Mean Arterial Blood Pressure Measurements Research Articles

Transcranial Doppler sonography indicates critical brain perfusion during hemorrhagic hypotension in dogs.

This study investigated the effects of hemorrhagic hypotension on cerebral blood flow velocity and brain electrical activity (by electroencephalogram [EEG]). Eleven mongrel dogs were anesthetized with isoflurane (1 minimum alveolar anesthetic concentration [MAC]) and catheters were placed into both femoral arteries and veins for mean arterial blood pressure (MAP) measurement, blood withdrawal, and drug administration. Brain temperature, arterial blood gases, and pH were maintained constant. EEG was recorded from temporoparietal recording sites versus a frontal reference. A pulsed transcranial Doppler (TCD) probe (2 MHz, Transpect, Medasonics) was placed on the dura via a temporal bone window to measure mean (Vmean, cm/s) and diastolic blood flow velocity (Vdiast, cm/s) in the middle cerebral artery. At the end of the surgical preparation, isoflurane was discontinued and all animals received fentanyl (bolus, 25 micrograms/kg intravenously (IV); infusion, 50 micrograms.kg-1.h-1 IV) plus 50% N2O/O2 during 30 min of equilibration. After recordings of baseline data, the dogs were hemorrhaged at a rate of 80-100 mL/min. The observation interval was 14 min. EEG spectral edge frequency (SEF 95%) and Vmean did not change when MAP was decreased from 109 +/- 10 to 63 +/- 7 mm Hg. This indicates preserved neuronal function and intact autoregulation of cerebral blood flow. Below MAP of 49 +/- 9 mm Hg, a shift of the EEG to lower frequencies was associated with decreases in Vmean and Vdiast. EEG burst suppression occurred at a MAP of 31 +/- 7 mm Hg, paralleled by a loss of the diastolic flow velocity pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood pressure and cardiovascular reflex development in fetal sheep. Relation to hypoxaemia, weight, and blood glucose.

We measured mean arterial blood pressure (MAP), fetal heart rate (FHR), the baroreflex, weight, blood gases, blood glucose and lactate in chronically instrumented fetal sheep for 14 days from Day 105 to Day 109 gestation, with or without daily administration of 1 h of acute isocapnic hypoxaemia (arterial O2 partial pressure, PaO2, 11-13 mm Hg; 1 mm Hg = 133 Pa). Fetuses subjected to hypoxia showed no significant differences in MAP or FHR v. control fetuses. However, examination of all fetuses together revealed that there were two distinct groups: those showing a rise in MAP over the 14 days ('pressure up' group, PU), and those in which blood pressure did not increase or showed only a slight decrease ('pressure down' group, PD). PU fetuses were proportionately larger than PD fetuses. In contrast to PU fetuses, PD fetuses had lower blood glucose concentration, arterial O2 saturation (SaO2), PaO2, total haemoglobin, haematocrit and oxygen content, and higher lactate concentration, pH and PaCO2. PU fetuses showed a shift of the baroreflex MAP/R-R interval curve to the right, however, the PD group showed a shift upwards from Day 1 to Day 14. The PD group responded to hypoxia with a greater increase in MAP than the PU group. Thus, repeated acute moderate isocapnic hypoxia does not affect development of MAP or FHR in late gestation fetal sheep. However, MAP follows different trajectories in individual fetuses, related to fetal size and the availability of oxygen and/or glucose. Cardiovascular chemoreflexes and baroreflexes are also different, depending on the MAP trajectory. These data indicate an important association between growth and blood pressure development, and also show that differences in growth are associated with changes in cardiovascular control.

Pregnant rats are refractory to the natriuretic actions of atrial natriuretic peptide.

