Rise In Mean Arterial Blood Pressure Research Articles

Autoregulation of retinal arterioles in patients with diabetes mellitus and normal probands

Measurement of myogenic autoregulation of retinal arterioles was demonstrated by the use of the Retinal-Vessel-Analyzer (Carl Zeiss, Jena). The purpose of the presented study was to find a significant difference of this myogenic response in a group of healthy individuals vs. a group of patients with pathologic conditions. As a group of patients with known pathology in microcirculation patients with type 1 diabetes were chosen. By isometric exercise an identical rise in mean arterial blood-pressure was provoked in 20 patients with type-1 diabetes and 20 matched healthy volunteers. The myogenic response of retinal arterioles was measured in both groups by the use of the Retinal-Vessel-Analyzer. The Wilcoxon test was used for statistical analysis within the two groups whereas both groups were compared with each other by the use of the Mann-Whitney test. Having the same age and same blood-pressure rise (p = 0.624) a significant better myogenic response was found in the healthy subjects vs. the diabetic group (p = 0.008). In the diabetic group no correlation was found between myogenic response and duration of diabetes (p = 0.982) or HbA1c values (p = 0.83). In this study significant loss of autoregulation in patients with type 1 diabetes is demonstrated. By the use of the Retinal-Vessel-Analyzer noninvasive testing of the function of autoregulation of retinal arterioles is possible. This method might prove to be of great value in early detection of diabetic vessel pathology.

Systemic adenosine increase during cold pressor test is dependent on sympathetic activation.

1. Following local vasoconstriction-inducing stimuli, such as the cold pressor test (CPT), significant changes occur in haemodynamics, with a rise in arterial blood pressure and heart rate (HR) due to the activation of the sympathetic nervous system. Among the compensatory mechanisms to local ischaemia, the endogenous nucleoside adenosine (ADO) has been suggested to play a relevant role by contributing to sympathetic stimulation. The possibility was investigated that CPT-induced increases in plasma ADO levels were not only an expression of the increased production of ADO in the ischaemic area, but also a consequence of systemic sympathoexcitatory mechanisms, thus showing a bidirectional involvement of the mechanisms of ADO formation. 2. The CPT was performed in 15 volunteers and mean arterial blood pressure (MABP) and HR were evaluated, together with plasma levels of noradrenaline (NA) and ADO in the tested and contralateral arm. The 15 subjects were then divided into three groups of five that were treated with either 5 mg transdermal clonidine weekly, 100 mg atenolol daily or 600 mg aminophylline twice daily. After 1 week treatment, the same test was repeated in the respective groups. 3. The CPT induced a rise in MABP and HR and an increase in plasma levels of NA and ADO. Increases in ADO were more pronounced in the tested arm. Clonidine blunted the haemodynamic response and NA release, while increases in ADO increase were reduced to a greater extent in the contralateral arm rather than the tested arm. Atenolol only affected MABP and HR without any effect on NA and ADO levels. Theophylline did not show any effect on CPT-induced changes. 4. In conclusion, local vasoconstriction and ischaemia induced in one arm following CPT are associated with haemodynamic changes dependent on the activation of the sympathetic system. The observed increase in plasma levels of ADO seems to be, in part, a direct expression of local responses to ischaemia (pre-dominant in the tested arm), but also appears as the consequence of systemic sympathoexcitatory mechanisms. Such increases in ADO are not dependent on a beta 1-adrenoceptor-mediated mechanism. Finally, theophylline, at a therapeutic dose, has no effect on the response to CPT.

The role of heart rate in the modulation of the decreased cardiac output induced by acute nitric oxide synthesis inhibition in anaesthetized dogs.

1. The role of the heart rate modulating the decrease in cardiac output induced by the nitric oxide synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was investigated in anaesthetized dogs. This was achieved in dogs in which a positive pacemaker (PM) cable was located at the right ventricle. 2. The haemodynamic events were evaluated: mean arterial blood pressure (MABP), systemic vascular resistance index (SVRI), stroke volume index (SVI), heart rate (HR) and cardiac index (CI). 3. The infusion of L-NAME (0.01-10 mg kg(-1)) in the animals with the PM off caused a dose-dependent rise in MABP and SVRI, accompanied by significant decreases of HR and SVI. A resulting decrease in CI was observed at all doses of L-NAME used. 4. In the animals with the PM on, HR was maintained stable. Under this condition, the increase in MABP and SVRI as well as the decrease in SVI induced by the L-NAME infusion did not significantly differ from the PM-off animals. However, the resulting decreased CI was markedly attenuated compared to PM-off animals but significant decreases in CI were still observed at higher doses of L-NAME. 5. The results suggest that HR plays an important role in the L-NAME-mediated decreased cardiac output but other factors might also be involved.

