Hemodynamics of hemorrhage in the conscious rat and chicken

1986 ◽  
Vol 251 (5) ◽  
pp. R846-R850 ◽  
Author(s):  
J. M. Ploucha ◽  
G. D. Fink

Hemodynamic responses to hemorrhage in conscious chicks (n = 10, 233 g) and rats (n = 10, 309 g) were compared. The animals were fitted with miniature pulsed Doppler aortic flow probes 2 days (chickens) or 5 days (rats) before catheterization, and the experiment began 1 (chickens) or 2 (rats) days later. Mean arterial pressure (MAP) and cardiac output (CO) were recorded continuously and simultaneously digitized to compute total peripheral resistance (TPR). MAP, CO, and TPR values were graphed on-line by a microcomputer and stored for later analysis. A 4-ml hemorrhage reduced MAP and CO by 25 and 43% in the rat, and 15 and 4% in the chickens, respectively. The fall in CO in the rat was due to reduction of stroke volume (SV) unlike the birds where SV was well maintained. TPR was elevated 65% in the rats and fell 13% in the chickens. The minimal fall in CO and SV in these conscious birds suggests that anesthetic agents used previously (i.e., urethane, paraldehyde, phenobarbital, and pentobarbital sodium) suppressed cardiac function. However, they do not account for the lack of a peripheral vascular response during hemorrhage. The chicken apparently maintains MAP by a volume regulating mechanism operating independently of peripheral vascular tone inasmuch as circulating fluid volume restitution is rapid and occurs without vasoconstriction. The rat maintains MAP through reflex cardiac and peripheral vascular responses which eventually may contribute to transvascular fluid loss and the ultimate collapse after prolonged hemorrhagic hypotension.

1961 ◽  
Vol 200 (4) ◽  
pp. 755-758 ◽  
Author(s):  
C. W. Nash ◽  
C. Heath

The influences of hypercapnia and hyperventilation on peripheral vascular responses to adrenaline and noradrenaline were observed in lightly anesthetized dogs. Changes in the carotid artery blood flow and pressure induced by intra-arterial doses of these amines were measured before, during and after the respiratory changes. During hypercapnia and low blood pH there was a reduced peripheral vascular response, while during hyperventilation and a high pH the vascular response to these drugs increased. However, a fall in blood pressure and flow, and a reflex elevation of the peripheral resistance occurred during both the hyperventilation and the posthypercapnic periods. It appeared that the elevated responses to the amines during those periods of high vasomotor tone may have been produced, in part at least, by the geometric factors involved in resistance, and not entirely by an increased response of the vascular smooth muscle.


1988 ◽  
Vol 64 (6) ◽  
pp. 2582-2588 ◽  
Author(s):  
K. C. Kregel ◽  
P. T. Wall ◽  
C. V. Gisolfi

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70–150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10–15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.


1986 ◽  
Vol 250 (6) ◽  
pp. H1093-H1101 ◽  
Author(s):  
A. L. Siren ◽  
E. Powell ◽  
G. Feuerstein

In the present study the effects of thyrotropin releasing hormone (TRH) and its stable analogue, CG3703, on cardiac output (thermodilution, Cardiomax) and regional blood flow (BF; directional pulsed Doppler technique) were investigated in hypovolemic hypotension in the rat. In urethan-anesthetized rats TRH (0.5 or 2 mg/kg ia) or CG3703 (0.05 or 0.5 mg/kg ia) reversed the bleeding (27% of the blood volume)-induced decreases in mean arterial pressure (MAP) and cardiac index (CI) and increased the heart rate (HR) and total peripheral resistance index (TPRI) in a dose-related manner. In the conscious rat exposed to a 45% hemorrhage, CG3703 (0.5 mg/kg ia) significantly raised MAP, HR, and TPRI with maximum changes of +67 +/- 6 (SE) mmHg, +123 +/- 30 beats/min, and +101 +/- 2%, respectively, CG3703 (0.5 mg/kg ia) also further enhanced the hemorrhage-induced reduction of hindquarter, mesenteric, and renal BF. The changes in BF in saline-treated vs. CG3703-treated rats 2 h after the bleeding were -32 +/- 6 vs. -55 +/- 6% (P less than 0.001) in hindquarter, -9 +/- 8 vs. -61 +/- 11% (P less than 0.001) in mesenteric, and -2 +/- 9 vs. -33 +/- 9% (P less than 0.01) in the renal artery; the changes in vascular resistance +30 +/- 7 vs. +309 +/- 167% (P less than 0.001) in hindquarter, -4 +/- 8 vs. +349 +/- 244% in the mesenteric, and -10 +/- 9 vs. +80 +/- 10% (P less than 0.01) in the renal artery. The survival rate after the 45% hemorrhage was significantly reduced by both TRH and CG3703.(ABSTRACT TRUNCATED AT 250 WORDS)


2013 ◽  
Vol 126 (8) ◽  
pp. 545-556 ◽  
Author(s):  
Fiorentina Roviezzo ◽  
Antonella De Angelis ◽  
Luana De Gruttola ◽  
Antonio Bertolino ◽  
Nikol Sullo ◽  
...  

