Effect of carotid sinus stimulation on resistance and critical closing pressure of the canine hindlimb

1993 ◽  
Vol 264 (5) ◽  
pp. H1560-H1566 ◽  
Author(s):  
I. Shrier ◽  
S. N. Hussain ◽  
S. Magder
Keyword(s):  
Carotid Sinus ◽  
Arterial Compliance ◽  
Vagus Nerves ◽  
Arterial Perfusion ◽  
Carotid Sinus Stimulation ◽  
Critical Closing Pressure ◽  
Occlusion Technique ◽  
Electromagnetic Flow Probe ◽  
Venous Resistance ◽  
Closing Pressure

Sympathetically mediated changes in blood pressure are thought to occur through changes in arterial resistance (Ra). To test whether the critical closing pressure (Pcrit) could also play a role, we pump-perfused the vascularly isolated canine hindlimb at constant flow. Carotid sinuses were isolated and both vagus nerves cut. Carotid sinus (Pcar), arterial, perfusion (Pper), and venous (Pv) pressures and flow to the hindlimb (Q, electromagnetic flow probe) were measured. By decreasing pump flow to zero over time periods of 1-10 s and measuring the pressure at zero-flow, it was possible to estimate arterial compliance and Pcrit. Ra was calculated as (Pper - Pcrit)/Q. Venous resistance was calculated as (Pel - Pv)/Q, where Pel is the pressure in the compliant region obtained by the double-occlusion technique. Raising Pcar from 115 +/- 7 to 203 +/- 10 mmHg (n = 6) decreased Pcrit from 49.7 +/- 4.3 to 25.9 +/- 2.6 mmHg and Ra from 10.7 +/- 1.2 to 6.8 +/- 0.9 mmHg.min.100 g-1.ml-1 (P < 0.05). Lowering Pcar from 119 +/- 6 to 71 +/- 6 mmHg (n = 6) increased Pcrit from 37.0 +/- 3.3 to 61.0 +/- 8.5 mmHg and Ra from 10.0 +/- 1.6 to 14.0 +/- 2.4 mmHg.min.100 g.ml-1 (P < 0.05). Arterial compliance increased when Pcar was raised (P < 0.05) and decreased when Pcar was decreased (P < 0.1). Venous resistance did not change when Pcar was altered. In conclusion, changes in carotid sinus stimulation alters blood flow to the hindlimb through changes in both Pcrit and Ra.

A square-pulse flow method for measuring characteristics of the arterial bed

1976 ◽  
Vol 40 (3) ◽  
pp. 425-433 ◽  
Author(s):  
M. G. Bottomley ◽  
G. W. Mainwood
Keyword(s):  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Mean Value ◽  
Pressure Response ◽  
Arterial System ◽  
Response Curves ◽  
Arterial Tree ◽  
Pulse Flow ◽  
Critical Closing Pressure ◽  
Closing Pressure

A device was designed to provide a “square” pulse of blood flow into the arterial system. Pulses were injected into the carotid artery of the rabbit during transient cardiac arrest. Analysis of pressure response curves generated by the flow provides information as to the state of the arterial tree. With certain assumptions it is possible to estimate from these curves lumped values of peripheral resistance, critical closing pressure, and arterial compliance. In a series of 12 rabbits the mean value of peripheral resistance was found to be 0.21 +/- 0.7 mmHg-ml-1-min and critical closing pressure was estimated to be 23.6 +/- 3.8 mmHg. This method gives two possible values for arterial compliance 0.036 +/- 0.010 and 0.055 +/- 0.010 ml-mm-1 based, respectively, on the rise and decay curves of the pressure response. The theory and limitations of the method are discussed. The use of the method is illustrated in following the response to increased PCO2 and hemorrhage.

scholarly journals Influence of critical closing pressure on systemic vascular resistance and total arterial compliance: A clinical invasive study

2017 ◽  
Vol 110 (12) ◽  
pp. 659-666 ◽  
Author(s):  
Denis Chemla ◽  
Edmund M.T. Lau ◽  
Philippe Hervé ◽  
Sandrine Millasseau ◽  
Mabrouk Brahimi ◽  
...  
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Total Arterial Compliance ◽  
Critical Closing Pressure ◽  
Closing Pressure

Critical Closing Pressure During a Controlled Increase in Intracranial Pressure

2018 ◽  
pp. 133-137
Author(s):  
Katarzyna Kaczmarska ◽  
Magdalena Kasprowicz ◽  
Antoni Grzanka ◽  
Wojciech Zabołotny ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Critical Closing Pressure ◽  
Closing Pressure

Cerebral Critical Closing Pressure During Infusion Tests

2016 ◽  
pp. 215-220 ◽  
Author(s):  
Georgios V. Varsos ◽  
Marek Czosnyka ◽  
Peter Smielewski ◽  
Matthew R. Garnett ◽  
Xiuyun Liu ◽  
...  
Keyword(s):  
Critical Closing Pressure ◽  
Closing Pressure

Central neural respiratory response to carotid sinus nerve stimulation in newborns

