Factors affecting lung microvascular pressure.
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Biomedical subjects
Publications and source records attributed to J Bhattacharya.
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We punctured subpleural microvessels in 19 isolated blood-perfused dog lung lobes to determine the effect of 5-hydroxytryptamine (5-HT) on the pulmonary microvascular pressure profile. Maintaining lobe airway pressure at 6 cmH2O and lobe venous pressure at 10 cmH2O we infused saline alone (10 microliter/min) in 10 control lobes and 5-HT in saline solution (100--150 micrograms/min) in 9 lobes. We measured pressures in subpleural microvessels using micropipettes connected to a servo-null system. The 5-HT infusion doubled lobar vascular resistance. In all microvessels upstream from the 150-micrometer venules, pressure was higher than in the control lobes. In contrast to the control lobes, pressure dropped markedly from the lobar artery to the 50-micrometer arterioles and from the venous capillaries to the 50-micrometer venules. We conclude that 5-HT not only constricted arterioles, but also raised lung microvascular pressure by constricting postcapillary venules.
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Microvascular pressures in the pulmonary circulation were measured under the pleural surface of the isolated perfused dog lung by the servo-null technique. Strong glass micropipettes with short beveled tips were used, with a suction ring to stabilize the lung's surface. Of the total vascular resistance, 45 percent was in the alveolar wall capillaries themselves. Most of the remaining resistance was in the arterioles. There was negligible pressure drop in venules with diameters larger than 20 micrometers.
When cannulation of the left ventricle and the left atrium were compared as methods for measuring for measuring renal blood flow distribution with radioactive microspheres in 9 conscious and 6 anesthetized rabbits, there were no differences between the two injection routes. Left ventricular cannulation per se did not affect cardiac output, nor the percentage of the cardiac output supplying the kidneys; but cardiac outputs estimated by thermodilution by injections via this route were up to 10% greater than those from left atrial injection. The advantages of left ventricular cannulation for experiments on regional blood flow distribution in conscious animals are discussed.
We determined the relationship between the amount of edema and changes in blood flow in the isolated, perfused, and ventilated lower lobe of dog lung. We held vascular pressure constant and measured lobe weight and flow continuously. Vascular pressures were set to produce minimal weight gain in four lobes (controls) and large weight gain in six lobes (edema). In all lobes, the outflow pressure exceeded alveolar pressure at end expiration (zone III conditions). The control lobes gained an average of 20% in weight over 4 h, but blood flow remained constant. They showed interstitial edema histologically and extravascular lung water was increased 38%. The edema lobes gained weight rapidly, ultimately tripling their weight. In these lobes, blood flow remained constant until lobe weight had doubled; then flow decreased progressively to low levels. These lobes showed extensive alveolar edema histologically and extravascular lung water was increased 238%. Pulmonary blood flow is not affected by interstitial edema, but is markedly reduced when alveolar flooding occurs.
Experiments in conscious rabbits were designed to determine whether the effects of mannitol on renal blood flow and sodium and water excretion depend on increased renal prostaglandin synthesis. Compared to controls mannitol caused: a) increased glomerular filtration rate, naturesis, and water diuresis, that were unaffected by meclofenamate, b) increased outer cortical flow, that was prevented by meclofenamate, and c) decreased inner cortical flow, that was accentuated by meclofenamate. Thus the diuretic effect of mannitol occurred independently of increases in renal blood flow or prostaglandin synthesis. Changes in renal blood flow distribution with mannitol may be due to altered renal prostaglandin synthesis secondary to changes in tissue osmolarity.
1. The effect on renal blood flow regulation of unilateral renal denervation followed by administration of a prostaglandin synthesis inhibitor has been studied in nine conscious rabbits.2. Renal blood flow distribution was estimated using radioactive microspheres injected via a pre-implanted left ventricular cannula. Cardiac output was estimated by thermodilution. Measurements were made before and after intravenous injection of Meclofenamate, Parke Davis Ltd (4 mg/kg).3. Renal denervation caused a fall in renal cortical catecholamine concentration of approximately 50% by 48 hr.4. Resting renal blood flow did not differ significantly between denervated and innervated kidneys.5. Meclofenamate caused a significant rise in arterial pressure from a mean of 59 to 70 mmHg. In innervated kidneys, Meclofenamate caused a fall in renal blood flow from 8.1 +/- 0.6 (mean +/- S.E. of mean) to 6.5 +/- 0.4 ml./min.g kidney weight while in denervated kidneys it caused a fall from 8.9 +/- 0.7 to 6.25 +/- 0.3 ml./min.g. After Meclofenamate flow was redistributed away from the inner cortex in the innervated kidney and paradoxically towards the inner cortex in the denervated one.6. It was concluded that in conscious animals, resting sympathetic tone has little effect on renal blood flow. The exaggerated reduction in flow in the outer cortex of the denervated kidney following Meclofenamate may indicate denervation hypersensitivity to circulating catecholamines unmasked by reduced synthesis of vasodilator prostaglandins. Alternatively, renal sympathetic nerves may normally prime prostaglandin synthesis in the outer cortex.
