Maximum Mean Arterial Pressure Research Articles

Intramuscularly Administered Dexmedetomidine Attenuates Hemodynamic and Stress Hormone Responses to Gynecologic Laparoscopy

The hemodynamic and endocrine effects of three different doses of dexmedetomidine (0.6, 1.2, and 2.4 micrograms/kg), oxycodone (0.13 mg/kg), and saline solution, injected intramuscularly 45-60 min before induction of general anesthesia, were compared in a double-blind, randomized study involving 100 women undergoing gynecologic diagnostic laparoscopy. Anesthesia was induced with thiopental (4.5 mg/kg) and maintained with 0.3% end-tidal isoflurane and 70% nitrous oxide in oxygen. Arterial blood pressure and heart rate increased after endotracheal intubation and during laparoscopy in all groups, but the maximal mean arterial pressure after tracheal intubation was lower in the dexmedetomidine 2.4-micrograms/kg group (104 mm Hg [SD 19]) than in the saline solution group (130 mm Hg [SD 12]). Dexmedetomidine (2.4 and 1.2 micrograms/kg) attenuated the maximal heart rate after intubation (84 [SD 11] and 101 beats/min [SD 15], respectively) compared with saline solution (116 beats/min [SD 19]). On the other hand, 40% of the patients in the dexmedetomidine 2.4-micrograms/kg group received atropine in the postanesthesia care unit for bradycardia (heart rate < or = 40 beats/min). Preoperative anxiety and sedation before and after preanesthetic medication were evaluated by the patients with the aid of a profile of mood-state questionnaire; only dexmedetomidine 2.4 micrograms/kg produced significant anxiolysis and sedation. Plasma concentrations of norepinephrine, epinephrine, 3,4-dihydroxyphenylglycol, cortisol, and beta-endorphin increased less in the dexmedetomidine 2.4-micrograms/kg group in response to tracheal intubation and surgery than in the saline solution group.

Cardiovascular reactivity and plasma prolactin response to mental stress in normals and hypertensives.

Central dopaminergic activity (CDA) may be involved in blood pressure control as a negative modulator of sympathetic outflow. In this study the plasma PRL changes produced by mental stress (a colour-word conflict test, CWT) were investigated in normals (NT, n.15) and stable hypertensives (HT, n.16) and the PRL response, as a possible index of CDA was correlated to the cardiovascular and the plasma renin activity (PRA) responses as indexes of peripheral sympathetic outflow. A significant (p less than 0.05) slight decrease in mean values of PRL was observed in normals after the CWT but no change was found in hypertensives. No correlation was found between the PRL responses to CWT and the maximal mean arterial pressure changes or the PRA changes whether the groups were considered separately or together. These findings indicates that PRL does not appear to be a reliable index of the CDA involved in blood pressure control.

Blood pressure in the midtrimester and future eclampsia

The purpose of this report was to investigate the potential usefulness of average mean arterial pressure, maximal mean arterial pressure, and maximal diastolic pressure during the second trimester in predicting the development of eclampsia in 207 nulliparas and 20 multiparas with eclampsia. In the nulliparas, both the mean arterial pressure and the maximal mean arterial pressure during the second trimester were greater than or equal to 90 mm Hg in 22% and 34% of the patients, respectively. For the multiparas, the percentages with greater than or equal to 90 mm Hg were 30% and 35%, respectively. Only 8.7% of nulliparas with eclampsia had a maximal diastolic pressure during the second trimester greater than or equal to 80 mm Hg and no patient had a diastolic pressure of greater than or equal to 90 mm Hg. A review of the literature suggests that the mean arterial pressure observed during the second trimester has poor predictive value for future development of preeclampsia-eclampsia. We conclude that there is no correlation between second-trimester blood pressure recordings and subsequent eclampsia.

Failure of plasma norepinephrine to consistently reflect sympathetic activity in humans.

To determine whether venous plasma norepinephrine concentrations consistently reflect changes in sympathetic nervous activity, the influence of mental arithmetic, static handgrip, and submaximal bicycle exercise on intra-arterial blood pressure, heart rate, and plasma norepinephrine was studied in 51 subjects with untreated essential hypertension (mean age, 46 years; range, 16-69 years). At rest, plasma norepinephrine was unrelated to age or blood pressure. Mental arithmetic increased mean arterial pressure from 108 +/- 18 to 127 +/- 18 mm Hg (mean +/- S.D.; p less than 0.001) and heart rate from 69 +/- 7 to 93 +/- 13 beats/min (p less than 0.001) but not plasma norepinephrine (547 +/- 297 to 518 +/- 250 pg/ml). Isometric exercise raised mean arterial pressure from 115 +/- 18 to 148 +/- 21 mm Hg (p less than 0.001) and heart rate from 76 +/- 9 to 95 +/- 13 beats/min (p less than 0.001) but not plasma norepinephrine (683 +/- 253 to 741 +/- 253 pg/ml). Bicycle exercise increased mean arterial pressure from 114 +/- 20 to 146 +/- 26 mm Hg (p less than 0.001), heart rate from 77 +/- 9 to 128 +/- 19 beats/min (p less than 0.001), and plasma norepinephrine from 645 +/- 228 to 1151 +/- 462 pg/ml (p less than 0.001). Both the maximum mean arterial pressure and the peak heart rate attained during bicycle exercise were related to the exercise plasma norepinephrine level (r = 0.33, p less than 0.02 and r = 0.28, p less than 0.03, respectively). Increases in plasma norepinephrine with exercise were not greater in older or more hypertensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