1984 ◽  
Vol 56 (6) ◽  
pp. 1614-1620 ◽  
Author(s):  
E. E. Lawson ◽  
W. A. Long
Keyword(s):  
Respiratory Activity ◽  
Carotid Sinus ◽  
Control Level ◽  
Carotid Sinus Nerve ◽  
Respiratory Response ◽  
Vagus Nerves ◽  
Newborn Piglets ◽  
Initial Control ◽  
Respiratory Centers ◽  
Adult Cats

During exposure to hypoxia newborns hypoventilate following a brief period of hyperventilation. Failure of integration of the afferent signals from peripheral O2 chemoreceptors due to immaturity of the central respiratory centers could explain this paradoxical respiratory response. To test this hypothesis we have utilized anesthetized, paralyzed, mechanically ventilated newborn piglets and lambs (less than 11 days) and old piglets (19–35 days). The vagus nerves were cut in each animal. Respiratory activity was quantified by integration of phrenic neural activity. A carotid sinus nerve (CSN) was isolated and electrically stimulated for periods of 1–6 min. In all three groups of animals respiratory activity was continuously elevated throughout the period of CSN stimulation. After CSN stimulation respiratory activity immediately declined about 25% from the stimulated value. Thereafter respiratory activity declined in an exponential fashion toward the initial control level of respiratory activity. The time constant of this latter decay was 84.2 s in the young piglets, 83.2 s in the old piglets, and 63.0 s in the lambs. These results indicate that the respiratory centers of newborn piglets and lambs can maintain integration of continuous afferent CSN activity. Further, the respiratory afterdischarge that follows CSN stimulus cessation is similar to that of adults. These studies indicate that, during periods of O2 sufficiency, the central respiratory centers of newborns respond in a qualitatively similar manner to CSN stimulation as do adult cats.

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

2004 ◽  
Vol 286 (1) ◽  
pp. R94-R100 ◽  
Author(s):  
Zonghai Ruan ◽  
Toshishige Shibamoto ◽  
Tomohiro Shimo ◽  
Hideaki Tsuchida ◽  
Tomonobu Koizumi ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Protoporphyrin Ix ◽  
Fold Increase ◽  
Liver Weight ◽  
Zinc Protoporphyrin ◽  
Hepatic Congestion ◽  
Occlusion Technique ◽  
Venous Resistance ◽  
Synthase Inhibitor ◽  
Guinea Pig Liver

The pathophysiology of the hepatic vascular response to anaphylaxis in guinea pig is not known. We studied effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused livers derived from guinea pigs sensitized with ovalbumin. We also determined whether nitric oxide (NO) or carbon monoxide (CO) modulates the hepatic anaphylaxis. The livers were perfused portally and recirculatingly at constant flow with diluted blood. With the use of the double-occlusion technique to estimate the hepatic sinusoidal pressure (Pdo), portal venous resistance (Rpv) and hepatic venous resistance (Rhv) were calculated. An antigen injection caused venoconstriction characterized by an increase in Rpv greater than Rhv and was accompanied by a large liver weight gain. Pretreatment with the NO synthase inhibitor NG-nitro-l-arginine methyl ester, but not the heme oxygenase inhibitor zinc protoporphyrin IX, potentiated the antigen-induced venoconstriction by increasing both Rpv and Rhv (2.2- and 1.2-fold increase, respectively). In conclusion, anaphylaxis causes both pre- and postsinusoidal constriction in isolated guinea pig livers. However, the increases in postsinusoidal resistance and Pdo cause hepatic congestion. Endogenously produced NO, but not CO, modulates these responses.

Carotid chemoreceptors and vagi in hypoxic and cyanide-induced tachycardia in the dog

1981 ◽  
Vol 240 (6) ◽  
pp. H874-H880 ◽  
Author(s):  
P. D. Gupta ◽  
M. Singh
Keyword(s):  
Heart Rate ◽  
Carotid Sinus ◽  
Adrenergic Blockade ◽  
Vagus Nerves ◽  
Carotid Chemoreceptors ◽  
Control Heart ◽  
Systemic Hypoxia ◽  
Spinal Section ◽  
High Control ◽  
Control Heart Rate

We investigated the mechanisms underlying heart rate changes resulting from systemic hypoxia in anesthetized artificially ventilated dogs with low control heart rate (less than or equal to 93 beats/min). We observed that systemic hypoxia evoked tachycardia in intact dogs that was not significantly different from that evoked in dogs with beta-adrenergic blockade (BB). Also, tachycardia elicited in dogs with BB plus spinal section at C3 (BBSS) was significantly greater than in dogs with BBSS plus bilateral section of carotid sinus nerves. Furthermore, under various anesthetics, intracarotid injection of sodium cyanide induced a tachycardia response in dogs with low control heart rate (less than or equal to 97 beats/min) and a bradycardia response in dogs with high control heart rate (greater than or equal to 130 beats/min). These results suggest that 1) when the resting cardiac parasympathetic tone is high, systemic hypoxia evokes tachycardia which is mediated predominantly through efferent vagus nerves and 2) the stimulation of carotid chemoreceptors causes excitation of both cardioacceleratory and cardioinhibitory reflexes, the resultant response being dependent on the prevalent autonomic drive.

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