Normal pregnant women and rats undergo a volume expansion. Atrial natriuretic peptide (ANP) is involved in volume homeostasis and is stimulated in response to volume expansion in nonpregnant animals, resulting in natriuresis and diuresis. The conscious, chronically catheterized rat was used to measure mean arterial blood pressure (MABP) and renal responses to administered ANP (160 ng.kg-1.min-1 i.v.) to determine if the actions of ANP are altered by pregnancy. These experiments examined virgin (n = 7) and pregnant rats, studied on gestational days 7-9 (n = 9) and 15-17 (n = 7). Renal clearance studies (with inulin and p-aminohippurate) were conducted in control conditions and during 60 min of ANP infusion. After the ANP infusion, plasma ANP concentrations were measured in virgin and pregnant rats. MABP fell with ANP infusion to similar absolute values in virgins (112 +/- 2 to 80 +/- 6 mmHg), 7- to 9-day pregnant (114 +/- 2 to 91 +/- 3 mmHg), and 15- to 17-day pregnant (107 +/- 2 to 88 +/- 4 mmHg) rats although the percent decline in MABP in 15- to 17-day pregnant rats was less than in virgins. Plasma ANP concentrations were similar in all groups. ANP had no effect on glomerular filtration rate, renal plasma flow, or renal vascular resistance in virgin or pregnant rats. ANP increased sodium excretion in virgins and in 7- to 9-day pregnant rats (+102 +/- 27 and +135 +/- 47%, respectively) but not in 15- to 17-day pregnant animals (+23 +/- 22%).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of diprotonated phosphate in evoking muscle reflex responses in cats and humans

Lactic acid and H+ evoke muscle reflexes that raise sympathetic nerve activity. Whether these substances are direct afferent stimulants or markers for the acidification of other substances is unknown. Diprotonated phosphate (H2PO4-), a possible mediator of fatigue, increases as the cell acidifies and phosphate is produced. Its role in evoking muscle reflexes is unknown. We used 31P-nuclear magnetic resonance to measure forearm muscle H+ and H2PO4- and microneurography to measure muscle sympathetic nerve activity (MSNA, peroneal nerve) during a handgrip protocol designed to dissociate H+ from H2PO4-. Ischemic handgrip (50% maximal voluntary contraction x 2 min) was followed by a 1-min rest period during which the muscle was freely perfused. This was followed by a second bout of ischemic handgrip and a 5-min recovery. In seven of eight subjects, MSNA correlated with H2PO4-, whereas it correlated with pH in only one subject. To determine whether muscle reflex responses are evoked by H+, lactic acid, monoprotonated phosphate (HPO4(2-), or H2PO4-, we injected H+, lactate, H2PO4- [all 50 mM in 10 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffered to pH 6], and HPO4(2-) (50 mM, pH 7.5 in 10 mM HEPES) into the arterial supply of the triceps surae of the cat (n = 9) as we measured mean arterial blood pressure (MAP). H2PO4- increased MAP more than HPO4(2-), H+, or lactate (27.1 +/- 3.7 vs. 5.0 +/- 1.3, 4.6 +/- 3.1, and 7.7 +/- 3.2 rise in mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Hemodilution and Resuscitation on Tumor Interstitial Fluid Pressure, Blood Flow, and Oxygenation

