Effects of tension, duty cycle, and arterial pressure on diaphragmatic blood flow in dogs

1989 ◽  
Vol 66 (2) ◽  
pp. 968-976 ◽  
Author(s):  
S. N. Hussain ◽  
C. Roussos ◽  
S. Magder
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Duty Cycle ◽  
Phrenic Nerve Stimulation ◽  
Gradual Decline ◽  
Transdiaphragmatic Pressure ◽  
Duty Cycles ◽  
Severe Hypotension ◽  
Internal Mammary ◽  
Pressure Part

We investigated the selective effects of changes in transdiaphragmatic pressure (Pdi) and duty cycle on diaphragmatic blood flow in supine dogs at normal arterial pressure (N), moderate hypotension (MH), and severe hypotension (SH) [mean arterial pressure (Part) of 116, 75, and 50 mmHg, respectively]. The diaphragm was paced at a rate of 12/min by bilateral phrenic nerve stimulation. Left phrenic (Qphr-T) and left internal mammary (Qim-T) arterial flows were measured by electromagnetic flow probes. Changes in Pdi and duty cycle were achieved by changing the stimulation frequencies and the duration of contraction, whereas Part changes were produced by bleeding. With N and at a duty cycle of 0.5, incremental increases in Pdi produced peaks in Qphr-T and Qim-T at 30% maximum diaphragmatic pressure (Pdimax) with a gradual decline at higher Pdi. With MH and SH, blood flow peaked at 10% Pdimax. At any given Pdi, blood flow was lower with MH and SH in comparison to N. The effect of duty cycle was tested at two levels of Pdi. With N and at low Pdi (25% Pdimax), blood flow rose progressively with increases in duty cycle, whereas at moderate Pdi level (50% Pdimax) blood flow peaked at a duty cycle of 0.3, with no increase thereafter. With MH, blood flow at low Pdi rose linearly with increasing duty cycle but to a lesser extent than with N, and at a moderate Pdi flow peaked at a duty cycle of 0.3. With SH, blood flow at low and moderate Pdi was limited at duty cycles greater than 0.3 and 0.1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragmatic blood flow in the dog

1986 ◽  
Vol 60 (2) ◽  
pp. 554-561 ◽  
Author(s):  
H. Bark ◽  
S. M. Scharf
Keyword(s):  
Blood Flow ◽  
Duty Cycle ◽  
Stimulus Frequency ◽  
Phase Flow ◽  
Transdiaphragmatic Pressure ◽  
Relaxation Phase ◽  
Duty Cycles ◽  
Tension Time ◽  
Phrenic Artery ◽  
Electromagnetic Flow Probe

In anesthetized mongrel dogs we measured the blood flow in the left phrenic artery (Qdi), using an electromagnetic flow probe, before and during supramaximal phrenic nerve stimulation (pacing). This was done at constant respiratory rate (24/min) but at three different stimulation frequencies at a duty cycle of 0.4 (20, 50, and 100 Hz) and at three different duty cycles at a stimulation frequency of 50 Hz (duty cycle = 0.2, 0.4, and 0.8). Qdi was unchanged during diaphragm contraction until transdiaphragmatic pressure (Pdi) was greater than approximately 11 cmH2O, whereafter it began to decrease, reaching zero at Pdi approximately 20 cmH2O. Thus, when Pdi was greater than 21 cmH2O, all flow occurred during relaxation. Qdi averaged over the entire respiratory cycle (Qt) was less at duty cycle = 0.8 than under the other conditions. This was because of decreasing length of relaxation phase rather than a difference of relaxation phase flow (Qr), which was maximal during all conditions of phrenic stimulation. During pacing-induced fatigue, Qt actually rose slightly as Pdi fell. This was due to an increase in contraction phase flow while Qr remained constant. The relationship between Qt and tension-time index was not unique but varied according to the different combinations of duty cycle and stimulus frequency.

