Quantitative studies of the vasculature of the carotid body in the chronically hypoxic rat.

The carotid bodies of rats made chronically hypoxic by breathing 12% O2 in a normobaric chamber (inspired PO2 91 mmHg) were compared with those of controls. Serial 5-microm sections of the organs were examined using an interactive image analysis system. The total volume of the carotid bodies was increased by 64%. The total vascular volume rose by 103% and was likely due to an increase in size of the large vessels (>12 microm lumen diameter) because the small vessel (5-12 microm lumen diameter) volume did not increase significantly while the small vessel density tended to decrease. The extravascular volume was increased by 57%. Expressed as a percentage of the total volume of the organ, the total vascular volume did not change, but the small vessel volume was significantly decreased from 7.83 to 6.06%. The large vessel volume must therefore have been increased. The proportion occupied by the extravascular volume was virtually unchanged (84 vs 82%). In accordance with these findings, the small vessel endothelial surface area per unit carotid body volume was diminished from 95.2 to 76.5 mm-1, while the extravascular area per small vessel was increased from 493 to 641 microm(2) or by 30%. In conclusion, the enlargement of the carotid body in chronic hypoxia is most likely due to an increase in total vascular volume, mainly involving the "large" vessels, and to an increase in extravascular volume. This is in contrast to our previously published findings indicating that in the spontaneous insulin-dependent diabetic rat the enlargement of the carotid body is due solely to an increase in extravascular volume.

The carotid body of the spontaneous insulin-dependent diabetic rat.

The carotid bodies from adult spontaneous insulin-dependent diabetic rats (strain BB/S) were perfusion-fixed at normal arterial blood pressure with 3% phosphate-buffered glutaraldehyde and compared with the organs from control rats (strain BB/Sc) prepared in the same way. Serial 5-micron sections were cut, stained, and using an interactive image analysis system, were analysed to determine the volumes of the carotid body and its vascular and extravascular compartments. There was no evidence of systemic arterial disease in the carotid stem arteries in either group of animals, and the microvasculature of the organs appeared normal by light microscopy. The volume of the carotid body was unchanged 3 months after the onset of diabetes but was increased at 6 months. The total vascular volume of the organ was unchanged, but the volume of the small vessels (5-12 microns) was increased. In the control group the small vessels comprised 5% of the total volume of the carotid body, or about 44% of the vascular compartment. The percentage of small vessels increased at 3 months in the diabetic group, but had returned to normal at 6 months. The extravascular volume followed the same pattern as the total carotid body volume and so did not change appreciably when expressed as a percentage of the total volume of the organ. The increase in size of the carotid body in diabetic rats is due, therefore, to an augmented extravascular volume. In one diabetic specimen the carotid sinus nerve showed signs of diabetic neuropathy, axonal swelling and intramyelinic oedema. The clinical implications of these results are discussed.

A morphological study of the size of the vascular compartment of the carotid body in a non-human primate (Cercopithecus ethiopus), and a comparison with the cat and rat.

The carotid bodies from 5 adult non-human primates (mean body weight 2.9 kg) were perfusion-fixed at normal arterial blood pressure with 3% phosphate-buffered glutaraldehyde. Serial 5-microns sections were cut, stained, and, using an interactive image analysis system, determinations were made of the volumes of the carotid body and of its vascular and extravascular compartments. The total volume of the carotid body was, on average 0.21 mm3, the total vascular volume contributing 9.7%. The small vessels (5-12 microns diameter) comprised 5.4% of the total volume of the carotid body, or about 56% of the vascular compartment; these estimates were similar to values obtained for the cat and rat. The mean small vessel endothelial area, per unit of extravascular volume (which is assumed to consist largely of type 1 and 2 cells) was 61.8 mm-1 in the primate and 69.7 mm-1 in the cat. A value was not available for the rat. Estimates of the carotid body tissue specific blood flow were 31, 61 and 104 ml/min/100 g organ tissue in the primate, cat and rat, respectively. It was emphasised that these values were not to be confused with estimates of carotid body specific blood flow based on values for total organ blood flow and the dissected weight of the organ.

Quantitative studies of the vasculature of the carotid body in fetal and newborn sheep.