Hemodilution due to hemorrhage may increase tumor blood flow (TBF) by lowering blood viscosity and decrease tumor interstitial fluid pressure (TIFP) by moving fluid from the interstitium to the vascular compartment and by lowering microvascular pressure (MVP), mainly due to the decrease in systemic pressure. To test this hypothesis, we measured mean arterial blood pressure (MABP), TIFP, hematocrit, relative TBF (RBC flux), and intratumor p O2 during hemorrhage and volume restitution in severe combined immunodeficient mice, bearing LS174T human colon adenocarcinoma xenografts. MABP and TIFP significantly decreased after 0.2 ml of blood (∼12% of blood volume) was withdrawn. MABP decreased from 87.5 ± 3.9 mmHg (mean ± standard error) to 59.8 ± 4.8 mmHg (n = 5, P = 0.01) within 2.5 rain after the withdrawal of blood and then returned to control value within 10 min. TIFP gradually decreased from 18.7 ± 2.3 mmHg to 11.3 ± 0.9 mmHg after 1 hr (n = 8, P = 0.01), while RBC flux increased by a factor of 1.99 ± 0.38 (n = 5, P = 0.02). The systemic hematocrit decreased from 51.2 to 45.9% (n = 7, P = 0.02). Tumor oxygenation did not significantly improve (median pO2 = for control, 28 mmHg, and median p O2 after blood withdrawal, 32 mmHg; P = 0.14). When 0.2 ml blood was withdrawn and replaced (within 2.5 min) with the same volume of normal saline, MABP significantly decreased from 86.4 ± 2.4 mmHg to 65.6 ± 4.6 mmHg (n = 11) at 1 hr post-treatment (P = 0.001). TIFP decreased, but not significantly, from 24.2 ± 2.9 mmHg to 20.4 ± 2.4 mmHg (P = 0.35). Blood withdrawals in excess of 0.3 ml significantly decreased MABP and TIFP without recovery during 1 hr of observation. Volume restitution with hyperoncotic/hyperosmotic 6.0% Dextran 70 and 7.5% saline had effects attributable to a direct transmission of systemic pressure to the tumor microcirculation and to a lowering of tumor venous resistance. These effects appear to be common to saline blood restitution and volume top-load with Dextran 70. In conclusion, mild hemorrhage (withdrawal of ∼12% of blood volume) can significantly lower TIFP without a reduction in TBF and pO2.

Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine

The influence of the release of endothelium-derived nitric oxide (NO) on the vasoconstrictor response to phenylephrine (PE) was evaluated before and after a single bout of dynamic exercise. Each rat ran on a motor-driven treadmill at 12-18 m/min, 10-18% grade until exhaustion (avg time 45 min). Sprague-Dawley rats (n = 6) were instrumented with a Doppler ultrasonic flow probe around the right common iliac artery. Just distal to the flow probe, a catheter was placed into the right iliac artery for local infusions. A Teflon catheter was placed in the descending aorta to measure mean arterial blood pressure (MAP) and heart rate (HR). PE (0.005-0.075 microgram/kg) and NO inhibitor N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME, 0.2-0.25 mg/kg) were injected into the functionally isolated hindlimb. HR and MAP were not altered by any of the injections because we selected doses below those which elicited systemic responses. Dose-response curves to PE were generated in the control and postexercise condition, with and without the NO synthase inhibitor L-NAME. Exercise significantly attenuated the maximal vasoconstrictor response to PE (45.6 +/- 1.6%). L-NAME enhanced the maximal vasoconstrictor response to PE 49.8 +/- 4.5% in the control condition and 121.4 +/- 5.9% in the postexercise conditions. Thus, although NO inhibition enhanced the vasoconstrictor response to PE in the control and postexercise conditions, the enhanced vasoconstrictor response to PE after L-NAME was significantly greater in the postexercise condition. Results suggest that NO contributes to the exercise induced attenuation of alpha 1-adrenergic receptor stimulation.

Neuropathological changes during generalized seizures in newborn monkeys

The brains of four 2-week-old marmoset monkeys were perfusion-fixed immediately after bicuculline-induced seizures lasting 1.5–4.3 h and were later examined by light and electron microscopy. Mean arterial blood pressure and rectal temperature measurements during seizures did not differ significantly from baseline. Plasma glucose concentrations decreased to the 1.5 mM range at the end of seizures, and arterial pH and bicarbonate were lower than in control animals, although arterial pO 2 and pCO 2 were maintained. Neuropathological changes were minimal. Swollen astrocytic processes surrounded some capillaries and some neurons in cerebral cortex, hippocampus, putamen and thalamus. Almost all the neurons examined looked normal, but mitochondrial swelling was present in a few. All but the most severe mitochondrial swelling, which occurred very rarely in one of four animals, is potentially reversible. The virtual absence of neuronal necrosis in these neonatal monkeys is consistent with the resistance to seizure-induced brain damage found in immature rats, and stands in sharp contrast to the damage seen in older animals. Lack of neuronal damage, however, does not rule out potential adverse effects of prolonged seizure activity on subsequent brain growth and development.