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Recently we demonstrated potassium secretion by the pars recta or by the descending limb of the juxtamedullary nephron. The purpose of this present investigation is to study the effect of a chronic high-potassium intake on this phenomenon. Fractional reabsorption of water and sodium by the juxtamedullary proximal nephron was decreased when compared to that in normal hydropenic rats. There was a striking increase in the fraction of filtered potassium at the end of the juxtamedullary descending limb from 94+/11% to 180+/18%, which was principally a result of enhanced potassium secretion. When the concentration of potassium in the collecting tubule fluid of potassium-loaded rats was reduced after the administration of amiloride, a sharp fall was observed in the amount of potassium which reached the end of the descending limb (64+/8%). A direct correlation was observed between the fraction of filtered potassium at the descending limb and the potassium concentration in the final urine (P less than 0.001). The findings suggest that potassium, like urea, normally undergoes medullary recycling, which is enhanced by chronic potassium loading.
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1. We have studied the effects of two prostaglandin synthesis inhibitors on renal cortical blood flow distribution in conscious rabbits. 2. Renal blood flow distribution was estimated by means of radioactive microspheres injected into chronically implanted left atrial cannulae. Cardiac output was measured by a thermodilution technique. 3. Measurements were made in groups of animals treated with either indomethacin, meclofenamate or control injections of phosphate buffer. 4. A method of microtome slicing of the renal cortex was developed to standardize measurements. Microtome sections were grouped into inner, middle and outer zones. After both indomethacin and meclofenamate there was a reduction in total renal blood flow with a redistribution of flow from inner to outer cortex. 5. Estimated renal vascular resistance rose in all three cortical zones. 6. The data support the hypothesis that renal prostaglandin synthesis is necessary for maintaining flow to the deep cortex. It is suggested that renal prostaglandins may also influence flow in more superficial zones. 7. Estimated total systemic vascular resistance was increased both with meclofenamate and indomethacin, suggesting an inhibiting effect of prostaglandins on arteriolar tone throughout a major part of the systemic circulartion.
1. Renal blood flow autoregulation was studied in anaesthetized greyhounds, using an electromagnetic flowmeter, before and after the administration of the prostaglandin-synthesis inhibitor, indomethacin, or phosphate buffer. 2. Indomethacin caused a reduction in renal blood flow at all levels of perfusion pressure, but did not affect the ability of the kidney to autoregulate. 3. The aburpt reinstatement of renal perfusion pressure from previously reduced levels caused a triphasic transient response in flow. Peak hyperaemia at the beginning of the transient was not affected by indomethacin. After indomethacin, the second phase of this flow transient showed an oscillatory pattern during which flow fell initially to levels significantly lower than control. 4. It is concluded that although indomethacin did not abolish steady-state autoregulation, renal prostaglandins may damp rapid oscillations in renal blood flow and thus contribute to the efficiency of autoregulation.
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The effects of furazolidone, erythromycin and azithromycin in inhibiting colonisation of Vibrio cholerae O1 and O139 in the rabbit intestine were tested. Both V. cholerae O1 and O139 highly colonised the gut in control rabbits. The colonisation of furazolidone-resistant strains in the rabbit intestine was prevented effectively by both erythromycin and azithromycin. In furazolidone-sensitive strains, the efficacies of erythromycin and azithromycin were very much comparable to furazolidone. These results suggested that azithromycin may be subjected to clinical trial in comparison to furazolidone and erythromycin for the treatment of cholera due to O1 and O139 infection in children.
The effect of propranolol and acebutolol therapy on serum lipoproteins was studied in thirty patients (mean age 43.9 +/- 8.7 years) with essential hypertension and/or stable myocardial ischaemia. Patients received six weeks therapy with propranolol (80-160 mg per day) and acebutolol (400-800 mg per day) each in random order and were changed over from one to the other beta-blocker after 6 weeks therapy. On propranolol treatment there was no significant effect on total cholesterol and LDL-cholesterol but the concentration of serum triglycerides (94.2 +/- 37.7 to 129.1 +/- 41.2 mg/dl) and VLDL cholesterol (18.9 +/- 7.8 to 26.1 +/- 8.1 mg/dl) significantly increased, concentration of HDL cholesterol (49.5 +/- 9.4 to 42.4 +/- 8.7 mg/dl) significantly decreased (p less than 0.01). Atherogenic index also worsened from 4.17 +/- 0.48 to 5.15 +/- 0.54 (p less than 0.05) on propranolol therapy. Acebutolol therapy, on the other hand, produced no significant change in the concentration of total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol and VLDL cholesterol.