Rise In Mean Arterial Pressure Research Articles

Platelet alpha2-adrenoceptors and diurnal changes of platelet aggregability in hypertensive patients

To analyse whether platelets from hypertensive patients have an increased responsiveness to aggregating agents during morning hours and whether these changes might be related to concurrent changes in platelet membrane alpha 2-adrenoceptor characteristics, plasma catecholamine and cortisol levels, and blood pressure values. Blood samples from 14 mild-to-moderate essential hypertensive males were collected in the morning (0700-0900 h) and the evening (1900-2100 h) to determine platelet aggregability responses to adrenaline and ADP, platelet alpha 2-adrenoceptor number and binding affinity to [3H]-yohimbine, plasma catecholamines and cortisol. During the same day patients underwent 24-h ambulatory blood pressure monitoring. The lowest concentration of adrenaline required to induce biphasic aggregation was significantly lower in the morning than in the evening, indicating an increased morning platelet aggregability to adrenaline; the minimum ADP concentration inducing aggregation was similar in morning and evening samples. There were no significant differences between morning and evening samples in platelet alpha 2-adrenoceptor number and binding affinity. Plasma adrenaline, noradrenaline and cortisol levels were higher in the morning than in the evening, but no correlation was observed between hormonal changes and the morning increase in platelet sensitivity to adrenaline. Ambulatory blood pressure recording showed abrupt morning elevations in systolic and diastolic blood pressures over sleeping values. However, morning blood pressure readings were not significantly different from those recorded during the rest of the day and in the evening. The morning rise in mean arterial pressure displayed a significant inverse correlation with the increased platelet sensitivity to adrenaline that was observed during the same hours. The results indicate that the increased morning responsiveness to adrenaline that was observed in platelets obtained from hypertensive patients does not appear to be mediated by changes in the characteristics of platelet membrane alpha 2-adrenoceptors, but morning blood pressure elevations might play some role in inducing this platelet hyper-reactivity.

Heterotopic heart transplantation: catheterization, endomyocardial biopsy, and coronary angiography of the donor heart

Follow-up after heart transplantation presently requires invasive techniques to assess graft viability and function. As the heterotopic transplant technique assumes a more important therapeutic role for patients not eligible for an orthotopic allograft, an understanding of the inherent challenges associated with management of these patients is mandatory to optimize patient care. Heterotopic transplant technique was used in 19 of 135 (14%) consecutive heart transplant procedures over a 41 month period. Invasive diagnostic procedures performed in follow-up revealed 1) adequate tissue for histologic evaluation in 140/158 (89%) biopsy procedures, 2) successful pulmonary wedge pressure measurements in 142/158 (90%) right heart catheterizations, and 3) successful coronary arteriography in 18 patients undergoing angiography (both vessels in 12 and one vessel in six patients). Thus, biopsy and surveillance procedures are feasible and productive in patients who have undergone heterotopic heart transplantation. Although heterotopic heart transplantation has become an increasingly utilized therapy for some patients with heart failure, there are no guidelines for routine biopsy and angiographic techniques in these patients. The objective of this study was to determine the feasibility of angiographic and endomyocardial biopsy procedures in heterotopic heart transplant recipients. The complete experience with heterotopic heart transplant recipients at Baylor College of Medicine and The Methodist Hospital over a 41 month period including endomyocardial biopsy, right heart catheterization, and selective coronary arteriography results were analyzed. Eighteen patients underwent 310 procedures without significant complications. Of 158 biopsy procedures, 140 (89%) yielded tissue adequate for histologic evaluation. Right heart pressures were obtained in almost all patients undergoing right heart catheterization. Pulmonary wedge pressures were obtained in 137 (90%). A rapid decrease in right heart pressures was noted following transplant; however, a gradual but significant rise in mean arterial pressure occurred. Eighteen selective coronary arteriogram procedures were performed; 12 (66%) resulted in successful cannulation of both coronary arteries. Of 12 patients followed for at least 1 year, five (40%) have developed evidence of allograft arteriopathy. The 1 and 2 year survival rates were 67% and 53%, respectively. Invasive diagnostic techniques can be performed safely and reliably and should not preclude the use of heterotopic heart transplantation in selected patients who are otherwise unsuitable for orthotopic transplantation.