Increments and Decrements in Mean Arterial Pressure as a Function of Audience Composition: An Averaging and Summation Analysis

Mean arterial blood pressure (MAP) measures were taken to assess performs' anxiety levels while they performed in front of heterogeneous and homogeneous audiences. The addition of one high school student to an audience of one faculty member lowered MAR whereas the addition of the same student to an audience of one high school student raised MAP In addition, subjects' MAP levels were elevated when their performance was observed by a faculty member and by two high school students relative to a setting in which no audience was present (i.e., an alone condition). The results support predictions made by the averaging-summation model and suggest that individuals are sensitive to both the average and the summative impact of evaluative audience members. 7he importance of considering the composition of audiences for predictions about individuals' anxiety levels is discussed.

Relationship between the hydralazine-induced changes in murine tumor blood supply and mouse blood pressure

The relationship between hydralazine-induced changes in blood pressure and tumor blood flow was investigated in restrained but non-anesthetized CDFI mice bearing C3H/Tif foot tumors. Mean arterial blood pressure measurements were made using the procedure of carotid cannulation, and tumor blood flow was estimated using laser Doppler flowmetry. Hydralazine doses from 0.1 to 5.0 mg/kg were tested. Following hydralazine administration the maximum changes in blood pressure and blood flow were apparent within 10–15 min and were maintained for at least 30 min after injection. Blood pressure decreased with increasing hydralazine dose, achieving a maximum reduction of 50% at 2.5 mg/kg. Tumor blood flow was found to be increased by 30% at the lowest hydralazine dose (0.1 mg/kg), even though blood pressure was decreased by 10% at this dose. At hydralazine doses producing a 15% or greater blood pressure drop, blood flow decreased, reaching an 80–90% reduction between 2.5 and 5.0 mg/kg.

Changes of blood pressure and cerebral arterio‐venous oxygen content differences (AVDo2) with and without bupivacaine scalp infiltration during craniotomy

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the effect of scalp infiltration with bupivacaine before incision was evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. All patients were given halothane 0.5% anaesthesia. Ten patients were given bupivacaine 0.25% and ten patients were given normal saline for scalp infiltration prior to incision. The study was performed in a double-blind randomized fashion. Significantly higher values of MABP (P less than 0.0005) after incision were found in the saline group compared to the bupivacaine group. Significantly lower values of AVDO2 (P less than 0.0005) after incision were seen in the saline group compared to the bupivacaine group. The results indicate that the increase in MABP associated with a decrease in AVDO2, suggesting an increase in CBF and cerebral hyperperfusion, is reduced by using bupivacaine scalp infiltration prior to incision.

The cerebral arterio‐venous oxygen content differences (AVDo2) during halothane and neurolept anaesthesia in patients subjected to craniotomy

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the haemodynamic changes during halothane and neurolept anaesthesia were evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. Ten patients were given 0.5% halothane anaesthesia and ten patients neurolept anaesthesia. MABP, AVDO2 and PaCO2 were measured after induction of anaesthesia, before and after incision, after opening and closure of the dura, at the time of extubation and 1 h later. Concerning MABP and PaCO2, no significant difference between the two groups was found. In both groups an increase in MABP was observed after incision (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group) and in the neurolept group after extubation (P less than 0.01). In both groups a decrease in AVDO2 was observed after incision (P less than 0.01) and after extubation (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group). During the operation AVDO2 values were significantly higher in the neurolept group (P less than 0.05). The results indicate that even a moderate increase in MABP after incision during neuroanaesthesia affects AVDO2 values, suggesting an increase in cerebral blood flow. The study suggests that autoregulation of cerebral blood flow might be better preserved during neurolept anaesthesia. A state of hyperperfusion of the brain after extubation was unveiled in both groups.

