scholarly journals PULMONARY VASCULAR RESPONSE TO INCREASING CARDIAC INDEX FOLLOWING SYSTEMIC HYPOTENSION IS MODIFIED BY PENTOBARBITAL ANESTHESIA

1987 ◽  
Vol 21 (4) ◽  
pp. 205A-205A
Author(s):  
Daniel P Nyhan ◽  
Bessie B Chen ◽  
Harold M Coll ◽  
Patrick W Clougherty ◽  
Paul A Murray
Keyword(s):  
Cardiac Index ◽  
Vascular Response ◽  
Systemic Hypotension ◽  
Pentobarbital Anesthesia

Pentobarbital anesthesia modifies pulmonary vasoregulation after hypoperfusion

1988 ◽  
Vol 255 (3) ◽  
pp. H569-H576
Author(s):  
B. B. Chen ◽  
D. P. Nyhan ◽  
H. M. Goll ◽  
P. W. Clougherty ◽  
D. M. Fehr ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Adrenergic Receptor ◽  
Conscious State ◽  
Conscious Dogs ◽  
Mixed Venous Blood ◽  
Vascular Response ◽  
Beta Adrenergic ◽  
Pentobarbital Anesthesia ◽  
Pulmonary Vasoconstriction ◽  
Receptor Block

Our objectives were 1) to investigate the extent to which the pulmonary vascular response to increasing cardiac index after a period of hypotension and hypoperfusion (defined as reperfusion) measured in conscious dogs is altered during pentobarbital sodium anesthesia, and 2) to determine whether pentobarbital anesthesia modifies autonomic nervous system (ANS) regulation of the pulmonary circulation during reperfusion. Base-line and reperfusion pulmonary vascular pressure-cardiac index (P/Q) plots were generated by stepwise inflation and deflation, respectively, of an inferior vena caval occluder to vary Q in conscious and pentobarbital-anesthetized (30 mg/kg iv) dogs. During pentobarbital anesthesia, controlled ventilation (without positive end-expiratory pressure) allowed matching of systemic arterial and mixed venous blood gases to conscious values. Marked pulmonary vasoconstriction (P less than 0.01) was observed during reperfusion in pentobarbital-anesthetized but not in conscious dogs. Both sympathetic alpha-adrenergic receptor block and total ANS ganglionic block attenuated, but did not abolish, the pulmonary vasoconstriction during reperfusion in pentobarbital-anesthetized dogs. Neither sympathetic beta-adrenergic receptor block nor cholinergic receptor block enhanced the magnitude of the pulmonary vasoconstrictor response to reperfusion during pentobarbital anesthesia. Thus, in contrast to the conscious state, the pulmonary vascular response to reperfusion is characterized by active, non-flow-dependent pulmonary vasoconstriction during pentobarbital anesthesia. This response is primarily, but not exclusively, mediated by sympathetic alpha-adrenergic vasoconstriction and is not offset by either sympathetic beta-adrenergic or cholinergic vasodilation. These results indicate, that, compared with the conscious state, pentobarbital anesthesia modifies pulmonary vasoregulation, during reperfusion following hypotension and hypoperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Paradoxical forearm vasodilatation and haemodynamic improvement during cardiopulmonary baroreceptor unloading in patients with congestive heart failure

1993 ◽  
Vol 84 (3) ◽  
pp. 271-280 ◽  
Author(s):  
Katsuhiko Nishian ◽  
Seinosuke Kawashima ◽  
Tadaaki Iwasaki
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Plasma Level ◽  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Normal Subjects ◽  
Lower Body ◽  
Vascular Response