Role of dorsal vagal motor nucleus in angiotensin II-mediated tachycardia in the conscious trout Oncorhynchus mykiss

Responses of heart rate (HR) and mean arterial blood pressure (MABP) were examined following microinjection of angiotensin II ([Asn 1,Val 5]AII) within the dorsal vagal motor nucleus (DVN) of the conscious trout's brainstem. AII (15–125 fmol) preferentially and significantly increased HR in a dose-dependent manner, but the rise in MABP was not dose-dependent and was only significant ( P<0.05) after injection of AII at a dose of 62.5 fmol. The cardiovascular action of AII was site-specific, since administrations of the peptide at a dose of 62.5 fmol, but outside the boundaries of the DVN, were devoid of any effect on HR or MABP. All the responses to DVN injections of AII were totally prevented by DVN injection of 1 nmol of losartan, a mammalian non-peptide AII subtype 1 (AT 1) receptor antagonist. The ability of DVN injection of AII to induce a tachycardic response was negatively correlated to HR basal values. In conclusion, these results indicate that, at femtomolar doses, AII exerts a central neurocardioregulatory role, involving a localized receptor closely related to the mammalian AT 1 receptor subtype within the DVN of the trout.

Effect of methylguanidine on rat blood pressure: role of endothelial nitric oxide synthase

1. The effect of acute i.v. administration of methylguanidine (MG) on mean arterial blood pressure (MABP) was investigated in anaesthetized male Wistar rats. 2. MG (1-30 mg kg-1 i.v.) produced an increase in MABP in a dose-dependent manner both in normal and in hexamethonium (5 mg kg-1, i.v)-treated rats. 3. L-Arginine (30 or 150 mg kg-1, i.v.), but not its enantiomer D-arginine (30 or 150 mg kg-1, i.v.), reversed the effect of MG on MABP in both normal and hexamethonium-treated rats. 4. L-Arginine (150 mg kg-1, i.v.) administered 2 min before MG (30 mg kg-1, i.v.) prevented the increase in MABP caused by MG in either normal or hexamethonium-treated rats. This effect was not observed with D-arginine (150 mg kg-1, i.v.). 5. Thus, the rise in MABP caused by MG in the anaesthetized rat is due to inhibition of endothelial NO-synthase activity. We speculate that the rise in the plasma concentration of endogenous MG associated with uraemia may contribute to the hypertension seen in patients with chronic renal failure.

Simultaneous influence of blood pressure, PCO2, and PO2 on cerebral blood flow velocity in preterm infants of less than 33 weeks' gestation.

In extremely preterm infants, the protective capacity for cerebral blood flow (CBF) autoregulation may be impaired or absent, which increases the risk for developing cerebral lesions. The purpose of this study was to quantify the simultaneous influence of several vital parameters, such as mean arterial blood pressure (MABP), PCO2, and PO2, on cerebral blood flow velocity (CBFv), which is used as a measure for CBF. In 16 mechanically ventilated infants of < 33 wk gestation, the CBFv in the internal carotid artery was measured every minute for 1 h by a computer-controlled pulsed Doppler device. MABP and transcutaneous PCO2 and PO2 were recorded as well. A multiple linear regression analysis was performed in each patient to determine the individual MABP, PCO2, and PO2 reactivities as a measure for CBF autoregulation. The medians (and ranges) of the whole group were an MABP reactivity of 7.5% (-12.5 to 20.1%) rise in CBFv/1 kPa rise in MABP, a PCO2 reactivity of 32.7% (-8.1 to 79.5%) rise in CBFv/1 kPa rise in PCO2, and a PO2 reactivity of -3.1% (-14.2 to 7.9%) fall in CBFv/1 kPa rise in PO2. In preterm infants, the individual's capacity for MABP-, PCO2-, and PO2-dependent CBF autoregulation can be estimated by means of the present method, even if the vital parameters change simultaneously.