S1P exerts a diverse set of vascular responses, and PAR-2 has been shown to be involved in vascular inflammation as well as in other inflammatory-based diseases. In the present study, we demonstrate that S1P-mediated vascular effect involves PAR-2 activation.


2008 ◽  
Vol 69 (3) ◽  
pp. 268
Author(s):  
M. Marinov ◽  
Z. Stoyanov ◽  
I. Boncheva ◽  
I. Vartanyan ◽  
T. Chernigovskaya

1980 ◽  
Vol 59 (s6) ◽  
pp. 315s-317s ◽  
Author(s):  
W. Rascher ◽  
R. Dietz ◽  
A. Schomig ◽  
J. Weber ◽  
F. Gross

1. In rats with deoxycorticosterone acetate (DOCA) hypertension basal plasma concentrations of noradrenaline and adrenaline correspond to those of sham-treated controls. 2. In DOCA-treated rats frusemide caused a more pronounced increase in plasma noradrenaline than in control rats. This difference was not observed for adrenaline. 3. In the isolated perfused hind-limb preparation the sensitivity to noradrenaline was already enhanced before blood pressure was elevated. 4. These results suggest that the adrenergic vascular tone is increased in DOCA hypertension in rats.


Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Stephanie W Watts

Serotonin (5-hydroxytryptamine, 5-HT) infusion in a normal conscious rat decreases mean arterial pressure (MAP), in part by reduction in total peripheral resistance. Microsphere experiments have shown 5-HT increases blood flow within the splanchnic vascular bed, with the greatest being in the intestine and spleen. Interestingly, 5-HT does not cause a direct relaxation of resistant (small or large) mesenteric arteries. The present study addresses the possibility of the venous circulation contributing to the 5-HT induced fall in blood pressure. Our working hypothesis is venous dilation, specifically dilation of veins measurable within the splanchnic vascular bed, contributes to 5-HT-induced hypotension. Using an ultrasound imaging system (Vevo 2100 imaging system; 21 MHz probe,Visual Sonics Inc.), telemetry-implanted, anesthetized male Sprague Dawley rats underwent cross-sectional imaging which was controlled for respiration and cardiac cycles. The following vessels were imaged: abdominal aorta (AA); portal vein (PV); abdominal inferior vena cava (IVC); and superior mesenteric vein (SMV). Following the collection of baseline MAP and vessel diameter measurements, Alzet osmotic mini-pumps containing vehicle (saline; n=9) or 5-HT (25 ug/kg/min; n=9) were implanted for 1 week. After, 24 hours of infusion, 5-HT increased the vein diameter (SMV 17.48±2%; PV 17.67±2%; IVC 46.87±8%) and maintained the AA diameter ( AA 0.93±1%) from baseline while reducing MAP (vehicle 101.93±3; 5-HT 84.68±2 mm Hg; p<0.05).One-week post removal of all osmotic mini-pumps, there was no difference in the MAP or diameter of all noted vessels between the two treatment groups. To correlate with in vivo findings, the PV and IVC, when isolated in a tissue bath for measurement of isometric force and contracted with endothelin 1, relaxed in a concentration dependent fashion to 5-HT and 5-carboxamidotryptamine (5-HT 1/7 receptor agonist;1 nM-10 uM). Collectively, these findings highlight the contribution of splanchnic venous dilation in 5-HT-induced hypotension and propose a possible mechanism for 5-HT reduction in blood pressure.


1978 ◽  
Vol 56 (3) ◽  
pp. 390-394
Author(s):  
Peter M. Szeto ◽  
Franco Lioy

In anesthetized, vagotomized cats with both carotid arteries occluded, a stretch of the walls of the thoracic aorta, performed without obstructing aortic flow, induced a significant reflex increase in arterial pressure (35 ± 2−26 ± 1 mmHg; systolic–diastolic). This pressure increase was accompanied by significant increases in peripheral resistance in the superior mesenteric (+30%), renal (+23%), and external iliac (+23%) vascular beds. The increase in iliac resistance observed in the skinned leg was comparable with that observed in the contralateral intact limb. All these vascular responses were drastically reduced by the administration of phenoxybenzamine. After α-adrenergic blockade no signs of reflex vasodilatation could be detected during aortic stretch in any of the vascular beds examined.


Sign in / Sign up

Export Citation Format

Share Document