Effects of contraction frequency and duty cycle on diaphragmatic blood flow

1985 ◽  
Vol 58 (1) ◽  
pp. 265-273 ◽  
Author(s):  
B. Buchler ◽  
S. Magder ◽  
C. Roussos
Keyword(s):  
Blood Flow ◽  
Duty Cycle ◽  
Contraction Time ◽  
Phrenic Nerve Stimulation ◽  
Contraction Frequency ◽  
Time Index ◽  
High Duty Cycle ◽  
Duty Cycles ◽  
Tension Time ◽  
Microsphere Method

The effects of diaphragmatic contraction frequency (no. of intermittent tetanic contractions/min) at a given tension-time index and of duty cycle (contraction time/total cycle time) on diaphragmatic blood flow were measured in anesthetized mongrel dogs during bilateral supramaximal phrenic nerve stimulation. Diaphragmatic blood flow was measured by the radionuclide-labeled microsphere method. Contraction frequency was varied between 10 and 160/min at duty cycles of 0.25 and 0.75. Diaphragmatic blood flow increased with contraction frequency from 1.47 +/- 0.13 ml X min-1 X g-1 (mean +/- SE) at an average of 18/min to 2.65 +/- 0.16 ml X min-1 X g-1 at 74/min (P less than 0.01) with a duty cycle of 0.25 and from 1.32 +/- 0.19 ml X min-1 X g-1 at an average of 15/min to 1.96 +/- 0.15 ml X min-1 X g-1 at 80/min (P less than 0.02) with a duty cycle of 0.75. At higher contraction frequencies diaphragmatic blood flow did not increase further at both duty cycles. In addition, diaphragmatic blood flow was higher with a duty cycle of 0.25 than 0.75 at all contraction frequencies. We conclude that frequency of contraction is a major determinant of diaphragmatic blood flow and that high duty cycle impedes diaphragmatic blood flow.

Contraction-dependent modulations in regional diaphragmatic blood flow

1990 ◽  
Vol 68 (5) ◽  
pp. 2019-2028 ◽  
Author(s):  
F. Hu ◽  
A. Comtois ◽  
A. E. Grassino
Keyword(s):  
Blood Flow ◽  
Duty Cycle ◽  
Time Course ◽  
Azygos Vein ◽  
Transdiaphragmatic Pressure ◽  
Parabolic Function ◽  
Internal Mammary ◽  
Anesthetized Dogs ◽  
Phrenic Artery ◽  
Artery Flow

Blood flow (Q) of the diaphragm was measured simultaneously with Doppler probes placed on diaphragmatic veins and an artery and by direct volumetric measurements obtained from cannulation of diaphragmatic blood vessels. The Doppler converting coefficients obtained were 6.27, 7.25, 4.21, and 41.07 ml.min-1.kHz-1 for left phrenic artery flow (Qpha), phrenic vein flow (Qphv), internal mammary vein flow (Qimv), and azygos vein flow (Qazv), respectively. The time course of Qpha, Qphv, Qimv, and Qazv after imposed patterns of diaphragmatic contraction was measured in nine anesthetized dogs. Each pattern consisted of various combinations of transdiaphragmatic pressure (Pdi), frequency of pacing (f), and duty cycle obtained by bilateral phrenic nerve stimulation. The dogs were prepared with chests open and loosely casted abdomens. Qpha, Qphv, Qimv, and Qazv were measured at rest (control, passive diaphragm, mechanical ventilation) and at two submaximal levels of stimulation (30 and 60% of Pdimax). The f was 10 or 30 cycles/min and the duty cycle was 0.25, 0.50, and 0.75. The results show 1) Qpha, Qphv, Qimv, and Qazv reached stable values (equilibration) after 30-36 s of pacing; 2) the steady Qpha, Qphv, and Qimv were linearly related to Pdi, and they were related by a parabolic function to duty cycle, whereas Qazv was not significantly affected by Pdi and increased linearly as a function of the duty cycle; 3) the diaphragmatic blood drainage was approximately 60% through the intercostal veins leading into the azygos trunk, 25% through the phrenic vein, and 15% through the internal mammary vein during pacing of the diaphragm at a duty cycle of 0.50 and 60% Pdimax; and 4) for a given pacing pattern, Qpha and Qphv increased with f, but Qimv and Qazv did not.