Responses evoked in the forearm vasculature on normal human subjects on repetition of mild, indirect cooling.

We have studied responses evoked in the forearm vasculature of normal subjects by mild cooling of the contralateral hand; it was transferred from thermoneutral water at -33 degrees C to water at 16 degrees C for 2 min. Total forearm blood flow was measured by venous occlusion plethysmography, cutaneous red cell flux was monitored with a laser Doppler flowmeter and arterial pressure was recorded by semi-automatic sphygmomanometry. In each of two groups (I and II) of twelve and 15 subjects, mild cooling evoked a rise in mean arterial pressure, but in each group, approximately half (six and eight respectively) showed a decrease in total forearm vascular resistance (FVR) in response to the first cool immersion (dilator group), while the remainder showed an increase in FVR (constrictor group), apart from one of group II who showed no change in FVR. Cutaneous vascular resistance tended to increase in both the dilator and constrictor groups, but this did not reach statistical significance. When cooling was repeated six times in group II, the decrease in FVR (-18% from control) in the dilator group reversed to an increase in FVR (+25%) by the sixth immersion, while the increase in FVR (+55%) in the constrictor group persisted through to the sixth immersion (+23%). We propose that mild cooling evokes a primary reflex vasoconstrictor response in forearm muscles, but that this can be overcome in some subjects by the characteristic muscle vasodilatation of the alerting response which is evoked by novel, or noxious stimuli; the latter is known to habituate on repetition of the stimulus.

Rectal Nifedipine for the Management of Intraoperative Hypertension

The effect of rectal administration of nifedipine for the management of intraoperative hypertension was studied in 12 adult neurosurgical patients, physical status II and III. A rise in mean arterial pressure (MAP) of > 20 mm Hg over the preoperative value was taken as the point at which rectal nifedipine (150 micrograms kg-1) was administered. Onset of action of nifedipine was observed in 4.5 +/- 1.5 min (mean +/- SD) with a peak effect at 30.8 +/- 10.7 min. MAP decreased from 124 +/- 4.5 mm Hg to 97 +/- 2.4 mm Hg. Heart rate and central venous pressure were unchanged. Endoscopic examination of the rectal mucosa 48 h after administration of nifedipine did not show any abnormality. Rectal nifedipine was found to be effective and safe for the management of intraoperative increases in arterial blood pressure as well as being convenient to administer to patients undergoing neurosurgical procedures.

Cardiovascular actions of dogfish urotensin II in the dogfish Scyliorhinus canicula

Bolus injections of synthetic dogfish urotensin II (0.1-1.0 nmol) into the celiac artery of the conscious dogfish Scyliorhinus canicula (n = 8) resulted in sustained and dose-dependent increases in arterial blood pressure and pulse pressure. A maximum rise in mean arterial pressure of 10.5 +/- 1.2 mmHg (equivalent to 38.6 +/- 4.2% over mean basal values) and a maximum increase in pulse pressure of 3.9 +/- 0.8 mmHg was elicited by injection of 0.5 nmol of peptide. In comparison, a bolus injection of epinephrine (5 nmol) elicited a rise of 24.8 +/- 3.3% in mean arterial pressure. Bolus injection of 0.5 nmol synthetic goby (Gillichthys mirabilis) urotensin II under the same conditions did not elicit a significant hypertensive response. When dogfish urotensin II (0.5 nmol) was administered 3 min after an intra-arterial injection of phentolamine, the rise in arterial blood pressure was completely abolished. Dogfish urotensin II produced a dose-dependent contraction (pD2 = 6.58 +/- 0.07; n = 8) of isolated rings of vascular muscle prepared from the first afferent branchial artery of the dogfish. A maximum contractile force of 1.3 mN was produced by 10(-5) M peptide. The urotensin II-induced contraction of the vascular rings was unaffected by pretreatment with tetrodotoxin (1 microM) or indomethacin (14 microM). It is concluded that urotensin II has potent hypertensive activity in the dogfish that is mediated, at least in part, through release of catecholamines, but the sustained nature of the pressor response suggests that the peptide may have a direct action on the heart.

