HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

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.


1958 ◽  
Vol 193 (1) ◽  
pp. 147-150 ◽  
Author(s):  
René Wégria ◽  
J. Nakano ◽  
J. C. McGiff ◽  
D. F. Rochester ◽  
M. R. Blumenthal ◽  
...  

In the anesthetized dog, acute arteriovenous fistulae sufficient to increase the cardiac output by from 16 to 130% resulted in an increase in the coronary blood flow even in the presence of a definite and even marked drop in the mean arterial blood pressure. The arteriovenous fistulae also resulted in an increase of the cardiac work and oxygen consumption as well as the cardiac efficiency.


1956 ◽  
Vol 186 (3) ◽  
pp. 525-528 ◽  
Author(s):  
G. B. Spurr ◽  
Steven M. Horvath ◽  
Enid Allbaugh Farrand

Chlorpromazine in doses of 2 and 5 mg/kg has been found to produce an initial hypotension in anesthetized dogs which was followed by return of the mean arterial blood pressure to near control levels. During the next 60–65 minutes there was a secondary decline in the pressure to hypotensive levels. Both an initial and secondary hypotension were the result of a decrease in peripheral vascular resistance.


In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.


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.


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.


1960 ◽  
Vol 199 (2) ◽  
pp. 221-225 ◽  
Author(s):  
Kathryn Ballard ◽  
Allan Lefer ◽  
George Sayers

Heart-lungs from intact rats were perfused with blood from intact rats (intact-intact preparations) or with blood from adrenalectomized rats (intact-adrenalectomized preparations). Left ventricular work index (LVWI) was employed to evaluate performance of the heart-lung and calculated as the product of cardiac output and mean arterial blood pressure. In confirmation of a previous report from this laboratory, LVWI was less for intact-adrenalectomized preparations than for intact-intact preparations. Aldosterone, added to perfusion blood from adrenalectomized rats to make a concentration of 2 x 10–3, 8 x 10–3 or 3.2 x 10–2 µg/100 ml, increased LVWI of the intact-adrenalectomized preparation to that of the intact-intact preparation. Extracts of plasma from intact rats, which may be expected to contain corticosteroids, were also capable of increasing LVWI of the intact-adrenalectomized preparation. Extracts of plasma from adrenalectomized rats were inactive.


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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