, but decreased the mean venous flow. Partial occlusion of the aorta augmented coronary venous pressure and coronary venous flow, while systolic coronary venous resistance remained unchanged. Adenosine increased peripheral and central coronary venous pressure and venous flow; it reduced peripheral coronary artery pressure. Adenosine augmented flow per systole and reduced venous resistance more than the other interventions. Dipyridamole decreased left ventricular, aortic, and central coronary artery systolic pressures and systolic venous resistance. It increased the venous flow, mean flow per systole, and coronary venous pressure, even though intramyocardial pressure remained unchanged. Nitroglycerine elevated coronary venous pressure and flow, as well as venous flow per systole, even though it decreased left ventricular, aortic, and central coronary artery pressures. Nitroglycerine significantly decreased coronary venous resistance. It is concluded that coronary venous resistance may be an important resistive component to consider when the total coronary circulation is studied.     

Regional vascular influences on tail-cuff measurements of drug-induced changes in systolic pressure.

When drug effects are quantified using the tail-cuff method, changes in systemic arterial pressure are extrapolated from those occurring in the caudal artery. The validity of this extrapolation was tested in anesthetized rats by recording drug-induced changes in phasic arterial pressure simultaneously from catheters inserted into the lower abdominal aorta, carotid, and caudal arteries. Pressor responses to norepinephrine or angiotensin were of equal magnitude at all three sites, but phentolamine reduced systolic pressure in the aorta or caudal artery more than that in the carotid artery. Unlike previous discrepancies between carotid and tail-cuff systolic pressures, aortic hypotension caused by injections of phentolamine or pentolinium in awake normotensive or spontaneously hypertensive rats was accurately predicted by the tail-cuff method. Because drug-induced changes in diastolic pressure always varied much less than those in systolic pressure, should indirect measurement of diastolic pressure become technically feasible, it might be preferable for assessing drug effects on blood pressure.     

Roentgeno-endovascular dilation of aortic coarctation]

The potentialities of roentgeno-endovascular dilation (RED) of various types of coarctation and aortic stenoses were studied in 12 patients aged 9 to 27. RED was performed by two Grüntzig's catheters with balloons not less than 7 mm in diameter. The main criterion of RED efficacy was a gradient of systolic pressure which was on the decrease by 25-40 mm Hg after using one catheter, and by 40-70 mm Hg after using both catheters. The same method was applied to dilation of stenosis of the abdominal aorta. The proposed method is low invasive and most effective in patients with aortic segmentation of segmental type, and makes it possible to avoid in many cases surgical intervention.     

Lack of additional action of oxygen on pulmonary artery pressure at the peak of verapamil or captopril action in pulmonary hypertension secondary to mitral stenosis]

The aim of the study was to investigate whether oxygen causes a further decrease in pulmonary artery pressure after administration of calcium channel blocker-verapamil-or angiotensin converting enzyme inhibitor-captopril-in the secondary pulmonary hypertension. We studied 37 patients with the secondary pulmonary hypertension (mean pulmonary artery systolic pressure = 56.1 mm Hg) due to mitral stenosis. After having completed hemodynamic diagnostic procedures, basal oxygen test was performed and pulmonary artery pressure was recorded at 10 min of oxygen breathing. Then, 10 mg of verapamil was injected into the pulmonary artery of 16 patients and 21 patients received 75 mg of oral captopril. At the peak of vasodilation, 30 min after verapamil and 90 min after captopril administration, pulmonary artery pressure was recorded and oxygen test was repeated. Baseline oxygen test produced a statistically significant decrease in pulmonary artery pressure. Verapamil and captopril also lowered pulmonary artery systolic and diastolic pressures. The second oxygen test did not cause a further decrease in the pulmonary artery pressure; mean pulmonary artery systolic pressure was 52.3 +/- 23.7 mm Hg, pulmonary artery diastolic pressure 22.7 +/- 10.6 mm Hg before and 49.1 +/- 23.8 mm Hg and 23.0 +/- 13.5 mm Hg, respectively after the test in verapamil group, and 47.0 +/- 15.5 mm Hg and 21.7 +/- 8.4 mm Hg before and 46.6 +/- 15.4 mm Hg, respectively in captopril subset. The results may support the thesis that vasodilating effect depends rather on the degree of pulmonary vascular changes than on the vasodilatory mechanism of particular drugs.     