Influence of labetalol on cocaine-induced coronary vasoconstriction in humans

purpose: Although labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown. patients and methods: In 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9). results: Of 40 coronary arterial segments analyzed, cocaine induced a 13% ± 10% (mean ± standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 ± 14 mm Hg after cocaine, 110 ± 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 ± 1.37 mm 2 after cocaine, 3.37 ± 1.32 mm 2 after labetalol; p = NS). conclusion: Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

Hemodynamic Changes Associated with Tourniquet Use Under Epidural Anesthesia for Total Knee Arthroplasty

Epidural anesthesia is administered commonly for total knee arthroplasty, a procedure using a thigh tourniquet. Tourniquet use has been associated with intraoperative hypertension and with occasional circulatory collapse after deflation. The purpose of this study was to define the hemodynamic changes in this setting.We prospectively studied 373 consecutive patients having a total knee arthroplasty performed under epidural anesthesia, with continuous electrocardiogram and radial artery pressure monitoring. Results were analyzed using Student's t-test, correlation coefficients, analysis of variance, or chi-square analysis. Alpha was set at 0.01.There was a 4 +/- 11 mmHg rise in mean arterial pressure throughout the period of tourniquet application (p less than 0.001); no clinically significant hypertension occurred. After tourniquet deflation, there was a 19.2 +/- 12% reduction in mean arterial pressure, occurring within one minute. The magnitude of mean arterial pressure reduction failed to correlate with any clinical parameter other than vasopressor use. There was a small subset of patients who had a fall in heart rate and a more profound degree of hypotension after tourniquet deflation, but these patients could not be identified before tourniquet release.In this setting, tourniquet-induced hypertension is rare. However, hypotension after deflation is common, occurs rapidly, and correlates poorly with clinical parameters.

Stability of cardiovascular reaction patterns across subjects and situations

The hemodynamic response to sequences of ventricular fibrillation and defibrillation includes an adrenergic component that is important for the maintenance of blood pressure after successful defibrillation. Because calcium channel blocking drugs have antiadrenergic effects, we hypothesized that they might blunt the adrenergic response to defibrillation. Ventricular fibrillation was induced in 35 closed-chest dogs. Each recaived 4 to 7 direct current transthoracic shocks at three energy levels to determine defibrillation energy requirements. Heart rate and blood pressure were recorded. Energy sequences were repeated after 45 minutes of no intervention (control, n = 5) or after 45-minute infusions of diltiazem (0.1 mg/kg/min, n = 10), verapamil (0.1 mg/kg bolus plus 0.01 mg/kg/min, n = 10), or nifedipine (40 μg/min for 3 minutes plus 2 to 20 μg/min adjusted to maintain a 10 mm Hg drop in mean arterial pressure, n = 10). Our results show that the normal post-shock rise in mean arterial pressure was blunted by the calcium channel blockers diltiazem (systolic arterial pressure at 15 and 60 seconds post-shock, pre-drug versus post-drug: 102 ± 9 versus 64 ± 9 mm Hg and 113 ± 10 versus 87 ± 6 mm Hg; p < 0.05) and verapamil (108 ± 9 versus 78 ± 12 mm Hg and 113 ± 7 versus 90 ± 10 mm Hg, p < 0.05). There were no differences in blood pressure responses after nifedipine treatment or no drug. Heart rate responses were not altered by diltiazem or verapamil; after nifedipine administration, post-shock heart rates were slower. After treatment with diltiazem and verapamil there was a modest reduction in percent shock success across all energy levels (diltiazem: 28% ± 7% versus 17% ± 6%, 71% ± 9% versus 52% ± 14%, and 87% ± 13% versus 82% ± 11% at 25 J, 50 J, and 100 J, respectively [ p < 0.05 ]; verapamil: 50% ± 14% versus 15% ± 2%, 64% ± 11% versus 44% ± 14%, and 82% ± 9% versus 72% ± 13%, respectively [ p < 0.05 ]). Nifedipine did not alter shock success rates. This study suggests that calcium channel blocking drugs blunt the adrenergic response to defibrillation.

