Pleural liquid pressure in dogs measured using a rib capsule

We have developed a minimally invasive method for measuring the hydrostatic pressure in the pleural space liquid. A liquid-filled capsule is bonded into a rib and a small hole is cut in the parietal pleura to allow direct communication between the liquid in the capsule and the pleural space. The pressure can be measured continuously by a strain gauge transducer connected to the capsule. The rib capsule does not distort the pleural space or require removal of intercostal muscle. Pneumothoraces are easily detected when they occur inadvertently on puncturing the parietal pleura. We examined the effect of height on pleural pressure in 15 anesthetized spontaneously breathing dogs. The vertical gradients in pleural pressure were 0.53, 0.42, 0.46, and 0.23 cmH2O/cm height for the head-up, head-down, supine, and prone body positions, respectively. These vertical gradients were much less than the hydrostatic value (1 cmH2O/cm), indicating that the pleural liquid is not in hydrostatic equilibrium. In most body positions the magnitudes of pleural liquid pressure interpolated to midchest level were similar to the mean transpulmonary (surface) pressure determined postmortem. This suggests that pleural liquid pressure is closely related to the lung static recoil.     

Pleural and extrapleural interstitial liquid pressure measured by cannulas and micropipettes

In 15 anesthetized apneic, oxygenated rabbits we simultaneously measured pleural liquid and interstitial extrapleural parietal pressures by using catheters and/or cannulas and micropipettes connected to a servonull system. With the animal in lateral posture, at an average recording height of 4.4 +/- 0.9 (SD) cm from the most dependent part of the cavity, the extrapleural catheter and the pleural cannula yielded -2.5 +/- 0.6 and -5.5 +/- 0.2 cmH2O; the corresponding values for micropipette readings in the two compartments were -2.4 +/- 0.6 and -5.4 +/- 0.4 cmH2O, respectively (not significantly different from those measured with catheters and cannulas). In the supine animal, interstitial extrapleural catheter pressure data obtained at recording heights ranging from 15 to 80% of pleural cavity lay on the identity line when plotted vs. the micropipette pressure values simultaneously gathered from the same tissues. We conclude that 1) micropipettes and catheters-cannulas yield similar results when recording from the same compartment and 2) the hydraulic pressure in the parietal extrapleural interstitium is less negative than that in the pleural space.     

Lung microvascular pressure profile measured by micropuncture in anesthetized dogs

We have micropunctured the lung in the open thorax of 17 anesthetized dogs to measure microvascular pressure. After intravenous pentobarbital sodium (25 mg/kg), we exposed the left lung through a wide left thoracotomy, which required rib excision. Through a double-lumen endotracheal tube, we ventilated the right lung to maintain normal blood gases and pH while we held the left lung motionless at an inflation pressure of 5 cmH2O. To reduce motion on the surface of the left lower lobe, we resected the left upper lobe, placed a Plexiglas baffle between the lobe and the heart, and held the lobe surface in a suction ring. In accordance with procedures we have previously described, we micropunctured subpleural vessels to measure microvascular pressure. At base line when alveolar pressure exceeded left atrial pressure (zone 2 conditions), 21, 38, and 41% of the total pressure drop occurred, respectively, in the arterial, microvascular, and venous segments. When we raised left atrial pressure above alveolar pressure (zone 3 conditions), the corresponding pressure drops were 30, 55, and 20% of total. The blood flow in the superficial layer of the lung averaged 15% less than the flow in the deeper layers as measured by distribution of 99mTc-albumin macroaggregates. We conclude that the intact and the isolated lung preparations in dog exhibit similar distributions of subpleural microvascular pressure.     