Morphological changes of the anterior spinal artery during aortic cross-clamping and effect of prostaglandin E1 with perfusion

This investigation was designed to evaluate the morphological changes of anterior spinal artery (ASA) and its reaction to prostaglandinE1 (PGE1) during aortic cross-clamping. ASA during 30 min cross-clamping was observed with charge-coupled device (CCD) and ASA diameter (ASAD) was measured. Group A: Infrarenal aorta was cross-clamped. Group B: Infrarenal aorta was cross-clamped and aorta above the bifurcation was snared. The aortic segment between clamp and snare was perfused with blood. Group C: PGE1 of 100 ng/kg/min was added to perfusate of Group B. The aortic segmental pressures in group B and C were about 30% of the proximal systolic arterial pressure and were significantly higher than distal pressure of group A. After cross-clamping, ASAD decreased about 80% of before cross-clamping in group A. By segmental perfusion of which pressure was about 30% of proximal systolic arterial pressure, ASAD remained almost 90% in group B. By administration of PGE1, ASAD was significantly increased in group C. The changes of ASAD were significantly different between group A and C, and between group B and C.     

Canine coronary venous pressures: responses to positive inotropism and vasodilation

The epicardial coronary venous pressure in 16 dogs was compared with coronary arterial pressure as well as aortic, intraventricular, and intramyocardial pressures. Partial aortic occlusion augmented intraventricular (IVP), intramyocardial (IMP), aortic (AP), and coronary arterial pressures. Peripheral coronary venous pressure was also elevated. Dobutamine significantly augmented IVP and IMP but not aortic or central coronary artery pressures; this agent significantly elevated coronary venous systolic pressure (28/8 to 84/12 mmHg) (1 mmHg = 133.322 Pa). Nitroglycerine decreased IVP, IMP, and AP significantly. Central coronary arterial pressure also fell significantly, but coronary venous pressures remained unchanged. In contrast dipyridamole resulted in no change in IVP, IMP, AP, or coronary arterial systolic pressures; however, the peripheral coronary venous systolic pressure became significantly elevated. Thus the two vasodilators, nitroglycerine and dipyridamole, had different effects upon coronary venous pressure. These data reinforce the recently expressed view that coronary veins behave in a complex fashion and further suggest that their pressures are dependent upon coronary artery pressure, intramyocardial pressure, and coronary venous tone.     

Blood pressure: distribution in students of junior and senior high schools in Saint John,NB.

Blood pressures were recorded for 8950 students (82.4% of the total student population) of the junior high and high schools of Saint John, NB. Among the boys the mean systolic pressure rose from 104 mm Hg at age 12 to 117 mm Hg at age 18; among the girls the rise was from 105 to 110 mm Hg. The mean diastolic pressure also rose, from 61 to 67 mm Hg, in both sexes. These data are similar to those found in epidemiologic studies in Montreal and Bogalusa, Louisiana. However, the mean systolic values are lower by 10 mm Hg than those in an Edmonton study and the norms published by a United States task force. Recording methods could explain some of the observed differences, but population differences may also contribute. The discrepancies suggest that the current standards for children and adolescents need to be reassessed.     

The effects of changes in heart rate and aortic systolic pressure on left ventricular myocardial oxygen consumption in lambs

To determine whether changes in heart rate and aortic systolic pressure contribute equally to the determination of left ventricular myocardial oxygen consumption, we independently varied heart rate and pressure and compared the resultant oxygen consumption for similar rate-pressure products. In 6 young lambs which underwent atrioventricular node ablation, we varied heart rate by ventricular pacing at 250 beats/min, 300 beats/min, and 120 beats/min while aortic pressure remained stable and varied aortic systolic pressure by infusion of phenylephrine (to 132 +/- 15 mm Hg and 155 +/- 14 mm Hg) and by infusion of sodium nitroprusside (to 79 +/- 6 mm Hg) while heart rate was maintained stable at 200 beats/min. The 3 levels of change in aortic systolic pressure were chosen so that the ratepressure product during the pressure changes matched the rate-pressure product during the heart rate changes. We found that left ventricular myocardial oxygen consumption was the same at all 3 levels of the rate-pressure product whether heart rate was changed and pressure remained stable or pressure was changed and heart rate remained stable. Also, the correlation between oxygen consumption and the rate-pressure product was similar for both heart rate and pressure changes. During nitroprusside infusion at a fixed heart rate, oxygen extraction was significantly lower than during pacing at a heart rate of 120 beats/min when the rate-pressure product was comparable because of the direct vasodilatory effects of nitroprusside. We conclude that heart rate and aortic systolic pressure contribute equally to left ventricular myocardial oxygen consumption at the same rate-pressure product, even though there may be differences in myocardial blood flow and oxygen extraction.     