Severe birth asphyxia and abnormal cerebral blood-flow velocity.

Thirty-four fullterm infants with postasphyxial encephalopathy (PAE) were studied with ultrasound to assess cerebral blood-flow velocity (CBFV). A control group of 126 healthy infants also had CBFV recordings during the first week of life. Measurements for the majority of the asphyxiated group fell into two abnormal patterns in relation to the control group: four had low CBFV (less than 2 SD below the mean) and 17 had high CBFV (greater than or equal to 2 SD above the mean); all had severe PAE. Median age at the first high measurement was 26 hours. There were no statistically significant differences between infants with normal and abnormal CBFV in measurements of PaCO2 or mean arterial blood-pressure. A Pourcelot Resistance Index (PRI) less than 0.55 was common in the presence of high CBFV, but never seen with low measurements. 21 of the 34 infants died of their asphyxial insult and four of the survivors have severe cerebral palsy at a median age of two years. Three of the four with low CBFV died, and no infant with CBFV greater than 3 SD survived without severe impairment. The positive predictive value of CBFV measurements less than 2 SD or greater than 3 SD for death or severe impairment is 94 per cent, compared with 83 per cent for low PRI alone. The authors believe that high CBFV is the result of vasoparalysis of cerebral arterioles and that it represents a form of irreversible cerebral injury.

Differential effects of sleep stage on coronary hemodynamic function during stenosis.

We have demonstrated in a previous study that in the normal heart REM sleep induces surges in heart rate and coronary blood flow which are abolished by bilateral stellectomy. To study the effects of sleep in the stenosed coronary circulation, dogs were instrumented with Doppler flow probes and hydraulic occluders around the left circumflex coronary artery to measure coronary blood flow and to produce a 60% flow reduction. Catheters were placed in the aorta to measure mean arterial blood pressure. Electrodes were implanted via the frontal sinus to identify sleep stages. In the absence of stenosis, mean blood pressure was 95 +/- 3 mmHg, HR was 111 +/- 4 bpm, and coronary blood flow was 33 +/- 2 ml/min. During stenosis, REM induced episodic increases in heart rate which were accompanied by 38% decreases in coronary blood flow. We conclude that in the stenosed coronary circulation, REM sleep produces episodic sinus tachycardia and coronary blood flow reduction.

Myocardial insulin resistance during acute endotoxin shock in dogs.

Myocardial insulin responsiveness was determined in open-chest pentobarbital sodium-anesthetized dogs before and after endotoxin administration. Animals were instrumented to measure mean arterial blood pressure (MABP), heart rate (HR), and coronary blood flow. Myocardial glucose uptake and myocardial oxygen uptake (MVO2) were determined during a basal control period and after a hyperinsulinemic-euglycemic clamp procedure over a wide range of insulin concentrations. The clamp was accomplished by intravenously infusing insulin (0-4000 mU/min) and 20% glucose in sufficient amounts to maintain arterial glucose concentrations within 5 mg/dl of the control value. In a separate series of experiments, myocardial insulin responsiveness was determined by use of a single dose of insulin (4000 mU/min). This was done to determine whether antecedent insulin infusions during the sequential clamp procedure would affect the responsiveness of the heart. In control experiments, myocardial glucose uptake increased without any changes in HR, MVO2, or MABP. Maximum myocardial glucose uptake occurred at an insulin infusion rate between 400 and 4000 mU/min. A single concentration of insulin resulted in similar increases in myocardial glucose uptake as with the sequential clamp protocol. Acute endotoxin shock was induced by bolus injection of 1 mg/kg Salmonella typhimurium endotoxin (Difco Labs, Detroit, MI). One hour after administration of endotoxin, basal myocardial glucose uptake was decreased compared with the control animals. After 1 h of endotoxin shock, the heart was refractory to all concentrations of insulin, suggesting the site for altered insulin response was being mediated by a postreceptor mechanism.