Prostaglandins modulate baroreflex-induced changes in blood pressure and myocardial function in anesthetized dogs

The purpose of our study was to investigate the role of prostaglandins in the changes in myocardial function and peripheral and coronary vascular resistance which accompany a generalized increase in sympathetic tone caused by carotid baroreflex unloading in the anesthetized dog. Bilateral carotid artery occlusion (BCO) with heart rate held constant by electrical pacing (150 beats/min) resulted in increases in systolic, (33%) diastolic (40%), and mean (35%) arterial pressures, LV systolic pressure (33%) and left ventricular (LV) dP/dt (37%). After blockade of prostaglandin synthesis with indomethacin (N = 11) or meclofenamate (N = 6) the increases in systolic (41%), diastolic (45%), and mean (41%) arterial pressures, LV systolic pressure (39%), LV dP/dt (52%), and cardiac work caused by BCO were significantly greater, in spite of the initially higher baseline values (11-18%) following the administration of the drugs. In contrast, the changes in circumflex coronary blood flow and coronary vascular resistance to BCO were essentially the same before and after inhibition of prostaglandin synthesis. Systemic prostaglandin synthesis may, therefore, play a significant role in the control of systemic arterial pressure and myocardial function, most probably by modulating the release of norepinephrine from adrenergic nerve terminals, without adversely affecting coronary blood flow regulation.     

Juxtacardiac pressure in closed-chest dogs

We studied pressure (Ppc)-volume (Vpc) relationships of the pericardial sac by inserting air into it at constant end-diastolic heart volume in six dogs. The lungs were inflated by positive alveolar pressure while pleural pressure was monitored using the esophageal balloon technique. Ppc-Vpc relationships were measured at transpulmonary pressures (PL) of 30, 10, and 5 cmH2O in each of three states: closed chest, open chest with lung separation, and open chest with the pericardium dissected free of its mediastinal attachment. Ppc in the closed-chest condition was more positive than Ppc in the open chest with lung separation, with increase of Vpc and PL, which suggests that the lungs compress the pericardium. Ppc in the open-chest condition with lung separation was also more positive than Ppc in the pericardium after it was dissected free, which suggests that mediastinal attachment compresses the pericardium. It is suggested that lungs in the closed-chest condition as well as mediastinal attachment reduce the heart expansion by a similar magnitude.     

Haemodynamic effects of respiratory alkalosis independent of changes in airway pressure in anaesthetized newborn dogs

We have recently reported a decrease in cardiac output in newborn dogs during respiratory alkalosis which is independent of changes in airway pressure. The present study was designed to characterize the mechanism responsible for this reduction in cardiac output. Twelve newborn coonhounds were anaesthetized with pentobarbital, paralyzed with pancuronium and hyperventilated to an arterial carbon dioxide tension (PaCO2) of 20 torr. Subsequent changes in PaCO2 were achieved by altering the FiCO2. Measurements were made after 30 min at either 40 or 20 torr PaCO2. The sequence of PaCO2 levels was randomized. Compared to normocarbia, respiratory alkalosis resulted in significantly decreased cardiac output (279 +/- 16 to 222 +/- 10 ml/min per kg, mean +/- SEM, P less than 0.001), stroke volume (1.60 +/- 0.10 to 1.24 +/- 0.06 ml/kg; P less than 0.001), maximum left ventricular dP/dt (1629 +/- 108 to 1406 +/- 79 mmHg/s, P less than 0.01) and left ventricular end diastolic pressure (3.9 +/- 0.4 to 2.9 +/- 0.3 mmHg; P less than 0.001). The decrease in cardiac output during respiratory alkalosis is manifest through a decrease in stroke volume, which is due, at least in part, to the decrease in left ventricular end diastolic pressure. The decrease in maximum left ventricular dP/dt is likely a reflection of the decrease in preload, however, a change in myocardial contractility cannot be excluded. We speculate the decrease in filling pressure may be due to an increase in venous capacitance.     

Pleural pressure as a function of body position in rabbits

Pleural pressure was measured at end expiration in spontaneously breathing anesthetized rabbits. A liquid-filled capsule was implanted into a rib to measure pleural liquid pressure with minimal distortion of the pleural space. Capsule position relative to lung height was measured from thoracic radiographs. Measurements were made when the rabbits were in the prone, supine, right lateral, and left lateral positions. Average lung heights in the prone and supine positions were 4.21 +/- 0.58 and 4.42 +/- 0.51 (SD) cm, respectively (n = 7). Pleural pressure was -2.60 +/- 1.87 (SD) cmH2O at 50.2 +/- 7.75% lung height in the prone position and -3.10 +/- 1.22 cmH2O at 51.4 +/- 6.75% lung height in the supine position. There was no difference between the values recorded in the prone and supine positions. Placement of the capsule into the right or left chest had no effect on the magnitude of the pleural pressure recorded in rabbits in right and left lateral recumbency (n = 12). Measurements over the nondependent lung were repeatable when rabbits were turned between the right and left lateral positions. Lung height in laterally recumbent rabbits averaged 4.55 +/- 0.52 (SD) cm.     

