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Biomedical subjects

H Bark

Publications and source records attributed to H Bark.

49 records · Page 3Linked to original sources
PubMed1987

Effect of inspiratory muscle fatigue on perception of effort during loaded breathing.

The present study examined the relationship between the intensity of the sense of effort during inspiratory threshold loading and the severity of inspiratory muscle fatigue. Studies were performed on normal subjects in whom the magnitude of airway pressure developed (Pm) and the duty cycle of breathing (TI/TT) were constrained to achieve a pressure-time integral (i.e., Pm/Pmax X TI/TT) 24% of maximum. In separate trials, the same pressure-time index (24%) was achieved using two widely different patterns of pressure magnitude and duty cycle to allow the effects of changes in the pattern of inspiratory muscle contraction on sensation and fatigue to be assessed. The intensity of the sense of effort was assessed using a category (Borg) scale. The severity of inspiratory muscle fatigue was assessed both from changes in the centroid frequency of the diaphragm electromyogram and from changes in the maximum static inspiratory pressure. Loaded breathing produced inspiratory muscle fatigue and a progressive increase in the sense of effort over time in all subjects. The rate at which the inspiratory muscles fatigued was the same with the two patterns of loading. In contrast, the rate of growth in the intensity of the sense of effort varied significantly as a function of the pattern of loaded breathing. The sense of effort increased at a faster rate with the high pressure-short duty cycle pattern of contraction as compared with the low pressure-long duty cycle pattern. As a result, the intensity of the sense of effort was not uniquely related to the severity of inspiratory muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effect of phrenic nerve stimulation on neural transmission and diaphragmatic force generation in the dog.

The effect of supramaximal bilateral phrenic nerve stimulation on neural transmission and diaphragmatic force generation was studied in anesthetized dogs. Different combinations of duty cycle and stimulation frequency were examined during intermittent stimulation (pacing) for 15 min. The effect of different stimulation frequencies was also examined during continuous stimulation for 60 sec. Force declined more with increasing stimulation frequency and duty cycle with intermittent stimulation, and with increasing stimulation frequency with continuous stimulation. Neural transmission decreased with increasing stimulation frequencies. The changes were always greater with continuous than with intermittent stimulation. We found no unique relationship between changes in neural transmission and changes in force generation, suggesting that if neural transmission failure is causally responsible for fatigue, it does so by a very complex mechanism.

Action Potentials↗
PubMed1986

Diaphragmatic blood flow in the dog.

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.

Animals↗
PubMed1986

Effect of alterations in muscle fiber length on diaphragm blood flow.

A variety of studies have examined the response of diaphragmatic blood flow (Qdi) to rhythmic pleiometric (i.e., shortening) and isometric contractions. The effect of changes in diaphragm fiber length on Qdi are, however, unknown. The present study examined the effect of changes in diaphragm fiber length on Qdi and the effect of alterations in length on the response of Qdi to increases in diaphragm contractile activity. Studies were performed on 21 anesthetized mechanically ventilated dogs in which a strip of costal diaphragm was developed in situ. The strip was immobilized in a rigid metal frame that permitted precise adjustment of muscle length. Strip blood flow was assessed with a drop counter attached to a catheter in the branch of the phrenic vein draining the strip. Strips were electrically stimulated via intramuscular electrodes, and the isometric tension developed was measured with a force transducer. Fiber length was expressed as a percentage of the length at which active isometric tension was maximum (Lo). With the diaphragm at rest, steady-state blood flow fell by 59 +/- 6% (SE) (P less than 0.001) as fiber length was increased from 92 to 107% Lo. Blood flow also varied as a function of length when muscles contracted rhythmically (15 contractions/min, duty cycle 50%) to generate isometric tensions equal to 20 and 80% of maximum. As fiber length increased from 92 to 106% Lo, Qdi fell by 36 +/- 6% (SE) when tension was 80% of maximum (P less than 0.01) and by 38 +/- 6% (SE) when tension was 20% of maximum (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Blood flow to the canine diaphragm during hemorrhagic shock.

Previous studies have shown impairment of diaphragm function during shock. It is possible that the mechanism for this is decreased diaphragm perfusion, which leads to decreased function because of limitation of oxygen transport. In order to examine the degree to which oxygen transport is limited during shock, we measured the changes in blood flow to and oxygen consumption of the diaphragm during controlled hemorrhage. Blood flow through the left phrenic artery (Qdi) was measured with an electromagnetic flow probe as systemic arterial pressure (Pa) was decreased. The Pa-Qdi relationship was found to be linear with slope of approximately 0.145 ml/torr/min, and extrapolated pressure at zero flow of approximately 40 torr in normal control subjects. Inspiratory loading and infusion of isoproterenol led to a parallel shift in the Pa-Qdi curve such that there was a decrease in the extrapolated pressure at zero flow to 9 to 13 torr. Infusion of dopamine led to a parallel shift of the Pa-Qdi curve such that there was an increase in the extrapolated pressure at zero flow from approximately 34 to approximately 45 torr. In the normal control subjects, there was a decrease in oxygen consumption associated with the decrease in Qdi, but this was not true for either loading or isoproterenol. We conclude that during hypotension, blood flow to the diaphragm decreases. However, the diaphragm retains the ability to increase its blood flow in response to metabolic or pharmacologic stimuli. This is done primarily by a parallel shift in the pressure-flow relationship, which may represent a change in the critical closing pressure of the phrenic vasculature.

Animals↗
PubMed1984

Function of canine diaphragm with hypovolemic shock and beta-adrenergic blockade.

