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This paper describes three pieces of 19th century resuscitation apparatus. These pieces, and the widespread literature on the subject, illustrate the interest in artificial respiration in this period.
A 56-year-old patient was admitted to hospital because of difficulties in swallowing and in opening his mouth. The serological transaminases were increased. Over the next 6 weeks a bioptically proven polymyositis (more proximally located) caused a respiratory insufficiency which had to be treated by artificial respiration. A tetraplegia connected with a large increase of creatine-kinase was also seen. The general investigations were focused on malign processes with a particular search for bronchial carcinoma. At first a kidney cyst detected by ultrasound but was classified as harmless by several investigators. Finally, a computer tomogram of the abdomen demonstrated a cystic degenerated renal carcinoma, which had been cytologically tested also. The clinical course showed a typical aspect of a paraneoplastic syndrome: after extended nephrectomy a distinct regression of the musculary symptoms developed, but with the development of metastases the symptoms increased again. The interdependence of polymyositis and primary renal carcinoma would appear to be proven.
BACKGROUND: During laparoscopic cholecystectomy the arterial-end-tidal CO2 gradient (Fa-ETCO2) has been variously shown to be unchanged, increased, decreased or even negative. The goal of this study was to evaluate Fa-ETCO2, and to determine the proper contribution of VECO2 and VA in regard to the increase of FETCO2. METHODS: Ventilatory patterns were studied in 15 ASA 1-2 patients (mean age +/- SD: 48.5 +/- 15.0) undergoing laparoscopic cholecystectomy, with intraperitoneal CO2 insufflation limited to 12 mmHg, 15 degrees head-up position, during general anaesthesia and controlled ventilation. The following were studied before, during and after the pneumoperitoneum: FaCO2, FETCO2, nasopharyngeal temperature; dead space ventilation, and expired volumes using the Single Breath Test for CO2. VA was calculated as the alveolar fraction of expired VT multipled by the respiratory frequency. RESULTS: During pneumoperitoneum it is shown that: 1) Fa-ETCO2 either decreases and becomes even negative (n = 8) (P < 0.01), or stays unchanged (n = 7), but never elevates; 2) VECO2 increases (peak value: +22.6%) (P < 0.01); 3) VA is unchanged, and 4) dead space ventilation, determined in 7 patients, remains unchanged. CONCLUSION: We conclude that only exogenous CO2 loading, and not VA, can explain such increase in FETCO2 and FaCO2, in cases of limited CO2 insufflating pressure in ASA 1-2 patients.
The cerebral and cerebellar lesions of the cats that were exposed to 0.3% carbon monoxide gas under artificial respiration were examined by an electron microscope at different intervals. During the first few days, the most outstanding features were segmental empty axonal swelling, dilatation of the extracellular space, swelling and necrosis of astrocytes and oligodendroglias, and lamellar separation of the myelin sheath predominantly in the deep cerebral white matter. These changes subsided within one week. Instead, collapsed myelin increased in number and phagocytosis of disintegrated myelin was occasionally observed. Astrocytes and oligodendroglias became prominent in size and number. Changes suggestive of selective damage of myelin or oligodendroglia was not encountered. We proposed that CO-followed by Wallerian degeneration. The pathogenesis of CO-encephalopathy was also discussed.
1. In eight adult cats intense, sharply circumscribed, monocular laser lesions were used to remove all cellular layers of the retina. The extents of the retinal lesions were subsequently confirmed with counts of alpha-ganglion cells in retinal whole mounts; in some cases these revealed radial segmental degeneration of ganglion cells distal to the lesion. 2. Two to 24 weeks later, area 17 (striate cortex; V1) was studied electrophysiologically in a standard anaesthetized, paralysed (artificially respired) preparation. Recording single- or multineurone activity revealed extensive topographical reorganization within the lesion projection zone (LPZ). 3. Thus, with stimulation of the lesioned eye, about 75 % of single neurones in the LPZ had 'ectopic' visual discharge fields which were displaced to normal retina in the immediate vicinity of the lesion. 4. The sizes of the ectopic discharge fields were not significantly different from the sizes of the normal discharge fields. Furthermore, binocular cells recorded from the LPZ, when stimulated via their ectopic receptive fields, exhibited orientation tuning and preferred stimulus velocities which were indistinguishable from those found when the cells were stimulated via the normal eye. 5. However, the responses to stimuli presented via ectopic discharge fields were generally weaker (lower peak discharge rates) than those to presentations via normal discharge fields, and were characterized by a lower-than-normal upper velocity limit. 6. Overall, the properties of the ectopic receptive fields indicate that cortical mechanisms rather than a retinal 'periphery' effect underlie the topographic reorganization of area 17 following monocular retinal lesions.