Charge movements measured during transverse-tubular uncoupling in frog skeletal muscle.

Capacity transients and slow asymmetric charge-movements are measured in frog skeletal muscle using the Vaseline-gap voltage-clamp technique. Capacity transients show a rapid phase lasting 10-30 microseconds, due to the charging of the surface membrane capacitance, and a slower phase lasting several milliseconds, consistent with the charging of the transverse tubular system (T-system). Exposure to isotonic CsF caused the ratio of the slowly-charging capacitance (Cslow) to the fast-charging capacitance to decline by 88 +/- 9% (n = 16). Electron micrographs of four fibers treated with CsF show disruption and disorganization of the T-system and sarcoplasmic reticulum membranes and a greater than 90% decrease in the number of dyads and triads. The role of CsF was investigated: Fibers exposed to CsF internally or externally, exhibit slower and less complete loss of Cslow than fibers exposed both internally and externally. Little loss of Cslow occurs during the external exposure to CsF. The bulk of loss occurs only after the fiber is returned to Ca++-containing solution. Elevated external Ca++ causes more rapid and more complete loss of Cslow. The time-course of Cslow loss is gradual, occurring over a period of 10 min to 2 h. The progressive loss of Cslow is accompanied by a progressive decline in the peak of the slow asymmetric charge-movement and a progressive slowing of charge movement kinetics. These effects are qualitatively accounted for by including gradual tubular uncoupling in a distributed model of charge movement proposed by B. Simon and K. G. Beam (1985, J. Gen. Physiol., 85:21-42).     

Intestinal helminths induce haematological changes in dogs from Jabalpur, India

The effect of canine intestinal helminths on the haematological profile of 200 dogs, of both sexes and variable age, visiting university veterinary clinics for routine examination was investigated. The dogs were assigned to parasitized (n?=?39) and non-parasitized (n?=?161) groups of animals. Coprological examination revealed a 19.5% prevalence of different species of the helminths. Of these animals, 10.25% had mixed infections with Ancylostoma caninum, Toxascaris spp. and Dipylidium caninum. The intensity of A. caninum infection was the highest, with mean egg counts of 951.43 (standard error 88.66), followed by Toxascaris 283.33 (standard error 116.81) and D. caninum. The parasitized animals had significantly lower levels of haemoglobin, packed cell volume and total erythrocyte counts than non-parasitized animals (P?相似文献   

Determinants of transdiaphragmatic pressure in dogs

We measured the transdiaphragmatic pressure (Pdi) during bilateral phrenic nerve stimulation and evaluated the determinants of its change with lung volume, chest wall geometry, and respiratory system impedance in supine dogs. Four rows of radiopaque markers were sewn onto muscle bundles of the costal and crural diaphragm between their origin on the central tendon and their insertion on the rib cage and spine. The length of the diaphragm (L) was determined from the projection images of marker rows using biplane fluoroscopy. Measurements were made at lung volumes between total lung capacity and functional residual capacity before and after the infusion of Ringer lactate solution into the abdominal cavity. In contrast to relaxation, during tetanic stimulation the active lengths of the muscle bundles were similar at all volumes, but the diaphragm assumed different shapes. Although the small differences in active muscle length with volume and liquid loads are consistent with only small changes in muscle force output, Pdi varied by a factor of greater than or equal to 5. There was no single L/Pdi curve that fitted all data during 50-Hz stimulations. We conclude that under these experimental conditions Pdi is not a unique measure of the force produced by the diaphragm and that lung volume, chest wall geometry, and respiratory system impedance are important determinants of the mechanical efficiency of the diaphragm as a pressure generator.