Evidence for a Cardiovascular Role of Central Galanin Neurons: Focus on Interactions with α2-Adrenergic and Neuropeptide Y Mechanisms

By means of immunocytochemical analysis using the indirect immunofluorescence method, and by means of receptor autoradiography using 125I-galanin as a radioligand, further evidence has been obtained for the existence of pre- and postsynaptic features of galanin neurons in the nucleus tractus solitarius (nTS) and the dorsal motor nucleus of the vagus (dmnX) of the male rat. Thus, a high density of galanin immunoreactive nerve terminals was found within the medial subnucleus of the nTS, in the periventricular region and within the medial part of the dmnX. High densities of 125I-galanin binding sites were found in the entire medial and lateral part of the nTS and in the dmnX as evaluated at a level approximately 1-2 mm rostral to obex. The physiological studies were performed in a-chloralose anesthetized male rats by injecting galanin in the nmolar range i.c. and measuring mean arterial blood pressure and heart rate (HR). The results showed a weak hypotensive action of galanin (3 nmol) and a clearcut tachycardic action (10 nmol). When administered simultaneously with clonidine no additive effects were observed on mean arterial blood pressure but the bradycardic action of clonidine was blocked and the tachycardic action of galanin prevailed. Similar results were obtained when galanin was injected simultaneously with NPY. These results indicate a cardiovascular role of galanin, and the morphological evidence favors the view that the galaninergic mechanism involved is located within the dorsal cardiovascular center of the medulla oblongata. The results obtained on the interaction of galanin synapses with α2-adrenergic and NPY mechanisms are of substantial interest, since they indicate that the descending fibers from the hypothalamic defense area by activating galaninergic mechanisms in the nTS can override the bradycardic action of α2-adrenoreceptor activation within the medulla oblongata and thus probably also the bradycardic effects of activation of the vasodepressor reflex arch.

Evaluation of a direct blood pressure measurement technique for canine toxicity studies

Repeated direct puncture of the central ear (intermediate auricular) artery to obtain mean arterial blood pressure in control and hypertensive dogs was evaluated. Unilateral nephrectomy and partial constriction of the contralateral renal artery were performed on four dogs to create hypertension. Ear artery blood pressure measurements and electrocardiograms were recorded twice pretest and after surgery at Weeks 1, 2, 4, 6, 8, 9, 10, and 11 on control ( n = 6) and hypertensive ( n = 4) dogs. Mean ear arterial blood pressures from the hypertensive dogs were significantly increased from Weeks 2 to 11. Indwelling omocervical artery catheters were implanted in both control and hypertensive dogs at Week 8. Mean omocervical artery blood pressures from hypertensive dogs were significantly increased at Weeks 8 through 11. Mean omocervical artery pressures were only significantly increased over mean ear artery pressures at Week 8 for control dogs and at Week 10 for hypertensive dogs. Nonspecific electrocardiographic changes in the ST-T segment and U waves occurred with greater frequency in hypertensive dogs than in control dogs. Hypertensive dogs developed subendothelial proliferation in the renal artery and aorta, and a proliferative vasculopathy in the heart and lungs. This ear artery technique was used successfully in two canine toxicity studies of different ICI pharmaceutical compounds. The ear artery method for measuring mean arterial blood pressure is suitable for canine toxicity studies and is a reasonably accurate measurement of systemic pressure.

An evaluation of blood pressure measurement.