Event-related potentials elicited by neutral stimuli and emotion-expressing human faces

The hemodynamic response to sequences of ventricular fibrillation and defibrillation includes an adrenergic component that is important for the maintenance of blood pressure after successful defibrillation. Because calcium channel blocking drugs have antiadrenergic effects, we hypothesized that they might blunt the adrenergic response to defibrillation. Ventricular fibrillation was induced in 35 closed-chest dogs. Each recaived 4 to 7 direct current transthoracic shocks at three energy levels to determine defibrillation energy requirements. Heart rate and blood pressure were recorded. Energy sequences were repeated after 45 minutes of no intervention (control, n = 5) or after 45-minute infusions of diltiazem (0.1 mg/kg/min, n = 10), verapamil (0.1 mg/kg bolus plus 0.01 mg/kg/min, n = 10), or nifedipine (40 μg/min for 3 minutes plus 2 to 20 μg/min adjusted to maintain a 10 mm Hg drop in mean arterial pressure, n = 10). Our results show that the normal post-shock rise in mean arterial pressure was blunted by the calcium channel blockers diltiazem (systolic arterial pressure at 15 and 60 seconds post-shock, pre-drug versus post-drug: 102 ± 9 versus 64 ± 9 mm Hg and 113 ± 10 versus 87 ± 6 mm Hg; p < 0.05) and verapamil (108 ± 9 versus 78 ± 12 mm Hg and 113 ± 7 versus 90 ± 10 mm Hg, p < 0.05). There were no differences in blood pressure responses after nifedipine treatment or no drug. Heart rate responses were not altered by diltiazem or verapamil; after nifedipine administration, post-shock heart rates were slower. After treatment with diltiazem and verapamil there was a modest reduction in percent shock success across all energy levels (diltiazem: 28% ± 7% versus 17% ± 6%, 71% ± 9% versus 52% ± 14%, and 87% ± 13% versus 82% ± 11% at 25 J, 50 J, and 100 J, respectively [ p < 0.05 ]; verapamil: 50% ± 14% versus 15% ± 2%, 64% ± 11% versus 44% ± 14%, and 82% ± 9% versus 72% ± 13%, respectively [ p < 0.05 ]). Nifedipine did not alter shock success rates. This study suggests that calcium channel blocking drugs blunt the adrenergic response to defibrillation.