Raised arterial pressure in parents of proteinuric insulin dependent diabetics.

Arterial pressure is raised early in the subset of insulin dependent diabetics at risk of later development of progressive renal failure, suggesting that liability to arterial hypertension may play a part in the aetiology of diabetic kidney disease. Evidence for a genetic basis was therefore sought by measuring the blood pressures of the 26 surviving parents of 17 insulin dependent diabetic patients with proteinuria and comparing them with those of the parents of 17 matched insulin dependent diabetic patients without proteinuria selected from the same cohort. Systolic and diastolic pressures were significantly higher in parents of the proteinuric (mean (SD) 161 (27)/94 (14) mm Hg) than in parents of the non-proteinuric patients (146 (21)/86 (11) mm Hg). The difference between the sample mean blood pressures was 15 mm Hg (95% confidence interval 3.3 to 26.7 mm Hg) for systolic pressure and 8 mm Hg (95% confidence interval 0.8 to 15.2 mm Hg) for diastolic pressure. These differences were independent of age, sex, and adiposity. There was a significant correlation between the mean arterial pressures in the proteinuric patients and the higher mean blood pressure in their parents. High blood pressure in non-diabetic parents may be a marker of susceptibility to clinical nephropathy in their insulin dependent diabetic offspring.     

Hemodynamic effects of pacing-induced tachycardia in valvular aortic stenosis.

The hemodynamic effects of tachycardia were studied in 13 patients with valvular aortic stenosis. Observations were made during sinus rhythm (average heart rate 80 beats/min) and two periods (P1 and P2) when atrial pacing increased the heart rate to 109 and 131 beats/min respectively. The cardiac index did not change, but the left ventricular stroke work index fell from 61.8 to 39.5 g X m/m2 (p less than 0.001) as the heart rate increased. The left ventricular end-diastolic pressure averaged 18 mm Hg during sinus rhythm and fell to about 11.5 mm Hg at P1 and P2 (p less than 0.001). The brachial arterial systolic pressure did not change during pacing, but the left ventricular systolic pressure fell from 208 mm Hg to 201 mm Hg during P1 (p less than 0.05) and 193 mm Hg during P2 (p less than 0.001). The mean systolic aortic valve gradient averaged 64 mm Hg during sinus rhythm and fell to 51 mm Hg during P2 (p less than 0.001), and the peak aortic valve gradient fell from 82 to 69 mm Hg during P2 (p less than 0.001). The left ventricular ejection time fraction increased from 26.9% during sinus rhythm to 31.9% during P1 (p less than 0.05) and 34.7% during P2 (p less than 0.005). Because of the prolonged left ventricular ejection time fraction and smaller stroke volume, a smaller pressure gradient developed across the stenosed valve at higher heart rates. The pacing test was of little value in assessing left ventricular function and thus is not useful during invasive investigations of valvular aortic stenosis.     

Comparison of the effect of simvastatin, spironolactone and L-arginine on endothelial function of aorta in hereditary hypertriglyceridemic rats

Hereditary hypertriglyceridemic (hHTG) rats are characterized by increased blood pressure and impaired endothelium-dependent relaxation of conduit arteries. The aim of this study was to investigate the effect of long-term (4 weeks) treatment of hHTG rats with three drugs which, according to their mechanism of action, may be able to modify the endothelial function: simvastatin (an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase), spironolactone (an antagonist of aldosterone receptors) and L-arginine (a precursor of nitric oxide formation). At the end of fourth week the systolic blood pressure in the control hHTG group was 148+/-2 mm Hg and in control normotensive Wistar group 117+/-3 mm Hg. L-arginine failed to reduce blood pressure, but simvastatin (118+/-1 mm Hg) and spironolactone (124+/-4 mm Hg) treatment significantly decreased the systolic blood pressure. In isolated phenylephrine-precontracted aortic rings from hHTG rats endothelium-dependent relaxation was diminished as compared to control Wistar rats. Of the three drugs used, only simvastatin improved acetylcholine-induced relaxation of the aorta. We conclude that both simvastatin and spironolactone reduced blood pressure but only simvastatin significantly improved endothelial dysfunction of aorta. Prominent increase in the expression of eNOS in large conduit arteries may be the pathophysiological mechanism underlying the protective effect of simvastatin in hHTG rats.     