Sustainable inspiratory pressures over varying flows, volumes, and duty cycles

1990 ◽  
Vol 69 (5) ◽  
pp. 1875-1882 ◽  
Author(s):  
T. L. Clanton ◽  
B. T. Ameredes ◽  
D. B. Thomson ◽  
M. W. Julian
Keyword(s):  
Tidal Volume ◽  
Duty Cycle ◽  
Dynamic Pressure ◽  
Breathing Patterns ◽  
Transdiaphragmatic Pressure ◽  
Lung Inflation ◽  
Duty Cycles ◽  
Pressure Time ◽  
Endurance Tests ◽  
Normal Humans

This study identifies the influence of flow (0.5-2.0 l/s), duty cycle (0.29-0.57), and tidal volume (1.08-2.16 liters) on sustainable inspiratory muscle pressure (Pmus) and transdiaphragmatic pressure (Pdi) development. Six normal humans performed endurance tests using an isoflow method, which allowed for measurements of maximum dynamic Pmus and Pdi, with controlled lung inflation. The subjects repeated maximum dynamic voluntary inspirations for 10 min. Pressures dropped exponentially from initial measurements at rest (Pmusi or Pdi) to sustainable values (Pmus or Pdis). As flow and tidal volume increased, maximum initial and sustainable pressures decreased significantly. However, at a constant duty cycle, the sustainable dynamic pressures remained predictable fractions of initial dynamic pressures (i.e., Pmuss/Pmusi or Pdis/Pdii), regardless of changes in flow and tidal volume. In contrast, as duty cycle increased, the sustainable fractions significantly decreased for both Pdi and Pmus. For example, at a duty cycle of 0.29, Pmuss/Pmusi was approximately 0.71, and at a duty cycle of 0.57, Pmuss/Pmusi was approximately 0.62. Calculated sustainable pressure-time indexes varied significantly between 0.16 to 0.32 for Pmus and 0.11 to 0.22 for Pdi over the breathing patterns studied. We conclude that 1) the maximum dynamic pressure that can be sustained at a given duty cycle is a predictable fraction of the maximum dynamic pressure that can be generated at rest when measured under the same conditions of inspiration and 2) the sustainable fraction of initial dynamic pressure significantly decreases with increasing duty cycle.

Sympathetic nerves reduce cerebral blood flow during hypoxia in awake rabbits

1984 ◽  
Vol 247 (3) ◽  
pp. H446-H451 ◽  
Author(s):  
D. W. Busija
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Sympathetic Nerves ◽  
The Other ◽  
Intact Side ◽  
Sham Surgery ◽  
Severe Hypotension ◽  
Cervical Ganglion ◽  
Cortical Gray Matter

Effects of sympathetic nerves on cerebral blood flow (CBF) during normoxia or hypoxia combined with hemorrhagic hypotension were examined in awake rabbits. One superior cervical ganglion was excised and sham surgery was performed on the other side. Five rabbits each were exposed to normoxia [arterial O2 tension (Pao2) greater than or equal to 78 mmHg] or hypoxia (Pao2 less than or equal to 39 mmHg). Cerebral blood flow was measured with 15-micron microspheres three times in each group: normotension [mean arterial pressure (MAP) 80-86 mmHg]; moderate hypotension (MAP 62-65 mmHg); and severe hypotension (MAP 49-50 mmHg). During normoxia, blood flow to cerebrum was 70 +/- 8 (SE) ml X min-1 X 100 g-1 during normotension and did not decrease during hypotension. Sympathetic nerves had no effect on CBF during normoxia. During hypoxia, blood flow to cerebrum was 243 +/- 21 ml X min-1 X 100 g-1 during normotension and fell as arterial pressure was lowered. Blood flow to denervated cerebrum was higher than on the intact side during normotension (13 +/- 4%), moderate hypotension (11 +/- 5%), and severe hypotension (12 +/- 4%). Similarly, blood flow to denervated cortical gray matter was higher during normotension (19 +/- 4%), moderate hypotension (16 +/- 6%), and severe hypotension (17 +/- 6%) when compared with the innervated side. In addition, blood flow to denervated cerebellum was higher than the innervated side during severe hypotension (27 +/- 17%).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular failure and apnea in shock

1989 ◽  
Vol 66 (1) ◽  
pp. 184-189 ◽  
Author(s):  
S. Nava ◽  
F. Bellemare
Keyword(s):  
Cardiac Arrest ◽  
Arterial Pressure ◽  
Venous Return ◽  
Initial Increase ◽  
Breathing Frequency ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Cardiovascular Failure ◽  
Anesthetized Dogs ◽  
The Right