Interoceptive processes in cardiac phobia and panic disorder

The hemodynamic response to sequences of ventricular fibrillation and defibrillation includes an adrenergic component that is important for the maintenance of blood pressure after successful defibrillation. Because calcium channel blocking drugs have antiadrenergic effects, we hypothesized that they might blunt the adrenergic response to defibrillation. Ventricular fibrillation was induced in 35 closed-chest dogs. Each recaived 4 to 7 direct current transthoracic shocks at three energy levels to determine defibrillation energy requirements. Heart rate and blood pressure were recorded. Energy sequences were repeated after 45 minutes of no intervention (control, n = 5) or after 45-minute infusions of diltiazem (0.1 mg/kg/min, n = 10), verapamil (0.1 mg/kg bolus plus 0.01 mg/kg/min, n = 10), or nifedipine (40 μg/min for 3 minutes plus 2 to 20 μg/min adjusted to maintain a 10 mm Hg drop in mean arterial pressure, n = 10). Our results show that the normal post-shock rise in mean arterial pressure was blunted by the calcium channel blockers diltiazem (systolic arterial pressure at 15 and 60 seconds post-shock, pre-drug versus post-drug: 102 ± 9 versus 64 ± 9 mm Hg and 113 ± 10 versus 87 ± 6 mm Hg; p < 0.05) and verapamil (108 ± 9 versus 78 ± 12 mm Hg and 113 ± 7 versus 90 ± 10 mm Hg, p < 0.05). There were no differences in blood pressure responses after nifedipine treatment or no drug. Heart rate responses were not altered by diltiazem or verapamil; after nifedipine administration, post-shock heart rates were slower. After treatment with diltiazem and verapamil there was a modest reduction in percent shock success across all energy levels (diltiazem: 28% ± 7% versus 17% ± 6%, 71% ± 9% versus 52% ± 14%, and 87% ± 13% versus 82% ± 11% at 25 J, 50 J, and 100 J, respectively [ p < 0.05 ]; verapamil: 50% ± 14% versus 15% ± 2%, 64% ± 11% versus 44% ± 14%, and 82% ± 9% versus 72% ± 13%, respectively [ p < 0.05 ]). Nifedipine did not alter shock success rates. This study suggests that calcium channel blocking drugs blunt the adrenergic response to defibrillation.

Heterogeneous receptors mediate endothelin-1-induced changes in blood pressure, hematocrit, and platelet aggregation.

Using selective endothelin (ET) receptor antagonists, we investigated which ET receptor subtypes mediate the changes in blood pressure and hematocrit produced by intraarterial injection of ET-1 in the anesthetized rabbit. In addition, the receptor through which ET-1 stimulates the release of prostacyclin (PGI2) and, hence, inhibits ex vivo platelet aggregation, was identified. FR 139317 (ETA antagonist, 0.6 mg kg-1 min-1 preceded by a loading dose of 3 mg kg-1 i.v.) and PD 145065 (nonselective ETA/ETB antagonist, 0.6 mg kg-1 min-1 preceded by a loading dose of 3 mg kg-1 i.v.) attenuated the ET-1 (1 nmol kg-1 i.a.)-induced rise in mean arterial pressure (MAP) by 89% and 75%, respectively. In contrast to FR 139317, PD 145065 also abolished the initial, transient depressor response brought about by ET-1. ET-1 caused a significant increase in hematocrit 15 min after its injection. PD 145065 caused a significantly greater inhibition of this hemoconcentration than FR 139317. ET-1 inhibited ex vivo platelet aggregation by 96%, measured 5 min after injection of the peptide. PD 145065, but not FR 139317, abolished the antiaggregatory effects of ET-1. Thus, the ET-1-induced vasoconstriction in the anesthetized rabbit is predominantly mediated via the ETA receptor, whereas the depressor and antiaggregatory actions of ET-1 are caused by activation of the ETB receptor. Moreover, activation of both receptor subtypes by ET-1 accounts for the increase in hematocrit produced by ET-1 in vivo.

Vasodilators inhibit acute alpha 1-adrenergic receptor-induced trophic responses in the vasculature.