Haemodynamics in the first seconds after coronary artery occlusion.

The changes in cardiac and in total haemodynamics, occurring during the first seconds of occlusion and the subsequent desocclusion of coronary arteries were studied on 28 dogs. The most intensive changes were observed after the trunk occlusion of the left coronary artery. Simultaneously with decreasing blood inflow into the myocardium its contractility and the systolic pressure in the left ventricle and the outflow from the coronary sinus began to fall rapidly. The systolic pressure in the left ventricle decreased within the first 10 s from 24 to 13-15 kPa (180 to 100-110 mm Hg), which means that the systolic pressure fell about 1 kPa (7-8 mm Hg) per second, or 0.5-0.6 kPa (4-5 mm Hg) per systole. At the same time the end-diastolic pressure in the left ventricle also increased from zero to 3-4 kPa (25-30 mm Hg). After the trunk desocclusion of the left coronary artery the systolic pressure in the left ventricle proceeded to fall by about 2-3 kPa (15-22 mm Hg). Only then, 20-25 s after the desocclusion, blood flow in the left coronary artery began to rise intensively and 4-6 s later the myocardial contractility and the systolic pressure in the left ventricle also increased. After unclamping (50-60 s), there was an overshoot of haemodynamic values above preocclusive values and then followed the compensatory phase. This phase lasted 80-90 s and on its peak the pressure and flow parameters increased by about 50-60% above preocclusive values. During the occlusion of ramus interventricularis anterior or ramus circumflexus for 30-60 s the haemodynamic parameters changed only slightly. The same was observed during trunk occlusion of the right coronary artery (30-60 s), but in that case many extrasystoles occurred.     

Wave reflection augments central systolic and pulse pressures during facial cooling

Cardiovascular events are more common in the winter months, possibly because of hemodynamic alterations in response to cold exposure. The purpose of this study was to determine the effect of acute facial cooling on central aortic pressure, arterial stiffness, and wave reflection. Twelve healthy subjects (age 23 +/- 3 yr; 6 men, 6 women) underwent supine measurements of carotid-femoral pulse wave velocity (PWV), brachial artery blood pressure, and central aortic pressure (via the synthesis of a central aortic pressure waveform by radial artery applanation tonometry and generalized transfer function) during a control trial (supine rest) and a facial cooling trial (0 degrees C gel pack). Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Measurements were made at baseline, 2 min, and 7 min during each trial. Facial cooling increased (P < 0.05) peripheral and central diastolic and systolic pressures. Central systolic pressure increased more than peripheral systolic pressure (22 +/- 3 vs. 15 +/- 2 mmHg; P < 0.05), resulting in decreased pulse pressure amplification ratio. Facial cooling resulted in a robust increase in AI and a modest increase in PWV (AI: -1.4 +/- 3.8 vs. 21.2 +/- 3.0 and 19.9 +/- 3.6%; PWV: 5.6 +/- 0.2 vs. 6.5 +/- 0.3 and 6.2 +/- 0.2 m/s; P < 0.05). Change in mean arterial pressure but not PWV predicted the change in AI, suggesting that facial cooling may increase AI independent of aortic PWV. Facial cooling and the resulting peripheral vasoconstriction are associated with an increase in wave reflection and augmentation of central systolic pressure, potentially explaining ischemia and cardiovascular events in the cold.     

Pulmonary circulation and right ventricular function in primary arterial hypertension]

Selected parameters of the pulmonary circulation and right ventricular performance were studied in 30 patients with primary arterial hypertension. Four patients belonged to the WHO class I, four to class I/II, 18 to class II and the remaining four to class III. Patients were eligible, if they were in sinus rhythm, without symptoms of left ventricular failure and diseases that night influence pulmonary pressures, and if drugs affecting cardiac performance could be withdrawn safely for 3 days. Ten healthy subjects served as control group. The mean pulmonary capillary wedge pressure and mean pulmonary artery pressure were similar in both groups. In contrast, the systolic pulmonary arterial pressure exceeded 30 mm Hg in 6 patients. Mean pulmonary vascular resistance was higher in examined patients than in the control group. Right ventricular end-diastolic pressure was above 5 mm Hg in as much as 50% of patients. Mean systolic ejection rate showed a tendency to decrease. The results indicate that part of patients with primary arterial hypertension exhibits disorders in the pulmonary circulation and right ventricular performance.     

Screen detected high blood pressure under 40: a general practice population followed up for 21 years.