A model of shock was developed in anesthetized dogs by limiting venous return with a balloon inflated in the right atrium. The change in ventilation (VE) in response to a sustained decrease in arterial pressure (Pa) to 50–60 Torr was studied by recording transdiaphragmatic pressure (Pdi) and diaphragm (Edi) and parasternal intercostal (Eic) electrical activity. Four dogs died of cardiac arrest after 20–60 min. In 11 dogs, VE, after an initial increase, decreased progressively until apnea occurred after 103 +/- 24 min, after 60% reductions in breathing frequency, Pdi, and Eic and a 30% fall in Edi. No decrease in diaphragm contractility was found in response to artificial phrenic nerve stimulation. The cardiocirculatory function deteriorated during shock until it became irreversible at apneic time. No recovery from apnea occurred without a recovery of Pa. We conclude that the fall in VE and ensuing apnea in this model resulted from a decrease in central respiratory neural output associated with a progressive deterioration of the cardiocirculatory function.

Effect of separate hemidiaphragm contraction on left phrenic artery flow and O2 consumption

1990 ◽  
Vol 69 (1) ◽  
pp. 86-90 ◽  
Author(s):  
F. Hu ◽  
A. Comtois ◽  
E. Shadram ◽  
A. Grassino
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Arterial Blood Flow ◽  
O2 Consumption ◽  
Phrenic Nerve Stimulation ◽  
Diaphragm Pacing ◽  
Transdiaphragmatic Pressure ◽  
Arterial Blood ◽  
Significant Difference

Phrenic arterial blood flow has been shown to increase during bilateral phrenic nerve stimulation (BPNS). However, the role of unilateral phrenic nerve stimulation [left (LPNS) or right (RPNS)] on the blood flow and O2 consumption of the contralateral hemidiaphragm is not known and is explored here. In six anesthetized, mechanically hyperventilated dogs, left phrenic arterial blood flow (Qlpha) was measured (Doppler technique). Supramaximal (10 V, 30 Hz, 0.25-ms duration) LPNS, RPNS, and BPNS at a pacing frequency 15/min and duty cycle of 0.50 were delivered in separate runs. Left hemidiaphragmatic blood samples for gas analyses were obtained by left phrenic venous cannulation. During RPNS, Qlpha and left hemidiaphragmatic O2 consumption (VO2ldi) did not change significantly compared with control. During LPNS and BPNS, there was a significant increase in Qlpha and VO2ldi (P less than 0.01). There was no significant difference in Qlpha and VO2ldi between LPNS and BPNS (P greater than 0.05). We conclude 1) that there is a complete independence of left-right hemidiaphragmatic circulation both at rest and during diaphragm pacing and 2) that during unilateral stimulation transdiaphragmatic pressure is not related to diaphragmatic blood flow.

Hypercapnia potentiates renal vasoconstriction during hemorrhagic hypotension in awake rabbits

1984 ◽  
Vol 246 (5) ◽  
pp. H671-H674
Author(s):  
D. W. Busija
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Renal Vasoconstriction ◽  
Hemorrhagic Hypotension ◽  
Severe Hypotension ◽  
Unanesthetized Animals ◽  
Renal Vascular

Although both hemorrhagic hypotension and hypercapnia increase renal vascular resistance (RVR) modestly, effects of interaction between these stimuli on RVR have not been examined systematically in unanesthetized animals. The purpose of this study was to test the hypothesis that renal vasoconstriction during hemorrhagic hypotension is affected by arterial CO2 tension (PCO2). Unanesthetized rabbits were placed into an environmental chamber, and six were exposed to normocapnia (PCO2 approximately 29 mmHg) and six to hypercapnia (PCO2 approximately 62 mmHg). Renal blood flow (RBF) was measured with 15-micrograms microspheres during 1) normotension [mean arterial pressure (MAP) 84-88 mmHg]; 2) moderate hemorrhagic hypotension (MAP 61-64 mmHg); and 3) severe hemorrhagic hypotension (MAP 44-50 mmHg). When MAP was normal, RBF was 437 +/- 59 and 345 +/- 59 ml X min-1 X 100 g-1 in the normocapnic and hypercapnic groups, respectively (NS; P greater than 0.05). In addition, RVR (MAP/RBF) was 0.22 +/- 0.04 in the normocapnic group and 0.32 +/- 0.08 mmHg X ml-1 X min X 100 g in the hypercapnic group (NS; P greater than 0.05). During moderate hypotension, RVR was 0.48 +/- 0.18 in the normocapnic group and 1.74 +/- 0.36 mmHg X ml-1 X min X 100 g in the hypercapnic group (P less than 0.05, comparison between groups). During severe hypotension, RVR was 0.46 +/- 0.14 and 3.13 +/- 1.13 mmHg X ml-1 X min X 100 g during normocapnia and hypercapnia, respectively (P less than 0.05, comparison between groups). Thus, in unanesthetized rabbits, although hypercapnia does not increase RVR compared with normocapnia when arterial pressure is normal, hypercapnia greatly potentiates renal vasoconstriction during hemorrhagic hypotension.