Increased sensitivity to pressor hormones in central diabetes insipidus.

Pressor sensitivities to infusions of arginine vasopressin (AVP), noradrenaline (NA) and angiotensin II (AII), as well as cardiovascular responses to head-up tilt, were assessed in subjects with central diabetes insipidus (CDI) and compared with those in normal control subjects. During incremental i.v. infusions of AVP at 0.2-5.0 pmol min-1 kg-1, mean arterial blood pressure (MABP) rose progressively in CDI subjects only and the rise was significantly greater than that which occurred in control subjects during their final infusion. The pressor effects of incremental i.v. infusions of NA and AII were greater, and the bradycardia associated with NA was more pronounced, in CDI subjects than in controls. Whole body tilt from supine to 45 degrees head-up was associated with increased heart rate and an insignificant rise in MABP in both groups, although a rise in plasma AVP occurred in control subjects only. These results demonstrate that subjects with CDI are more sensitive than control subjects to the pressor effects of NA and AII, and also develop sensitivity to the pressor effects of AVP. Their cardiovascular responses to head-up tilt remain intact. Presumably the increased vascular sensitivity to NA and AII in subjects with CDI is sufficient to compensate for their lack of AVP response during head-up tilt.

Dissociation of 24-hour catecholamine levels from blood pressure in older men.

Increased plasma norepinephrine levels have been observed in some persons with early essential hypertension. Although both plasma norepinephrine level and mean arterial blood pressure rise with age, little is known about the state of catecholamine secretion in elderly patients with essential hypertension. We studied the 24-hour cycle levels of plasma norepinephrine, epinephrine, and dopamine in 12 elderly hypertensive subjects and 13 age-matched normotensive controls (mean ages, 63.8 +/- 1.2 yr and 64.8 +/- 1.8 yr [SEM] respectively). Blood samples were obtained at bihourly intervals from 0900 to 2100 hours and every 30 minutes from 2100 to 0900 hours, during which time sleep and breathing were continuously monitored. A circadian rhythm was displayed in both groups by plasma epinephrine levels (mesor, 49 +/- 2 pg/ml and 38 +/- 1 pg/ml; amplitude, 15 +/- 2 pg/ml and 11 +/- 1 pg/ml; acrophase, 12.20 +/- 0.40 hr and 14.41 +/- 0.34 hr in the normotensive and hypertensive groups respectively) but not by plasma norepinephrine or dopamine levels. During the 24-hour cycle plasma epinephrine, but not norepinephrine or dopamine, levels were positively related to mean arterial blood pressure (r = 0.60 for the normotensive subjects, r = 0.57 for the hypertensive subjects, p less than 0.01 for both).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac substances that influence blood-pressure II. Potent pressor activity in rat and rabbit atrial muscle

In addition to their natriuretic, diuretic and vasodilator activities, freshly prepared aqueous extracts of either rat or rabbit atrial myocardium were shown to elicit significant increases in the blood-pressure of anaesthetized rats. Small aliquots (0.05 mℓ) intravenously administered caused a transient rise in mean arterial blood-pressure of up to 20%. Slow infusion of 0.4 mℓ right atrial extract (corresponding to about one half of a rabbit right atrial lobe) during 90 seconds caused the expected natriuresis and diuresis, together with a sustained elevation in arterial blood-pressure ( ca 25%) that returned to normal within 3 minutes. This potent pressor activity could not be detected in ventricular extracts. It was furthermore readily separable from the natriuretic peptides and catecholamines by ultrafiltration. The atrial pressor factor is a small proteolytically unstable molecule (300 – 1000 dalton).

1500 REGULATION OF CEREBRAL BLOOD FLOW VELOCITY (CBFV) IN LOW BIRTH WEIGHT (LBW) INFANTS WITH HYALINE MEMBRANE DISEASE (HMD)

