Carotid Blood Pressure in Normal and Tumor-Bearing Mice

1956 ◽  
Vol 184 (3) ◽  
pp. 599-604 ◽  
Author(s):  
Sachindra N. Pradhan ◽  
Betty Achinstein ◽  
Murray J. Shear

Blood pressure was measured directly in mice after cannulation of the carotid artery. The anesthetic was urethan in a single intraperitoneal dose of 1.4–1.6 mg/gm. The apparatus was a Technitrol Lilly manometer, or a Statham physiological transducer (Model P 23 D) with a Brush ‘Universal analyzer.’ The blood pressure was continuously recorded in some 400 CAF1 mice, both normal and bearers of Sarcoma 37. In 166 mice without tumor, the mean blood pressure varied from 35–110 mm of mercury; the average was 71 with a S.E. of ± 1. In 233 mice bearing 6-day-old implants of Sarcoma 37, the pressure varied from 40–110 mm.; the average was 78 ± 1 mm. Under these conditions of continuous recording of arterial blood pressure, about 40% of the animals lived for 2 hours; a few survived as long as 6 hours. The various patterns of blood pressure changes are described and illustrated.

2021 ◽  
Vol 7 (2) ◽  
pp. 815-818
Author(s):  
Robert Huhle ◽  
Thorsten Richter ◽  
Marcelo Gama de Abreu

Abstract Considering accuracy/precision cut-offs of 5 ± 8 mmHg and cut-off values for inter-class correlation coefficients (ICC=0.37...1, from DIN EN ISO 81060-2), absolute and relative errors in time independent measurement of blood pressure changes with non-invasive intermittent devices (NiBP) are derived mathematically for mean arterial blood pressure range of 40-180 mmHg. As a clinically relevant value for change of arterial blood pressure 20% of the baseline blood pressure is considered. The mean ratio between the change of BP measured by the NiBP and measured by the invasive reference device (TE%) were proposed as quality measure for the evaluation of NiBP device tracking capability. The proposed measure TE%is theoretically independent of absolute accuracy but depends on precision and ICC of a device. NiBP devices show considerable maximum TE% of 41% in tracking mean blood pressure changes respectively. In 10% of the measurements in the low blood pressure range TE% exceeding 100%. The mean 50th/90th TE% percentile over the whole blood pressure range were 25/61%, respectively. Furthermore, TE% was relatively insensitive to assumed blood pressure range but sensitive to ICC. NiBP devices have high relative error in tracking blood pressure changes that make those devices not well-suited for tracking blood pressure changes. The proposed tracking error allows the definition of reasonable accuracy/precision requirements of NBP devices.


1958 ◽  
Vol 192 (2) ◽  
pp. 345-352 ◽  
Author(s):  
W. J. Roberson ◽  
Steven M. Horvath

Twelve experiments were conducted on anesthetized and paired dogs of similar weights subjected to unimpeded, unregulated crossed circulation. Shunts were made between the carotid arteries and external jugular veins and free flow allowed for 60 minutes or longer. Statistically significant changes occurred in the mean femoral arterial blood pressures, carotid shunt blood flow, heart rate, cardiac output, cardiac work, percentage of cardiac output flowing through the shunt and pulmonary systolic and diastolic pressures of one or both animals from their control values. The mean arterial blood pressure remained at control levels for several minutes and then dropped precipitously to hypotensive levels. The lowest mean pressures between 42 and 49 mm Hg occurred within the first 16.5 minutes of the open shunt phase with a gradual return toward control levels. The volume of blood flowing through the shunt was increased initially 250% above the control carotid blood flow, followed by a reduction in flow after 15 minutes; the volume flow at this moment was still double precross circulation levels. A secondary increase in the shunt blood flow occurred throughout the remainder of the open shunt phase. In general, the heart rates and peripheral vascular resistance were slightly elevated during the open shunt phase while cardiac output and work decreased below their control values. A marked and similar increase in the percentage of the cardiac output flowing through the carotid artery was observed in both animals. During the 60 minutes of the recovery period mean arterial blood pressure, cardiac output and work tended to return to control levels while the carotid artery blood flow and pulmonary systolic and diastolic pressure remained slightly below their control values.


