Effects of progesterone and pregnancy on systemic and regional hemodynamics in rats

1998 ◽  
Vol 5 (1) ◽  
pp. 131A-131A
Author(s):  
P GANGULA ◽  
D DIPETTE ◽  
H ZHAO ◽  
R BUKOSKI ◽  
S SUPOWIT ◽  
...  
1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.


1991 ◽  
Vol 112 (6) ◽  
pp. 1745-1747 ◽  
Author(s):  
M. N. Ivashev ◽  
O. S. Medvedev ◽  
V. B. Koshelev ◽  
T. V. Ryasina

1990 ◽  
Vol 109 (1) ◽  
pp. 24-27
Author(s):  
E. Yu. Bychkova ◽  
E. R. Martynova ◽  
O. S. Medvedev ◽  
V. P. Krotov ◽  
F. E. Meertsuk

1989 ◽  
Vol 257 (3) ◽  
pp. H918-H926 ◽  
Author(s):  
M. M. Knuepfer ◽  
S. P. Han ◽  
A. J. Trapani ◽  
K. F. Fok ◽  
T. C. Westfall

Endothelin is a peptide with potent, long-lasting pressor effects characterized by increases in mesenteric and hindquarters vascular resistance and bradycardia following an initial, transient depressor response. This study examined the mechanisms of action of endothelin on regional hemodynamics in conscious, freely moving rats and on baroreflex sensitivity both in conscious and chloralose-anesthetized rats. The pressor response to endothelin (0.67 nmol/kg) was attenuated by nifedipine (25 micrograms/kg) and augmented by chloralose anesthesia. The bradycardia was attenuated by pentolinium (10 mg/kg), atropine methyl sulfate (0.5 mg/kg), or chloralose anesthesia. Hindquarter vaso-constriction was attenuated by nifedipine, pentolinium, and atropine, whereas mesenteric vasoconstriction was less sensitive to blockade. The vasopressin V1 antagonist, [d(CH2)5Tyr(Me)]-AVP (20 micrograms/kg), indomethacin (5 mg/kg), or verapamil (150 micrograms/kg) did not affect any of these cardiovascular responses. Renal sympathetic nerve activity was reduced similarly in chloralose-anesthetized rats to pressor responses elicited by either phenylephrine or endothelin, and the slope of the baro-reflex function curve after endothelin was similar to that of phenylephrine. These results suggest that endothelin is a potent vasoconstrictor in which its action on visceral and skeletal muscle vasculature is mediated by somewhat different mechanisms. Endothelin does not alter baroreceptor reflex control of sympathetic nerve activity or heart rate.


Author(s):  
Douglas Kondziolka ◽  
Bruce J. Nixon ◽  
Pierre Lasjaunias ◽  
Pierre Lasjaunias ◽  
William S. Tucker ◽  
...  

ABSTRACT:The common vascular anomalies of cerebral aneurysm and arteriovenous malformation may exist independently, or together as part of a closely related hemodynamic pairing. Resection or embolization of an AVM may be followed by a decrease in local blood flow, and lead to regression of a suitably situated proximal aneurysm. However, aneurysms located outside the angioarchitecture of the AVM, which remain flow-unrelated to the malformation, will likely not regress, and may in fact enlarge. Two cases are presented which demonstrate these vascular relationships, in order to better understand the regional hemodynamics of these anomalies prior to surgical or endovascular treatment planning.


1984 ◽  
Vol 247 (1) ◽  
pp. H35-H39 ◽  
Author(s):  
I. Kobrin ◽  
M. B. Kardon ◽  
W. Oigman ◽  
B. L. Pegram ◽  
E. D. Frohlich

The influences of the site of microsphere injection (intra-atrial vs. intraventricular) and positioning of the left ventricular catheter (aortoventricular vs. atrioventricular) on systemic, renal, and coronary hemodynamics were evaluated in anesthetized rats. The effect of anesthesia on aortoventricular catheter positioning was also evaluated. In anesthetized and open-chest preparations, the systemic and renal hemodynamics were not affected by catheter position or site of microsphere injection; however, myocardial blood flow was dependent on these variables. Variations in coronary blood flow were significantly greater when the catheter was in the aortoventricular position (34 +/- 3%) than with an atrioventricular catheter (11 +/- 2%, P less than 0.01), irrespective of whether the microspheres were injected into the atrium or ventricle. Comparison of anesthetized and conscious rats with aortoventricular catheter indicated lesser variability in coronary blood flow in the conscious rats (P less than 0.01). Therefore, the greater variability of coronary flow measurements in anesthetized rats was caused by the position of the cardiac catheter in the aortoventricular route. However, the variability caused by the aortoventricular catheter was much less in conscious rats. Therefore, coronary flow hemodynamic measurements (microsphere technique) are less variable when they are made in conscious rats.


1978 ◽  
Vol 234 (3) ◽  
pp. H244-H252 ◽  
Author(s):  
S. F. Vatner ◽  
M. Pagani ◽  
J. D. Rutherford ◽  
R. W. Millard ◽  
W. T. Manders

The effects of intravenous infusion of nitroglycerin (NTG), 8 and 32 microgram/kg.min for 7 min, and of sublingual NTG, 1.2 mg, were examined on direct and continuous measurements of systemic, coronary, and regional hemodynamics, left ventricular (LV) dimensions, pressures, and myocardial contractility in conscious dogs. NTG induced sustained reductions in LV dimensions and transient increases in heart rate and dP/dt, and decreases in mean arterial pressure. Initially NTG increased cardiac output and flows to the coronary, mesenteric, renal, and iliac beds, while systemic and regional vascular resistances fell. Later, cardiac output, cardiac work, and mesenteric and iliac flows fell significantly below control, and significant vasoconstriction in the systemic as well as mesenteric, iliac, and coronary beds was observed at a time when LV end-diastolic dimensions were still significantly reduced. Peripheral vasoconstriction was not observed with systemic NTG in deafferented dogs or when NTG, 1 microgram/kg.min, was infused intra-arterially into the iliac bed. Thus, systemic NTG induces a biphasic response consisting of initial arteriolar vasodilation followed by vasoconstriction in the mesenteric, iliac, coronary and systemic beds, which is presumably due to longer lasting effects on preload and to secondary reflex responses to the drug.


1982 ◽  
Vol 52 (3) ◽  
pp. 647-654 ◽  
Author(s):  
S. Enjeti ◽  
P. B. Terry ◽  
H. A. Menkes ◽  
R. J. Traystman

The role of mechanical interdependence in the perfusion of atelectatic lung was studied in two ways: a) regional hemodynamics were compared before (control) and after the development of lobar and sublobar atelectasis, and b) the effect of thoracotomy on regional hemodynamics was assessed. With lobar atelectasis mean lobar blood flow and vascular conductance decreased to 60% of control. Sublobar atelectasis caused mean sublobar blood flow and vascular conductance to decrease to 6% of control. Opening the chest after production of lobar atelectasis caused blood flow to fall to 50% of control. When sublobar atelectasis was produced in the open chest, sublobar blood flow decreased to 25% of control measurements made prior to thoracotomy. We conclude that with a closed chest, sublobar vascular distortion mediated by mechanical interdependence may be an important mechanism responsible for the differences in hemodynamic responses to atelectasis between lobes and sublobar regions.


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