1. To examine the contribution of paradoxical reflex forearm vasodilatation during unloading of cardiopulmonary baroreceptors to systemic haemodynamics, the responses of central and peripheral haemodynamics during lower-body negative pressure were measured in 24 patients with chronic congestive heart failure (New York Heart Association functional class II-IV) and were compared with those of 10 normal subjects. 2. Lower-body negative pressure of less than −20 mmHg caused a significant forearm vasoconstriction in normal subjects but not in patients with congestive heart failure. In the individual cases, however, eight patients (subgroup A) had a significant forearm vasoconstriction, whereas 10 patients (subgroup B) had a paradoxical forearm vasodilatation. The remaining six patients had a blunted forearm vascular response. Baseline pulmonary capillary wedge pressure (26 ± 3 versus 20 ± 1 mmHg, means ± SEM) and left ventricular wall stress in end-diastole (57 ± 6 versus 37 ± 4 g/cm2) were significantly (P <0.05) higher in subgroup B than in subgroup A. 3. During lower-body negative pressure of −20 mmHg, the plasma level of noradrenaline, systemic vascular resistance and cardiac index did not change significantly in subgroup A. In subgroup B, however, during this orthostatic stimulus systemic vascular resistance fell significantly from a baseline value of 2023 ± 109 to 1740 ± 110 dyns−1 cm−5 (P <0.01) and cardiac index increased significantly from a baseline value of 2.0 ± 0.1 to 2.5 ± 0.21 min−1 m−2 (P <0.01) despite there being no significant change in the plasma level of noradrenaline. 4. After treatment, a second bout of lower-body negative pressure was applied to seven patients in subgroup B. The forearm vascular response to the second bout of lower-body negative pressure was normalized. 5. These data suggest that the patients with more severe heart failure show a paradoxical forearm vasodilatation during mild lower-body negative pressure and that this altered cardiopulmonary baroreflex control of the circulation serves to improve the depressed cardiac performance.

PULMONARY VASCULAR RESPONSE TO CYCLOOXYGENASE PATHWAY INHIBITION MEASURED IN CONSCIOUS DOGS IS MODIFIED DURING PENTOBARBITAL ANESTHESIA

1988 ◽  
Vol 69 (3A) ◽  
pp. A127-A127
Author(s):  
D. P. Nyhan ◽  
B. B. Chen ◽  
D. M. Fehr ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Conscious Dogs ◽  
Vascular Response ◽  
Pentobarbital Anesthesia ◽  
Pathway Inhibition

Ultrastructural Changes of Canine Kidneys During 24-Hour Perfusion on a LI-400 Preservation System

1971 ◽  
Vol 29 ◽  
pp. 316-317
Author(s):  
M. O. Magnusson ◽  
D. G. Osborne ◽  
T. Shimoji ◽  
W. S. Kiser ◽  
W. A. Hawk
Keyword(s):  
Electron Microscopy ◽  
Electrolyte Solution ◽  
Ultrastructural Changes ◽  
Midline Incision ◽  
Short Term ◽  
Pentobarbital Anesthesia ◽  
Pulsatile Perfusion

Short term experimental and clinical preservation of kidneys is presently best accomplished by hypothermic continuous pulsatile perfusion with cryoprecipitated and millipore filtered plasma. This study was undertaken to observe ultrastructural changes occurring during 24-hour preservation using the above mentioned method.A kidney was removed through a midline incision from healthy mongrel dogs under pentobarbital anesthesia. The kidneys were flushed immediately after removal with chilled electrolyte solution and placed on a LI-400 preservation system and perfused at 8-10°C. Serial kidney biopsies were obtained at 0-½-1-2-4-8-16 and 24 hours of preservation. All biopsies were prepared for electron microscopy. At the end of the preservation period the kidneys were autografted.

Does low cardiac index predict a negative outcome in patients undergoing cardiac surgery?

2010 ◽  
Vol 58 (S 01) ◽  
Author(s):  
A Lehmann ◽  
AH Kiessling ◽  
P Schmuck ◽  
F Isgro ◽  
J Boldt ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Cardiac Index ◽  
Negative Outcome

The Hemodynamic and Fibrinolytic Response to Low Dose Epinephrine and Phenylephrine Infusions During Total Hip Replacement Under Epidural Anesthesia

1992 ◽  
Vol 68 (04) ◽  
pp. 436-441 ◽  
Author(s):  
Nigel E Sharrock ◽  
George Go ◽  
Robert Mineo ◽  
Peter C Harpel
Keyword(s):  
Heart Rate ◽  
Deep Vein Thrombosis ◽  
Cardiac Index ◽  
Total Hip Replacement ◽  
Epidural Anesthesia ◽  
Hip Replacement ◽  
Low Dose ◽  
Total Hip ◽  
Vein Thrombosis ◽  
Deep Vein