1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.


Author(s):  
Abigail Flower ◽  
Daniel Vasiliu ◽  
Tianrui Zhu ◽  
Robert Andris ◽  
Maryam Abubakar ◽  
...  

Objective This study aimed to evaluate the role of an objective physiologic biomarker, arterial blood pressure variability, for the early identification of adverse short-term electroencephalogram (EEG) outcomes in infants with hypoxic-ischemic encephalopathy (HIE). Study Design In this multicenter observational study, we analyzed blood pressure of infants meeting these criteria: (1) neonatal encephalopathy determined by modified Sarnat exam, (2) continuous mean arterial blood pressure (MABP) data between 18 and 27 hours after birth, and (3) continuous EEG performed for at least 48 hours. Adverse outcome was defined as moderate–severe grade EEG at 48 hours. Standardized signal preprocessing was used; the power spectral density was computed without interpolation. Multivariate binary logistic regression was used to identify which MABP time and frequency domain metrics provided improved predictive power for adverse outcomes compared with standard clinical predictors (5-minute Apgar score and cord pH) using receiver operator characteristic analysis. Results Ninety-one infants met inclusion criteria. The mean gestational age was 38.4 ± 1.8 weeks, the mean birth weight was 3,260 ± 591 g, 52/91 (57%) of infants were males, the mean cord pH was 6.95 ± 0.21, and 10/91 (11%) of infants died. At 48 hours, 58% of infants had normal or mildly abnormal EEG background and 42% had moderate or severe EEG backgrounds. Clinical predictor variables (10-minute Apgar score, Sarnat stage, and cord pH) were modestly predictive of 48 hours EEG outcome with area under curve (AUC) of 0.66 to 0.68. A composite model of clinical and optimal time- and frequency-domain blood pressure variability had a substantially improved AUC of 0.86. Conclusion Time- and frequency-domain blood pressure variability biomarkers offer a substantial improvement in prediction of later adverse EEG outcomes over perinatal clinical variables in a two-center cohort of infants with HIE. Key Points


1990 ◽  
Vol 68 (6) ◽  
pp. 2391-2393 ◽  
Author(s):  
T. Matsuse ◽  
Y. Fukuchi ◽  
T. Suruda ◽  
T. Nagase ◽  
Y. Ouchi ◽  
...  

We examined the effect of endothelin-1 (ET-1), a novel 21-residue vasoconstrictor peptide, on pulmonary resistance (RL) in Wistar rats. The lung volume, tracheal flow, and transpulmonary pressure of tracheotomized and paralyzed rats were measured with a fluid-filled esophageal catheter and a pressure-sensitive body plethysmograph. RL was calculated by the method of von Neergaard. The femoral artery was cannulated to measure the mean arterial blood pressure. Intravenous bolus administration of synthetic ET-1 provoked a dose-dependent increase in RL in rats. The bronchoconstricting effect reached maximum at 500 pmol/kg. This bronchoconstriction was observed in less than 5 min, increased up to 15 min, and was sustained for 60 min. ET-1 increased the mean arterial blood pressure in a dose-dependent manner. We conclude that ET-1 is a hitherto unknown potent bronchoconstrictor that has a sustained effect in vivo. The potential physiological and pathophysiological role of this new peptide in the development of respiratory disease warrants further investigation.


1961 ◽  
Vol 16 (2) ◽  
pp. 348-350 ◽  
Author(s):  
Florian Nykiel ◽  
Vincent V. Glaviano

In dogs with left adrenal cannulation, administration of 1 mg/kg of purified E. coli endotoxin resulted in a decrease in mean blood pressure and adrenal blood flow. These changes were accompanied by significant increases in levels of epinephrine in adrenal venous blood. Release of epinephrine by the adrenals in endotoxin shock was due to a neurogenic mechanism, since sectioning of the splanchnic nerves prevented secretion of epinephrine. The rise in epinephrine output from an intact adrenal was noted to occur only in the presence of a significant decrease in arterial blood pressure; therefore endotoxin causes adrenal stimulation from reflexes initiated by the hypothalamus or peripheral baroreceptors. Submitted on September 20, 1960