In adults arterial oxygen content (CaO2) and pCO2 are the major regulators of cerebral blood flow (CBF) while CBF is constant in the face of changes in mean arterial blood pressure (MABP). In this study Doppler ultrasonography was used to examine the effects of these factors on CBFV in non-asphyxiated LBW infants with HMD requiring mechanical ventilation. Infants were studied on days 1-7, 14 and 21. CBFV was measured in the anterior cerebral artery for determination of the Area Under the Velocity Curve (AUTC)/min. Blood flow velocity was measured in the carotid artery and Diastolic/Systolic ratio (D/S) determined. Hematocrit (HCT), blood gases, MABP and LA/AO ratio (echocardiogram) were measured. CaO2 was calculated from the hemoglobin dissociation curve. No infant had evidence of ductal shunting on the basis of a normal LA/AO ratio, absence of a murmur, normal pulses and a normal D/S ratio (+.32±.09) (m±sd). Data analysis (n=61) revealed a significant inverse relationship between CaO2 and AUTC/min (r=.46) (p<.01). A strong linear correlation was found between pCO2 and AUTC (r=.40) (p<.01). Despite a rise in MABP associated with postnatal age (r=.57), AUTC/min was constant over the observed range of MABP (29-67 mmHg). We conclude that autoregulation of CBF is present in non-asphyxiated LBW infants with HMD and that their CBF is not pressure-passive as previously suggested.

1356 THE EFFECT OF PHENOBARBITAL (PB) ON CEREBRAL BLOOD FLOW VELOCITY (CBFV) FOLLOWING ENDOTRACHEAL UZ3U SUCTION (ETS)

ETS produces a transient fall in PaO2 and a rise in mean arterial blood pressure (MABP). PB may decrease the neonatal response of CBFV as a result of ETS. 7 infants, mean birthweight 819g and mean gestational age of 27 wks, were studied in the first 20 hrs of life. Area under the velocity curve (AVC), peak systolic velocity (PSV), and end diastolic velocity (EDV) were measured with a doppler velocimeter before (C) and after (S) ETS at 3 time periods: prior to PB (baseline: 0), 2 hrs after and 4 hrs after an i.v. dose of 20 mg PB/kg. Heart rate, mean arterial blood pressure (MABP) and transcutaneous PO2(Tc PO2) were measured simultaneously with the doppler determinations. There were no changes at any time with PSV (values: 7.4 cm/sec) and EDV (values: 2.1 cm/sec). As shown above, ETS produced a significant rise in MABP and a fall in TcPO2. Four hours following PB treatment, the percent change in ΔAVC associated with ETS was reduced. We speculate that PB may modulate the response of ΔAVC to ETS.

Effect of induced hypertension on experimentally-induced cerebral arterial spasm.

Ten adult cats were anesthetized and ventilated by respirator. After the basilar artery was exposed transclivally and visualized with an operative microscope, mean arterial blood pressure (MABP) was raised gradually by intravenous drip infusion of norepinephrine (5-20 micrograms/kg) or angiotensin-II-amide (0.3-1.0 micrograms/kg). At various blood pressures, microphotographs were taken. There was no appreciable change in vessel diameter at a MABP ranging from 78 to 191 mmHg. The blood pressure was allowed to return to the initial baseline level. Arterial spasm was produced by the topical application of 0.2 M calcium gluconate, which decreased the arterial diameter by 13 to 58 percent for more than 60 min. Blood pressure was increased again after the production of the arterial spasm. Significant increases in the diameter of the arteries were produced by the drug-induced hypertension at levels of MABP ranging from 82 to 192 mmHg. The maximum arterial dilations ranged from 123 to 208 percent of the untreated control. The degree of dilation of the arteries almost paralleled the rise in MABP. Norepinephrine and angiotensin-II had a similar effect on both the blood pressure and the arterial diameter. Induced hypertension would be expected to improve blood flow parameters in the case of spastic cerebral arteries.

The effect of halothane anaesthesia on the asphyxiated foetal lamb in utero.

In a previous study, we examined the effects of halothane on the normal foetal lamb in utero. The most significant finding was a 33 per cent fall in foetal mean arterial blood pressure (MABP). Cardiac output and placental blood flow were not affected. To determine if the asphyxiated foetus would respond similarly, the following study was performed. Seven pregnant ewes were surgically prepared two days prior to study with maternal and foetal indwelling arterial and venous cannulas. An inflatable occlusion loop was secured around the umbilical cord. On the day of study, a tracheostomy was performed on each ewe. Microspheres were injected into the foetal circulation during the control period. The occlusion loop was inflated to produce foetal asphyxia and microspheres were again injected. The ewe was then anesthetized with halothane; and after 15 minutes, microspheres were injected into the asphyxiated foetus and halothane levels were measured. The asphyxiated foetuses showed a significant rise in MABP, fall in heart rate and fall in cardiac output from control. Blood flow to the brain was significantly increased and flow to the placenta and gut decreased. Exposure of the asphyxiated foetus to halothane resulted in a fall of MABP to control but no significant change in cardiac output or brain blood flow. The mean halothane level in the foetus was 46.0 mg X l-1 or 0.32 vol%. Exposure of the asphyxiated foetus to halothane for 15 minutes does not produce significant further deterioration of the foetal lamb in utero.