The accuracy of routine measurements by nursing staff of systemic arterial, central venous, pulmonary artery and pulmonary capillary wedge pressures was determined. There was a significant difference between direct mean arterial blood pressure measurements and routine indirect measurements by the nursing staff in the pressure range of 50--100 mmHg, whereas there was no significant difference between direct and indirect measurements when indirect measurements were made by specially trained hypertension clinic personnel. However, there was a good correlation between direct and indirect measurements in each instance, indicating that changes in blood pressure could be adequately followed by both groups. Systems commonly used to measure blood pressure directly were tested. Limits in frequency response preclude the routine direct measurement of systolic or diastolic blood pressures. If direct systolic and diastolic pressure measurements are required, it is necessary to check the performance of the amplifier and recording system, attach the transducer to the patient, and determine and adjust, if necessary, the natural frequency and damping coefficient of each system before each measurement. However, it is suggested that a knowledge of systolic and diastolic pressure measurements seldom improves patient management, and if mean pressures are accepted, reliable routine measurements may be obtained by the nursing staff. The digital display of the systems tested may be accepted for mean arterial pressure, but for accurate mean central venous and pulmonary capillary wedge pressure measurements, it is necessary to interpret the trace on a chart recorder; pulmonary artery pressure can often only be estimated.

Portal and aortic blood sampling technique in unrestrained rats

A composite cannula has been designed to permit blood sampling from the distal aorta and portal vein in unanesthetized, unrestrained rats. The aortic and portal cannulas were constructed from polyvinylchloride (PVC) tubing drawn to a fine tip and fused to polyethylene tubing (PE 50). The portal vein was cannulated via a mesenteric vein. The abdominal aorta was cannulated non-occlusively. Both vascular cannulas were securely tied to the abdominal wall. A silicone rubber duodenal cannula was inserted into the membraneous portion of the stomach and passed into the duodenal lumen. Its end was tunnelled under the skin to the rat's back and placed under a wound clip. The utility of these cannulas was illustrated by simultaneous sampling of aortic and portal vein blood during absorption of labelled amino acids. These chronic cannulas can be used to study behavioral or physiologic parameters while selectively infusing compounds into the duodenum or portal vein. The aortic cannula can be used to measure mean arterial blood pressure, to sample blood, or to infuse the caudal part of the rat.

Rapid measurement of blood pressure in the sick neonate.

We measured mean arterial blood pressure using a hydrostatic technique in 24 sick neonates who had umbilical artery catheters in place. Value for blood pressure obtained with this technique correlated significantly (r = 0.9844, P less than 0.01) with measurements obtained with standard strain gauge and electronic monitor. The method is simple, quick, and safe. It is particularly useful when the infant's size or clinical condition precludes the use of the sphygmomanometer or Doppler ultrasound device or in a setting, such as during transport, when standard electronic means of blood pressure measurement are unavailable.

Response of the circulation of pregnant sheep to angiotensin and norepinephrine before and after dexamethasone

We studied the vascular reactivity of the systemic and uterine circulations of six pregnant sheep. We placed catheters in a maternal carotid artery and a jugular vein, and then implanted an electromagnetic flow transducer around the uterine artery of the pregnant horn. After allowing 3 days for recovery from anesthesia and operation, we measured mean arterial blood pressure, heart rate, uterine blood flow, and calculated uterine vascular resistance, then separately infused angiotensin and norepinephrine in each ewe at the rate that produced a 20 torr pressor response. Dexamethasone, 0.2 mg. per kilogram of body weight, was then injected intravenously daily for 2 to 4 days. On the day following the final injection of dexamethasone, we separately infused angiotensin and norepinephrine at a rate that, before steroid treatment, produced a 20 torr pressor response. Administration of dexamethasone for 2 to 4 days did not change mean arterial blood pressure, heart rate, uterine blood flow, or uterine vascular resistance. Prior to steroid treatment, angiotensin increased blood pressure, decreased heart rate, but had no consistent effect on uterine blood flow or uterine vascular resistance; norepinephrine increased blood pressure without chenging heart rate, decreased uterine blood flow, and increased uterine vascular resistance. The changes produced by angiotensin and norepinephrine were the same after dexamethasone treatment. These studies indicate that dexamethasone does not influence systemic and uterine vascular reactivity during normal sheep pregnancy.