1959 ◽  
Vol 196 (4) ◽  
pp. 715-718 ◽  
Author(s):  
Leslie A. Kuhn ◽  
Lot B. Page ◽  
John K. Turner ◽  
Julian Frieden

Effects of progressive hemorrhage during severe cold exposure were studied in 17 unanesthetized dogs. The amount of blood required to be withdrawn to reduce the mean arterial blood pressure to 50 mm Hg by a standardized bleeding procedure was determined in the same animals at air temperatures of +25°C and –25°C. Cold-exposed dogs showed a statistically significant increased ‘resistance’ to hemorrhage in that an average withdrawal of 20% more blood was required to reduce mean arterial blood pressure to shock levels in the cold than in the same dogs at comfortable temperature. In six animals it was necessary to draw a minor, but measurably greater, amount of blood from a given dog to produce hypotension during cold exposure than when the procedure was performed at a comfortable temperature and, in two animals, a minor, but measurably less, amount of blood was withdrawn during cold exposure. In seven animals a significantly greater amount of blood was drawn in the cold than in a neutral environment, but in some of these animals the control bleeding was apparently substandard. In two animals the control bleedings were in the normal range and bleedings were substandard in the cold. Cortisone administration did not alter resistance to hemorrhage during cold exposure.


1989 ◽  
Vol 67 (5) ◽  
pp. 423-427 ◽  
Author(s):  
J. Kettler ◽  
B. Y. Ong ◽  
D. Bose

Pial arteriolar diameter changes inversely with changes in systemic arterial blood pressure. Such changes are consistent with autoregulatory functions. These responses are reduced by a brief period of hypoxia followed by reoxygenation. By using an open cranial window preparation we assessed the changes in pial arteriolar diameters during blood pressure changes in rats induced by hemorrhage and reinfusion of blood, before and after a brief period of hypoxia. The slopes of the changes in pial arteriolar diameter as a function of mean arterial blood pressure were −0.47 ± 0.26 μm/mmHg (mean ± SD; 1 mmHg = 133.3 Pa) before hypoxia and −0.11 ± 0.23 μm/mmHg after hypoxia in the untreated rats. In ouabain-treated rats, corresponding slopes were −0.42 ± 0.24 and −0.46 ± 0.22 μm/mmHg. The observed protective effects of ouabain might be a blockade of the Na–K pump in the sarcolemma of the vascular smooth muscle.Key words: vascular smooth muscle, electrogenic sodium pump, metabolic inhibition.


2002 ◽  
Vol 172 (2) ◽  
pp. 303-310 ◽  
Author(s):  
E Bojanowska ◽  
B Stempniak

To date, glucagon-like peptide 1(7-36) amide (tGLP-1) has been found to affect the neurohypophysial and cardiovascular functions in normotensive and normovolaemic rats. The aim of the present study was to investigate possible effects of tGLP-1 on the mean arterial blood pressure and the release of vasopressin and oxytocin under conditions of blood volume depletion in the rat. In the first series of experiments, the animals were injected i.p. with either 0.15 M saline or 30% polyethylene glycol (PEG). PEG caused an 18% reduction of blood volume 1 h after injection. No significant changes in the mean arterial blood pressure were found in either normo- or hypovolaemic rats during the experiment. tGLP-1 injected i.c.v. at a dose of 1 microg/5 microl 1 h after the i.p. injection increased similarly the arterial blood pressure in normo- and hypovolaemic rats. The plasma vasopressin/oxytocin concentrations were markedly elevated in hypovolaemic animals and tGLP-1 further augmented the release of both hormones. In the second study, hypovolaemia was induced by double blood withdrawal. The haemorrhage resulted in a marked decrease of the mean arterial blood pressure and in the elevated plasma vasopressin/oxytocin concentrations. tGLP-1 injected immediately after the second blood withdrawal increased the arterial blood pressure. In parallel, tGLP-1 enhanced significantly vasopressin and oxytocin secretion when compared with haemorrhaged, saline-injected rats. The results of this study indicate that tGLP-1 may affect the arterial blood pressure and the secretion of neurohypophysial hormones under pathological conditions brought about by blood volume depletion.


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