A Computerized System for Continuous Physiologic Data Collection and Analysis: Initial Report on Mean Arterial Blood Pressure in Very Low-Birth-Weight Infants

A system for continuous measurement and analysis of mean arterial blood pressure (MABP) by microcomputer is presented. The system allows prolonged recording and maintenance of fine detail by sequential evaluation and storage of up to 3,600 data points per hour. Fifteen preterm appropriate-for-gestational-age (AGA) infants weighing less than or equal to 1,500 g (very low birth weight) who were free of pulmonary and neurologic disease were monitored continuously from birth to 5 days of age. MABP was recorded via an umbilical arterial catheter with a pressure transducer and module interfaced with the microcomputer. Software was developed to analyze this stored data rapidly. MABP was found to correlate significantly with gestational age from 3 to 15 hours of age (P less than .05). Significant correlation was rare after 20 hours of age. MABP increased as a function of postnatal age in 11 infants. This increase was greater (0.31 to 0.54 mm Hg/h) for the least mature infants (27 to 29 weeks of gestation). The increase for the most mature infants (31 to 32 weeks of gestation) was low (0 to 0.24 mm Hg/h), and in three infants a small negative slope was seen. The steep rise in MABP during the first 40 hours of life in the least mature infants may be due to the perfusion requirements of extrauterine life. These pressures may be at or near the threshold for rupture of immature vascular beds such as are found in the subependymal germinal matrix and thus predispose to intraventricular hemorrhage.

Inhibition of adrenaline-forming enzyme in the brain prevents one-kidney, one-clip hypertension and deoxycorticosterone acetate-salt hypertension in the rabbit.

1. Phenylethanolamine N-methyltransferase (PNMT) converts noradrenaline into adrenaline and brain PNMT is elevated in spontaneously hypertensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In view of the evidence for the involvement of central adrenergic neurons in renal hypertension, we measured the blood pressure response in one-clip, one-kidney Goldblatt hypertensive and DOCA-salt hypertensive rabbits to the PNMT inhibitor SK&F 64139, injected into the lateral cerebral ventricles. 2. Intracerebroventricular injection of SK&F 64139 (10 micrograms/kg) significantly attenuated the mean arterial blood pressure rise in one-clip, one-kidney and DOCA-salt rabbits, at 4 and 8 weeks. 3. These findings support the idea the hypertension in this animal model required an intact adrenaline biosynthetic process, and that central catecholaminergic neurons may be involved in the pathogenesis of low-renin dependent forms of hypertension.

Blood pressure changes and oral contraceptive use: a study of 2676 black women in the southeastern United States.

Blood pressure (BP) and weight were measured on 2676 black women attending a large southeastern family planning clinic. Repeat measurements were made after a minimum of six and upt to 24 months on 673 women who continuously used nonhormonal contraceptive (OC) therapy, and 1390 women who continuously used OCs. The mean change in systolic blood pressure (SBP) adjusted for initial BP and change in per cent ideal body weight is +1.44 mmHg in the new users of OC. This slight increase in SBP is statistically significant (p = 0.04) relative to the +0.41 mmHg increase observed in the control group. However, the adjusted diastolic blood pressure (DBP) change (+0.46 mmHg in new OC users and +1.54 mmHg in the control group) fails to support the hypothesis of a greater increase in DBP in new OC users. The adjusted mean rise in mean arterial BP does not differ significantly between new OC users and the control group. The proportion of women developing a DBP greater than or equal to 90 mmHg during the average follow-up interval of one year is 2.4% in the control group, 1.0% in the new OC users and 0.2% in the continued OC users. These results provide evidence that OC use has no significant effect on the level of mean arterial BP in black women followed for 6-24 months; and fail to support the hypothesis of a causal relationship between OC use and elevated BP in black women.