In anesthetized mongrel dogs we investigated the effects of hypovolemia and beta-adrenergic stimulation on the decrease in force generation by the diaphragm [transdiaphragmatic pressure (Pdi)] during electrical stimulation of the phrenic nerves for 1 h. In seven normovolemic dogs with arterial pressure (Pa) of approximately 125 Torr, Pdi fell approximately 48% from an initial value of 35 +/- 4.8 Torr. In dogs made moderately hypovolemic, Pdi was actually higher than with normovolemia (P less than 0.01). In dogs made severely hypovolemic, Pa approximately 50 Torr, Pdi at the start of pacing was less than with normovolemia (25 +/- 1.5 Torr) and remained so during phrenic nerve stimulation. When beta-adrenergic blockade with propranolol was added to moderate hypovolemia, the values of Pdi became similar to those of severe hypovolemia. Analysis of the relative contributions of gastric pressure and pleural pressure revealed that the factor responsible for maintaining Pdi with moderate hypovolemia was pleural pressure. Changes in thoracic gas volume and chest wall configuration did not explain the changes we saw in diaphragm function. Analysis of the relationship between rib cage motion and pleural pressure confirmed our finding of the greater pleural pressure generation with sympathetic stimulation that accompanies hypovolemia. These studies demonstrated that 1) severe hypovolemia impaired diaphragm function, 2) diaphragm function was maintained with moderate hypovolemia by beta-adrenergic stimulation, and 3) with hypovolemia-associated sympathetic stimulation there was an increase in force generation by the intercostal muscles.

Adrenergic beta-Antagonists↗
PubMed1984

"Second wind" during inspiratory loading.

Five human volunteers breathed through an inspiratory register to achieve a transdiaphragmatic pressure (Pdi) of 42-45% of the maximum, until fatigue. During the period of resistive breathing all subjects experienced at least one episode of a sudden feeling of relaxation and relief from dyspnea, i.e., "second wind." These episodes were accompanied by a sudden decrease in the neural stimulation to the diaphragm as reflected in the electromyogram (EMG). Changes in lung volume or chest configuration were eliminated as was recruitment of accessory muscles of inspiration during the "second wind"; thus, there appeared to be a change in the contractile function of the diaphragm such that the same force (Pdi) was achieved with less neural input. These results indicate that the phenomenon of "second wind" has physiologic correlates and may be subject to experimental verification and manipulation.

Adult↗
PubMed1980

Elevations in plasma ADH levels during PEEP ventilation in the dog: mechanisms involved.

In an attempt to define more precisely the various mechanisms involved in antidiuretic hormone (ADH) release during positive end-expiratory pressure ventilation (PEEP), experiments were performed on seven groups of dogs. PEEP-10 and PEEP-15 cmH2O caused significant elevations of plasma ADH from basal values of 24.9 +/- 5.2 pg/ml (mean +/- SE) to 64.6 +/- 14.2 and 106.0 +/- 20.6, respectively (P < 0.02, P < 0.005). The ADH levels returned to basal values after cessation of PEEP. This rise in ADH levels was prevented by an infusion of dextran prior to PEEP. The fall in blood pressure and cardiac output that occurred during PEEP was also prevented by the dextran infusion. Changes in ADH levels were unrelated to lung volume, left transmural pressure, and serum osmolality. Bilateral vagotomy and carotid sinus denervation was followed by an attenuated rise in ADH levels in terms of the percent rise above base line, but it did not significantly alter the absolute rise in ADH during PEEP. ADH levels were, however, reduced significantly by decreasing intracranial pressure by the removal of cerebrospinal fluid during PEEP. Propranolol administration prior to PEEP completely blocked plasma renin activity. Although the peak ADH levels were unaffected by propranolol, the rise was delayed. The results obtained indicate that a number of physiological factors may affect plasma ADH levels during PEEP. These include the carotid body and aortic arch baroreceptors as wells as sensors of intracranial pressure.

Animals↗
PubMed1977

Caffeine pharmacokinetics in young and adult dogs.

The pharmacokinetics of caffeine were studied in young (age: 1 day, 7 days, 14 days, 30-45 days) and adult dogs following a single intravenous dose of 50 mg/kg. Mean (+/-SE) plasma elimination half life (T1/2) was 47.5 (+/-5.35) h in 1-day-old puppies, as opposed to 6.66(+/-0.85) h in adult dogs. A rapid decrease in plasma T1/2 values occurred during the first 2 weeks of life. At about 14 days of age caffeine plasma T1/2 was similar to that of adults. The volume of distribution was greatest (0.94+/- 0.03 liters/kg) and the total body clearance was smaller (2.81 +/- 0.73 liters/kg/min X 10(-4)) in the 1-day-old animals. The much smaller body clearance of caffeine in the newborn as compared to the adult dog could be due to a lower rate of metabolism and/or renal excretion of this drug in the young.

Age Factors↗
PubMedDate not supplied

Spirocerca lupi infection in the dog: aberrant migration.

The nematode Spirocerca lupi (S. lupi), a parasite of dogs and other carnivores, affects mainly the esophagus and the aorta leading to gastrointestinal, respiratory, and circulatory signs. Aberrant migration of the worm to unusual anatomical structures, especially the thoracic cavity, resulting in atypical clinical signs is being reported more frequently. Aberrant migration of S. lupi is reviewed, and two such cases (i.e., migration to the heart, causing an aortico-pulmonary "window-like" opening, and to a subcutaneous abscess in the caudal thoracic region) are presented.

Animals↗
PubMedDate not supplied

Halothane anaesthesia in the dromedary camel.

It was shown that the effects of halothane anaesthesia in the dromedary are similar to those of large domestic ruminants. As a general rule the equipment and techniques used for adult cattle may also be used in the dromedary. Endotracheal intubation may be more difficult in camels because of their narrow oral cavities. Involuntary regurgitation is a particular hazard in dromedaries and every effort should be made to avoid this potentially life threatening complication.

Anesthesia, General↗