Cardiovascular hypertrophy plays an important role in the development and maintenance of hypertension. Hyperactivity of the sympathetic nervous system may be one of the initiating factors responsible for the stimulation of growth processes involved in these structural alterations. We have used a well-established early biochemical marker of cellular growth processes, induction of ornithine decarboxylase (ODC), to determine whether alpha 1-adrenergic receptor-induced vascular trophic responses are dependent on arterial pressure elevation. Hydralazine or felodipine were coadministered to control the alpha 1-adrenergic receptor agonist-induced rise in mean arterial pressure (MAP). Methoxamine (2, 5, or 10 mg/kg s.c.) increased the average MAP (up to 20 mm Hg) and vascular ODC activity (up to ninefold) above control rats over 4 hours. Concomitant administration of hydralazine (0.5, 1.25, or 5 mg/kg s.c.) or felodipine (100 or 250 micrograms/kg s.c.) with methoxamine (10 mg/kg) attenuated the alpha 1-adrenergic receptor-induced activation of ODC in the aorta and mesenteric resistance vasculature, as well as the MAP increases. Vasodilators alone did not lower basal vascular ODC activity. The major findings include: 1) alpha 1-adrenergic receptor activation dose-dependently induces vascular ODC activity concomitantly with MAP elevation, 2) vasodilators inhibited both the alpha 1-adrenergic receptor-induced MAP increases and the activation of mesenteric vascular and aortic ODC, and 3) the stimulus-response correlation between MAP elevation and mesenteric (r = 0.78) and aortic (r = 0.92) ODC activation was characterized by a logistic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of hypotension induced by Vibrio vulnificus lipopolysaccharide in the rat by inhibition of nitric oxide synthase

Intravenous infusion of Vibrio vulnificus lipopolysaccharide (LPS) (1 mg/kg body wt) in rats caused a dramatic drop in mean arterial pressure within 10 min and a further decline in mean arterial pressure and heart rate which lead to death between 25 and 70 min. Rats treated with LPS followed 10 min later by the intravenous infusion of N G-monomethyl-L-arginine (L-NMMA, 20 mg/kg body wt) showed an initial drop in mean arterial pressure owing to the LPS infusion, followed by a transient rise in mean arterial pressure which lasted for approximately 40 min after the infusion of L-NMMA. The pressure values then remained level for at least 150 min post-LPS infusion. Control rats treated with equivalent volumes of saline infusion showed stable values of mean arterial pressure and heart rate. Additional control rats receiving L-NMMA alone showed the transient rise in mean arterial pressure, followed by a return to the baseline values. The results indicate that the symptoms of endotoxic shock resulting from V. vulnificus LPS may result in part from the stimulation of the activity of nitric oxide synthase. Inhibition of nitric oxide synthase by L-NMMA is a possible treatment for toxic shock induced by V. vulnificus.

Measurement of local directional pressures in the brain with mass.

In order to understand the effects and the direction of pressure transmitted from a mass lesion through various brain structures, miniature strain gauges were inserted in different brain locations in eight anesthetized monkeys. Mass lesions were created by inflating a balloon in either of two locations--subcortical in four animals (Group I) and deep (lateral to the caudate nucleus) in the other four animals (Group II). Anterior-posterior directed pressures were thus measured from a gauge placed in the parietal lobe, and lateromedially directed pressures (LM-dPs) were measured from gauges in the temporal lobe and midbrain. Intracranial pressure, systemic mean arterial pressure, and cerebral blood flow were also monitored. After balloon inflation was begun, temporal changes in pressure were recorded from gauges as percentage increase or decrease from baseline measurements. In both groups, balloon inflation caused a gradual increase in the parietal lobe anterior-posterior directed pressure with a concomitant increase in intracranial pressure and a decrease in cerebral blood flow. The temporal lobe gauge in Group I recorded an initial negative followed by a positive LM-dP with further balloon inflation. In Group II, this gauge recorded a positive LM-dP throughout. The midbrain gauges in both groups recorded an initial positive followed by a negative LM-dP. This reversal in the direction of pressure in the midbrain occurred just before the supratentorial pressure reached a peak and was noted to be concurrent with a sudden rise in mean arterial pressure and a decline in cerebral blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of aging and hypertension on plasma angiotensin II and platelet angiotensin II receptor density.