Severe Hypotension Is Not Essential for Isoflurane Neuroprotection against Forebrain Ischemia in Mice

2003 ◽  
Vol 99 (5) ◽  
pp. 1145-1151 ◽  
Author(s):  
H. Mayumi Homi ◽  
Javier M. Mixco ◽  
Huaxin Sheng ◽  
Hilary P. Grocott ◽  
Robert D. Pearlstein ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Occlusion ◽  
Plasma Norepinephrine ◽  
Ischemic Insult ◽  
Bilateral Carotid Occlusion ◽  
Severe Hypotension ◽  
Bilateral Carotid ◽  
Neurologic Function

Background Volatile anesthetics provide protection in experimental models of global cerebral ischemia. To date, all models evaluated have included profound systemic arterial hypotension as a component of the ischemic insult. This study was designed to determine if isoflurane protection persists in a global insult devoid of hypotension. Methods C57BL/6J mice having a high incidence of posterior communicating artery atresia were anesthetized with isoflurane (1.2%) or fentanyl/N2O and subjected to bilateral carotid artery occlusion for 15 min or 20 min with normotension (80-110 mmHg mean arterial pressure) or for 10 min with hypotension (35 mmHg mean arterial pressure). Three days later, neurologic function and histologic damage were assessed. Other mice underwent measurement of intraischemic cerebral blood flow (4-iodo-N-methyl-[14C]antipyrine autoradiography) or plasma norepinephrine. Results Isoflurane reduced the percentage of hippocampal CA1 dead neurons (e.g., 10 min bilateral carotid occlusion + hypotension: 43 +/- 18 (isoflurane) vs. 67 +/- 20 (fentanyl/N2O), P = 0.003; 20 min bilateral carotid occlusion + normotension: 49 +/- 27 (isoflurane) vs. 71 +/- 22 (fentanyl/N2O), P = 0.003). Isoflurane also reduced CA3 damage and improved neurologic function under all conditions. Intraischemic forebrain blood flow was similar during bilateral carotid occlusion plus normotension for the two anesthetic states. Plasma norepinephrine values were greater when hypotension was added to the ischemic insult. Conclusions Isoflurane resulted in improved neurologic function and reduced histologic damage regardless of the presence or absence of systemic hypotension during the ischemic insult. This indicates that beneficial effects of isoflurane are most likely attributable to direct effects at the neuronal level as opposed to indirect effects resulting from interactions with profound hypotension.

Acoustic-Reflex Dynamics for Pulsed Signals

1978 ◽  
Vol 21 (2) ◽  
pp. 295-308
Author(s):  
Terry L. Wiley ◽  
Raymond S. Karlovich
Keyword(s):  
Duty Cycle ◽  
Acoustic Impedance ◽  
Normal Hearing ◽  
Broadband Noise ◽  
Threshold Shift ◽  
Temporary Threshold Shift ◽  
Acoustic Reflex ◽  
Stapedius Muscle ◽  
Duty Cycles

Contralateral acoustic-reflex measurements were taken for 10 normal-hearing subjects using a pulsed broadband noise as the reflex-activating signal. Acoustic impedance was measured at selected times during the on (response maximum) and off (response minimum) portions of the pulsed activator over a 2-min interval as a function of activator period and duty cycle. Major findings were that response maxima increased as a function of time for longer duty cycles and that response minima increased as a function of time for all duty cycles. It is hypothesized that these findings are attributable to the recovery characteristics of the stapedius muscle. An explanation of portions of the results from previous temporary threshold shift experiments on the basis of acoustic-reflex dynamics is proposed.

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