The relation between plasma urate and placental bed vascular adaptation to pregnancy

Placental bed biopsies were obtained at caesarean section from 34 women. Their plasma urate was directly related to maximum mean arterial pressure and inversely to adjusted birthweight; but it was related most closely to the histological appearances of the spiral arteries in the placental bed. Nine women had physiological changes in the spiral arteries: their mean urate (233, SD 28.9 mumol/l) was significantly (P less than 0.001) lower than the mean urate in those who did not have adequate physiological changes (339, SD 90.3 mumol/l) or that in the nine women who had atherosis (397, SD 153.2 mumol/l). Raised plasma urate appears to be better related to maternal vascular pathology than to the clinical condition or infant birthweight.

The relation between plasma urate and placental bed vascular adaptation to pregnancy

Summary. Placental bed biopsies were obtained at caesarean section from 34 women. Their plasma urate was directly related to maximum mean arterial pressure and inversely to adjusted birthweight; but it was related most closely to the histological appearances of the spiral arteries in the placental bed. Nine women had physiological changes in the spiral arteries: their mean urate (233, SD 28·9 μmol/l) was significantly (P &lt;0·00l) lower than the mean urate in those who did not have adequate physiological changes (339, SD 90·3 μmo1/l) or that in the nine women who had atherosis (397, SD 153·2 μmol/l). Raised plasma urate appears to be better related to maternal vascular pathology than to the clinical condition or infant birthweight.

Hypertension and brain oedema: an experimental study on acute and chronic hypertension in the rat.

To determine under what circumstances hypertension is associated with brain oedema, the specific gravity of the brain was measured in acutely hypertensive, renal hypertensive and spontaneously hypertensive rats. Maximum mean arterial pressure (MAP) in acute hypertension induced by intravenous amphetamine or bicuculline was 171 +/- 5 and 181 +/- 5 mmHg respectively. In spite of pronounced extravasation of Evans blue-albumin, there was no decrease in specific gravity except in the diencephalon in rats given bicuculline (p less than 0.05). Cortical and cerebellar samples from renal hypertensive rats (MAP 174 +/- 14 mmHg) were lighter than corresponding regions in normotensive rats (p less than 0.001) although the brains showed little or no macroscopic extravasation of Evans blue-albumin. Neither macroscopic protein leakage nor increase in water content was observed in brains from spontaneously hypertensive rats (MAP 210 +/- 5 mmHg). It is concluded that renal hypertension is more likely to lead to brain oedema than spontaneous genetic hypertension or acute hypertension.

Effects of acute hypertension on the extravasation of macromolecule in the temporal bone--the possible involvement of the blood-inner ear barrier.

In guinea pigs the radioactivity in the vascular beds was washed out by a cardiac perfusion of saline 15 min after the injection of 50 microCi of radioiodinated human serum albumin (RISA). The brain and temporal bones were dissected and a blood sample was obtained. To examine the degree of extravasation of RISA, the extravascular radioactivity in the tissues was measured and expressed as a ratio to that of the blood. Intravenous injection of amphetamine sulfate increased the extravasation in the brain and the temporal bone of the rat but did not increase it in either tissue of the guinea pig. It was proposed that this was because amphetamine did not cause the blood pressure of the guinea pig to reach the "critical level" which would cause the opening of the blood-tissue barrier. In the rat the degrees of extravasation in both the brain and the temporal bone paralleled the maximal mean arterial pressure caused by amphetamine. It is proposed on the basis of these data that there may exist a blood-inner ear barrier and that this barrier has the same characteristics as the blood-brain barrier.

Nifedipine, a new antihypertensive with rapid action.

Oral (17 cases) or sublingual (9 cases) administration of nifedipine (10 mg), a new coronary dilator, induced a prompt and large pressure reduction in patients with severe primary hypertension. Pressure started to fall within 20 and 5 min after oral and sublingual administration, respectively, and reached the lowest levels in the next 10 min. Maximal mean arterial pressure reduction averaged 36 mm Hg; 120 min after the drug, mean arterial pressure was diminished by 19.5% of control. The hypotension was mediated through diminished peripheral resistance associated with rise of cardiac output and pulse rate. Nifedipine was also administered siblingually in 3 cases with hypertensive encephalopathy and acute left ventricular failure with average systemic and pulmonary arterial pressures from 307/164 and 91/55 mm Hg, respectively, which fell to 237/115 and 68/35 mm Hg 15 min after 10 mg of the drug, and were further reduced to 176/89 and to 47/19 mm Hg by an additional 10 mg.

Cardiac performance of hypertensive aorta-constricted rabbits.

A heart-lung preparation with flow limited to the coronary vessels was used to study cardiac performance 4 to 120 days after severe constriction of the abdominal aorta in rabbits. Cardiac performance was evaluated by finding the maximum mean arterial pressure against which the heart could pump. Cardiac performance began to exceed the normal, range by the second or third post operative week and was well above normal after the first month. A high cardiac performance was not necessarily associated with marked ventricular hypertrophy. Animals died of heart failure within the first month, and all had developed a much more rapid rate of blood pressure increase than those that survived without signs of decompensation. We conclude that the basic cause of heart failure after severe aorta constriction is a rapid rise in arterial pressure which exceeds the rate at which the heart develops an improved performance.