Plasma renin activity (PRA) declines with age in normal individuals, but the effect of age on plasma angiotensin II (ANG II) is less clear. A decline in plasma ANG II with age could result in altered platelet ANG II receptor density since plasma hormone levels influence their target organ receptors. To investigate this possibility, PRA, plasma ANG II, and platelet ANG II receptor density were examined in 17 young, 12 middle-aged, and 14 elderly healthy normotensive volunteers. To assess whether hypertension altered receptor density, these variables were also examined in 23 hypertensive patients. In normotensives, there was a negative correlation between age and PRA (r = -0.43, P < .05), no significant change in basal plasma ANG II with age, and a weak positive correlation between age and ANG II receptor density (r = 0.34, P < .05). Multiple regression analysis revealed that the relationship between age and ANG II receptor density was independent of the associated rise in mean arterial pressure with age (P < .05). Platelet ANG II receptor density was not significantly related to PRA or plasma ANG II. ANG II receptor affinity did not change with age. Neither PRA nor ANG II receptor density or affinity differed between hypertensives and normotensives of similar mean age, but plasma ANG II was significantly lower in hypertensives compared with normotensives. We concluded that aging is associated with a decline in supine PRA. The small decrease in plasma ANG II was not significant. Platelet ANG II receptor density increased with age primarily due to a small group of elderly subjects with elevated receptor density. There was no change in ANG II receptor density or affinity in hypertensives despite apparently lower plasma ANG II in these patients.

Effect of magnesium sulfate on the vascular actions of norepinephrine and angiotensin II.

Magnesium sulfate is used for seizure prophylaxis in patients with preeclampsia. It also has significant effects on calcium metabolism and could, therefore, alter the pressor response to calcium-dependent vasoconstrictors. The present in vivo rat study examined the effect of magnesium sulfate to alter the pressor response to norepinephrine (NE) and angiotensin II (A II). Magnesium doses were chosen to approximate those used in treating preeclampsia. NE resulted in a significant rise in mean arterial pressure (delta MAP, 46 +/- 3.7 mmHg; p < 0.001). A II also resulted in a significant rise in MAP (delta MAP, 23 +/- 3.6 mmHg, p < 0.02). Magnesium sulfate alone had no significant effect on MAP but attenuated the pressor response to both NE (delta MAP, 16 +/- 1.5 mmHg) and A II (delta MAP, 12 +/- 2.5 mmHg). After discontinuation of the magnesium sulfate infusion, the control pressor responses to NE and A II were again seen (delta MAP, 39 +/- 3.5 mmHg and delta MAP, 28 +/- 4.2 mmHg, respectively). Although magnesium sulfate is not a primary antihypertensive agent, it may have effects on blood pressure by attenuating the actions of circulating vasoconstrictors.

Relationships between dopamine infusions and intracranial hemodynamics in patients with raised intracranial pressure

Dopamine, 1–10 μg/kg body weight/min was infused in 6 patients suffering from cerebrovascular diseases with elevated intracranial pressure and a critical cerebral perfusion pressure. Dopamine decreased intracranial pressure in 3 and increased it moderately in the other 3 patients. In all patients, the dopamine-induced rise of mean arterial pressure led to an increase of cerebral perfusion pressure. Transcranial Doppler ultrasonographic recordings of the middle cerebral artery in patients whose intracranial pressure declined revealed a decrease of the pathologically elevated cerebrovascular resistance, and an augmentation of cerebral blood supply. In conclusion, dopamine infusions may improve cerebral hemodynamics in some patients with severe brain edema. Such patients can be identified by intracranial pressure and Doppler monitoring.