OBJECTIVE--To assess hypertension detected under 40 in a general practice population. DESIGN--Prospective case-control study. SETTING AND SUBJECTS--Former coal mining community in south Wales. Systematic case finding for hypertension and associated risk factors applied to a mean total population of 1945 from age 20 on a five year cycle through 21 years. Mean population aged 20-39, 227 men and 213 women. Case criteria: age < 40 and mean systolic pressure > or = 160 mm Hg or diastolic pressure > or = 100 mm Hg. Age and sex matched controls randomly sampled from the same population. MAIN OUTCOME MEASURES--Mean initial pressures and pressures at follow up in 1989 or preceding death, and all cardiovascular events. RESULTS--25 men and 16 women met criteria. Estimated five yearly inceptions were 26/1000 for men and 18/1000 for women. Male group mean initial blood pressure was 164/110 mm Hg for cases, falling to 148/89 mm Hg at follow up. Five male cases died at mean age 47.8, compared with two controls at 49.5. Female group mean initial pressure was 172/107 mm Hg for cases, falling to 145/86 mm Hg at follow up. One female case died aged 50, no controls. 10 male cases had non-fatal cardiovascular events at mean age 40.2, compared with two controls at mean age 50.5. Four female cases had non-fatal events at mean age 47.2, compared with one control aged 58. Male differences were statistically significant. CONCLUSIONS--Hypertension under 40 is dangerous, commoner in men than women, rarely secondary to classic causes, and may be controlled in general practice on a whole community basis.     

Evaluation of blood pressure changes and heart rate in young health men based on results of a 24-hour monitoring of pressure]

Systolic and diastolic blood pressures and heart rate were monitored in a group of 20 young healthy men for 24 hours. Period of time between 8 o'clock a.m. and 10 o'clock p.m. was treated as waking state whereas period of time from 12 p.m. to 6 a.m. as sleep phase. Mean value of systolic blood pressure for waking state was 124.6 +/- 7.6 mm Hg, and for sleep phase 110.4 +/- 11.5 mm Hg. (p < .001). Mean diastolic blood pressures were also significantly different (76.5 +/- 5.9 mm Hg and 63.8 +/- 7.7 mm Hg, respectively), the same concerns heart rate (79.6 +/- 6.4 and 63.0-7.2 min-1, respectively). In both cases p < .001. To evaluate dependence of heart rate on systolic blood pressure in waking state the following calculation was made: HR = 0.230 x systolic blood pressure +51.4 (r = 0.24; p < .001) whereas for sleep phase r did not reach a level of statistical significance (HR = 0.074 x systolic blood pressure + 53.9; r = 0.094). Single or even multiple measurements of the arterial blood pressure are not sufficient to evaluate circadian changes.     

Blood pressure and five year survival in the very old

During 1977-8 we measured blood pressure in 561 old people (83% of those aged 85 or more living in Tampere) and analysed their five year survival according to their blood pressure group. The subjects were divided into six groups on the basis of their blood pressures (from <120 to >200 mm Hg systolic, from <70 to >110 diastolic). The greatest mortality was observed in those in the lowest systolic and lowest diastolic groups. Mortality was least in subjects with systolic pressures of 160 mm Hg or more and diastolic pressures of 90 mm Hg or more.The most essential finding in this series of the very old was an increased mortality in the lowest blood pressure groups.     

Acute effects of cold exposure on central aortic wave reflection.

The purpose of this study was to determine the effects of acute cold exposure on the timing and amplitude of central aortic wave reflection and central pressure. We hypothesized that cold exposure would result in an early return of reflected pressure waves from the periphery and an increase in central aortic systolic pressure as a result of cold-induced vasoconstriction. Twelve apparently healthy men (age 27.8 +/- 2.0 yr) were studied at random, in either temperate (24 degrees C) or cold (4 degrees C) conditions. Measurements of brachial artery blood pressure and the synthesis of a central aortic pressure waveform (by noninvasive radial artery applanation tonometry and use of a generalized transfer) were conducted at baseline and after 30 min in each condition. Central aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Cold induced an increase (P < 0.05) in AI from 3.4 +/- 1.9 to 19.4 +/- 1.8%. Cold increased (P < 0.05) both brachial and central systolic pressure; however, the magnitude of change in central systolic pressure was greater (P < 0.05) than brachial (13 vs. 2.5%). These results demonstrate that cold exposure and the resulting peripheral vasoconstriction increase wave reflection and central systolic pressure. Additionally, alterations in central pressure during cold exposure were not evident from measures of brachial blood pressure.