SummaryLower rates of deep vein thrombosis have been noted following total hip replacement under epidural anesthesia in patients receiving exogenous epinephrine throughout surgery. To determine whether this is due to enhanced fibrinolysis or to circulatory effects of epinephrine, 30 patients scheduled for primary total hip replacement under epidural anesthesia were randomly assigned to receive intravenous infusions of either low dose epinephrine or phenylephrine intraoperatively. All patients received lumbar epidural anesthesia with induced hypotension and were monitored with radial artery and pulmonary artery catheters.Patients receiving low dose epinephrine infusion had maintenance of heart rate and cardiac index whereas both heart rate and cardiac index declined significantly throughout surgery in patients receiving phenylephrine (p = 0.0001 and p = 0.0001, respectively). Tissue plasminogen activator (t-PA) activity increased significantly during surgery (p <0.0005) and declined below baseline postoperatively (p <0.005) in both groups. Low dose epinephrine was not associated with any additional augmentation of fibrinolytic activity perioperatively. There were no significant differences in changes in D-Dimer, t-PA antigen, α2-plasmin inhibitor-plasmin complexes or thrombin-antithrombin III complexes perioperatively between groups receiving low dose epinephrine or phenylephrine. The reduction in deep vein thrombosis rate with low dose epinephrine is more likely mediated by a circulatory mechanism than by augmentation of fibrinolysis.

scholarly journals A proof of principle study of atomoxetine for the prevention of vasovagal syncope: the Prevention of Syncope Trial VI

EP Europace ◽  
2019 ◽  
Vol 21 (11) ◽  
pp. 1733-1741 ◽  
Author(s):  
Robert S Sheldon ◽  
Lucy Lei ◽  
Juan C Guzman ◽  
Teresa Kus ◽  
Felix A Ayala-Paredes ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Stroke Volume ◽  
Vasovagal Syncope ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Study Drug ◽  
Norepinephrine Transporter ◽  
Volume Index ◽  
Head Up Tilt ◽  
Invasive Techniques

Abstract Aims There are few effective therapies for vasovagal syncope (VVS). Pharmacological norepinephrine transporter (NET) inhibition increases sympathetic tone and decreases tilt-induced syncope in healthy subjects. Atomoxetine is a potent and highly selective NET inhibitor. We tested the hypothesis that atomoxetine prevents tilt-induced syncope. Methods and results Vasovagal syncope patients were given two doses of study drug [randomized to atomoxetine 40 mg (n = 27) or matched placebo (n = 29)] 12 h apart, followed by a 60-min drug-free head-up tilt table test. Beat-to-beat heart rate (HR), blood pressure (BP), and cardiac haemodynamics were recorded using non-invasive techniques and stroke volume modelling. Patients were 35 ± 14 years (73% female) with medians of 12 lifetime and 3 prior year faints. Fewer subjects fainted with atomoxetine than with placebo [10/29 vs. 19/27; P = 0.003; risk ratio 0.49 (confidence interval 0.28–0.86)], but equal numbers of patients developed presyncope or syncope (23/29 vs. 21/27). Of patients who developed only presyncope, 87% (13/15) had received atomoxetine. Patients with syncope had lower nadir mean arterial pressure than subjects with only presyncope (39 ± 18 vs. 69 ± 18 mmHg, P < 0.0001), and this was due to lower trough HRs in subjects with syncope (67 ± 30 vs. 103 ± 32 b.p.m., P = 0.006) and insignificantly lower cardiac index (2.20 ± 1.36 vs. 2.84 ± 1.05 L/min/m2, P = 0.075). There were no significant differences in stroke volume index (32 ± 6 vs. 35 ± 5 mL/m2, P = 0.29) or systemic vascular resistance index (2156 ± 602 vs. 1790 ± 793 dynes*s/cm5*m2, P = 0.72). Conclusion Norepinephrine transporter inhibition significantly decreased the risk of tilt-induced syncope in VVS subjects, mainly by blunting reflex bradycardia, thereby preventing final falls in cardiac index and BP.

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