Resetting of the hypoxic sensitivity of the carotid chemoreceptors from the fetal to the adult arterial PO2 range follows the rise in PO2 which occurs after birth. The mechanism of this resetting is unknown. To study whether it is accompanied by a change in the carotid body microvasculature, 2 pairs of carotid bodies from fetal sheep (145 days gestation) and 2 pairs from 7-8 days-old lambs were examined. The ratio of the area of small vessels (6-16 microns diameter) or of larger vessels (greater than 16 microns diameter) to the total area of individual lobules of the carotid body was measured, using a semi-automatic image analysis system. This quantified the number and total cross-sectional area of small vessels and of larger vessels in 20 sections of 5 microns thickness taken at random from 200-350 sections cut from each carotid body. When the carotid bodies of the fetus and neonate were compared, the neonates showed increases in the percentage of the lobule area occupied by both small and large vessels, but the difference was only significant in the case of the larger vessels. There was no difference in the ratio of the area occupied by smaller vessels to the extravascular area of the lobule. Our results do not support the idea that the post-natal resetting of chemoreceptor sensitivity from the fetal to the post-natal range is accompanied by a change in the perfusion of the carotid body chemoreceptor cells.

Comparison of the size of the vascular compartment of the carotid body of the fetal, neonatal and adult cat.

The carotid bodies from full-term fetal cats, 3- to 4-day-old neonates and adult cats were perfusion-fixed at normal arterial blood pressure with 3% phosphate-buffered glutaraldehyde. Serial 5-microns sections were cut and stained by the MSB method. Using an interactive image analysis system, determinations were made of the volumes of the carotid body and of its vascular and extravascular compartments. Compared to the fetus, the carotid body of the neonate increased in volume by 51% and by 286% in the adult cat. There was a proportional increase in the volumes of the vascular compartment and of the small vessels (5-12 microns diameter) in that compartment. The volume of the small vessels, expressed as a ratio of the total volume of the organ, remained constant in the three animal groups at 5-7%. The small vessel endothelial surface area, expressed as a ratio of the extravascular volume (which was assumed to consist largely of type 1 and type 2 cells), was the same in the neonate as in the full-term fetus. Thus, there were no apparent quantifiable morphological features of the carotid body and its vasculature which would account for the resetting of the hypoxic sensitivity of the organ from the fetal to the adult range within a few days of birth.

Dimensions and volume of the carotid body in the adult cat, and their relation to the specific blood flow through the organ. A histological and morphometric study.

In perfusion-fixed preparations of the carotid body, morphological measurements were made on serial histological sections using an interactive image analysis system. The volume of the organ was found to be 0.247 +/- 0.092 mm3. This is considerably smaller than the previous estimates based on the measured postmortem wet weight. This means that the specific blood flow to the carotid body of 2,000 ml/min/100 g using the previously obtained values for the organ's total blood flow and postmortem wet weight may be an underestimate of the true value.

The Brighton resuscitation ambulances: a continuing experiment in prehospital care by ambulance staff.

Two ambulances from the existing fleet in Brighton and one in Hove are equipped with portable defibrillator-oscilloscope units. Selected attendants have been trained not only to defibrillate patients but also to perform endotracheal intubation and administer intravenous atropine and lignocaine for carefully defined indications. In the two years up to December 1975 the ambulances responded to 2253 calls which were considered possible emergencies. Retrospective analysis showed that half of these had been for patients with myocardial infarction, coronary insufficiency, or angina. The ambulances took a median time of five minutes to reach a patient. Attempts at resuscitation were made in 207 patients with circulatory arrest, of whom 160 had ventricular fibrillation. Coordinated rhythm was restored at least transiently in 66 patients, and 27 of them survived to leave hospital. Sixteen of the survivors had been in ventricular fibrillation before the arrival of the ambulance. The delay before admission to hospital was reduced: over 50% of patients carried in the ambulances were admitted within two hours of the onset of major symptoms. No extra ambulance staff have been employed for the scheme. The increased load on hospital services has been limited by encouraging a rational admission policy and also by early discharge.

Mobile coronary care provided by ambulance personnel.

Mobile coronary care has been provided in Brighton by ambulance personnel without immediate help from physicians or nurses. No additional vehicles or staff were required. The capital cost of the experiment was therefore small and additional running costs were negligible. The results have been monitored by retrospective analysis of electrocardiograms recorded in the ambulance and stored on magnetic tape. In the first 12 months of operation to July 1972, 1,082 patients with suspected cardiac emergencies were carried in two vehicles. Subsequent analysis showed that 76% of these patients had acute symptoms from ischaemic heart disease or had circulatory arrest. Eighty-six per cent. of arrhythmias were diagnosed correctly by the ambulance attendants. Though only eight cases of primary ventricular fibrillation occurred during or shortly before transit all were successfully reversed, and five of these patients subsequently left hospital alive. Other benefits of the scheme have included an appreciable reduction in the median delay between onset of presenting symptoms in patients with acute myocardial ischaemia and their admission to hospital.