Vasopressin responses to unloading arterial baroreceptors during cardiac nerve blockade in conscious dogs

We examined the relative contributions of afferent input from the heart and from arterial baroreceptors in the stimulation of arginine vasopressin (AVP) secretion in response to hypotension caused by thoracic inferior vena caval constriction (TIVCC). Afferent input from cardiac receptors was reversibly blocked by infusing 2% procaine into the pericardial space to anesthetize the cardiac nerves. Acute cardiac nerve blockade (CNB) alone caused a rise in mean arterial pressure (MAP) of 24 +/- 3 mmHg but no change in plasma AVP. If the rise in MAP was prevented by TIVCC, plasma AVP increased by 39 +/- 15 pg/ml, and if MAP was allowed to increase and then was forced back to control by TIVCC, plasma AVP increased by 34 +/- 15 pg/ml. Thus the rise in MAP during CNB stimulated arterial baroreceptors, which in turn compensated for the loss of inhibitory input from cardiac receptors on AVP secretion. These results indicate that the maximum secretory response resulting from complete unloading of cardiac receptors at a normal MAP results in a mean increase in plasma AVP of 39 pg/ml in this group of dogs. When MAP was reduced 25% below control levels (from 95 +/- 5 to 69 +/- 3 mmHg) by TIVCC during pericardial saline infusion, plasma AVP increased by 79 +/- 42 pg/ml. However, the same degree of hypotension during CNB (MAP was reduced from 120 +/- 5 to 71 +/- 3 mmHg) led to a greater (P less than 0.05) increase in plasma AVP of 130 +/- 33 pg/ml. Because completely unloading cardiac receptors can account for an increase of only 39 pg/ml on average in this group of dogs, the remainder of the increase in plasma AVP must be due to other sources of stimulation. We suggest that the principal stimulus to AVP secretion after acute CNB in these studies arises from unloading the arterial baroreceptors.

Hemodynamic evaluation of a chronically implanted, electrically powered left ventricular assist system: Responses to acute circulatory stress

Hemodynamic stress testing was performed in four calves with a chronically implanted left ventricular assist device consisting of a double-valved pump interposed between the left ventricular apex and the descending thoracic aorta. The device was powered either pneumatically (n = 1) or with a transcutaneous energy transmission system (n = 3). Hemodynamic evaluation (cardiac output and right and left ventricular and pulmonary and carotid artery pressures) was carried out at baseline and during all hemodynamically stressed states.Atrial pacing and ventricular pacing to a heart rate of 140 beats/min resulted in no significant change in right or left heart filling pressures or cardiac output. Preload reduction with nitro-prusside or transient inferior vena cava balloon occlusion resulted in a marked decrease in left ventricular pressure with preservation of mean arterial pressure. Phenylephrine administration resulted in a marked rise in mean arterial pressure with no change in cardiac output or filling pressure. Induction of ventricular fibrillation resulted in a decrease of mean left ventricular pressure to 11 ± 8 mm Hg, but mean arterial pressure was maintained at ≥50 mm Hg.It is concluded that a multicomponent, implantable, electrically powered assist system is capable of maintaining a normal cardiac output under a wide range of loading conditions and chronotropic states. Although this device is clearly preload dependent it is capable of maintaining normal systemic pressures during conditions of severe left ventricular dysfunction and circulatory collapse.

Effects of angiotensin II on atrial natriuretic peptide in pregnancy

To clarify the effects on angiotensin II and blood pressure on plasma atrial natriuretic peptide in pregnancy, angiotensin II was infused in 37 healthy, normotensive pregnant women in week 32 of gestation. Levels of atrial natriuretic peptide were determined with the women in a sitting position 3 days before the test and in the left lateral recumbent position immediately before and after the test. Levels of atrial natriuretic peptide were not influenced by parity or salt intake. They were found to be significantly higher in the left lateral recumbent position than in the sitting position. There was also a significant increase in atrial natriuretic peptide levels during angiotensin II infusion. A dose of angiotensin 11 <1.5 nglkglmin did not affect atrial natriuretic peptide levels. Rise in atrial natriuretic peptide levels was minimally correlated with rise in mean arterial pressure, as caused by acute vasoconstriction from angiotensin II infusion. Therefore it is suggested that, in pregnancy, the response of atrial natriuretic peptide to angiotensin II is mediated not only by changes in blood pressure but also by angiotensinergic receptor activity in the atria.