1. The effects of the intravenous injection of isoprenaline on heart rate and arterial pressure has been studied in dogs artificially respired with room air or with 12% oxygen-88% nitrogen.2. In dogs breathing room air, isoprenaline in doses from 0.02 to 500 mug/kg increased heart rate and reduced arterial pressure. Ventricular fibrillation was produced in one out of three dogs given 250 mug/kg. This was the only dog breathing room air which was killed by isoprenaline.3. In dogs breathing room air the repeated intravenous injection at 5-min intervals of 2.5 mug/kg increased heart rate and reduced arterial pressure. No ill effects were produced by six doses.4. In dogs respired with 12% oxygen-88% nitrogen the PaO(2) was reduced from 84 to 38 mm Hg with no changes in PaCO(2). In these dogs death was produced by doses of isoprenaline which in dogs breathing room air produced normal responses.5. The fatal dose of isoprenaline (10-50 mug/kg) reduced heart rate and arterial and pulse pressures; sinus rhythm persisted until arterial pressure was less than 50 mm Hg. Ventricular fibrillation did not occur; death occurred from cardiac asystole.6. Death was produced in a similar way in dogs with hypoxaemia by giving four or five doses of isoprenaline (2.5 mug/kg) at 5-min intervals or by two doses of 25 mug/kg.7. The final reduction in arterial pressure during a fatal response resulted from a reduction in cardiac contractility.8. These lethal effects of isoprenaline could be prevented by pretreatment with propranolol.
1 A method for stimulating the lumbar sympathetic outflow from the spinal cord of the rat is described which does not require artificial respiration of the animal.2 In some, but not all experiments continuous stimulation at 2 Hz or intermittently at 10 Hz accelerated the rate at which noradrenaline and dopamine-beta-hydroxylase accumulated central to a ligature on the sciatic nerve by approximately 40%.3 It is concluded that, although nervous activity is not necessary for axonal transport of transmitter granules in sympathetic neurones, intense nervous activity may accelerate the rate of granule transport.
1. Electrical stimulation (1 ms, 5 Hz, 80 V) for 5 or 15 s at the level of C4-T1 in the spinal canal of artificially respired pithed guinea-pigs (which had received intravenously (i.v.) (+)-tubocurarine chloride 2 mg kg-1, atropine sulphate 2 mg kg-1 and pentolinium tartrate 5 mg kg-1) caused constriction of airways, indicated by increased insufflation pressure. 2. This non-cholinergic constriction was inhibited by morphine (1-3 mg kg-1, i.v.), the peripherally acting mu-receptor agonist, H-Tyr-D-Arg-Phe-Lys-NH2 (DALDA, 0.1-1 mg kg-1, i.v.) or the alpha 2-adrenoceptor agonist B-HT920 (1-3 mg kg-1, i.v.). 3. The effects of either morphine (3 mg kg-1, i.v.) or DALDA (1 mg kg-1, i.v.) were inhibited by naloxone (3 mg kg-1, i.v.). Idazoxan (3 mg kg-1, i.v.) inhibited the anti-constrictor effect of B-HT920 (3 mg kg-1, i.v.), but not that of DALDA (0.1 mg kg-1, i.v.). 4. Thus activation of peripheral mu-opioid receptors or alpha 2-adrenoceptors inhibits airways constriction induced by non-cholinergic nerve stimulation in the pithed guinea-pig. This preparation therefore provides a further method for the in vivo examination of the effects of drugs on non-cholinergic tracheobronchial constrictor nerve function.
The effect of total right ventricular bypass peak flow-rate on the intrapulmonary shunt ratio was quantitatively investigated in animal tests. To give variations in the peak flow-rate (from pulsatile to intermediate to non-pulsatile), three types of blood pump (piston-bellows, screw, and centrifugal) were applied to dogs. The intrapulmonary shunt ratio was calculated from blood oxygen content drawn every 30 min from the outlet of the right ventricular bypass pump and from the femoral artery, while the canine lung was ventilated with 100% oxygen gas by an artificial respirator. The results show that when the intrapulmonary shunt ratio ranged between 0.095 and 0.392 there is no clear relation to the peak-flow-rate index (which varied from 1.1-17.0 l min-1 m-2) over the preceding 30 min. This study demonstrates that the intrapulmonary shunt ratio is able to be kept within the range of control values for 6 h even with a peak-flow-rate index of less than 4.0 l min-1 m-2.
Simultaneous recordings of the EEG, the electromyogram of the small intestine, the electrocardiogram, and femoral arterial pressure were monitored in 24 cats anesthetized with halothane, immobilized with gallamine, and artificially respirated. During pentylenetetrazol-induced generalized seizures, intestinal activity was blocked, as demonstrated by the disappearance of spikes from the EMG. This block was abolished by spinal cord section at C1-C2 level and partially abolished by bilateral adrenalectomy. These results demonstrate the existence of inhibitory sympathetic mechanisms during generalized experimental seizures.
The clinical characteristics of ALS in Finland were investigated. The study was based on the hospital records of 255 patients. No correlation was found between the disease and other previous illnesses. Muscular weakness was the most frequent complaint of the patients as their first symptom (149/255, i.e. 58 per cent). The duration of the disease was shortest (1.9 years) in male cases with the first symptoms in the bulbar area, and it was longest (3.4 years) in females with a spinal onset of the symptoms. The duration of the disease was in inverse relation to the age when it was contracted. Progressive muscular atrophy with fasciculations was considered the most important clinical sign of ALS. It was most frequently observed in the upper extremities including shoulders. Sensory disturbances were absent, sphincter abnormalities were reported in only three cases, bed sores did not exist, and there were no reports of impotence in the male patients. Two families with two familial cases in each were found, altogether two men and two women. Their disease did not differ from that of the rest of the series. The ALS patients soon became too disabled to work; 56 per cent bacame permanently disabled in less than 1 year's time, and only 9 per cent retained their working capacity for more than 2 years. The average length of stay at hospital was 32 days for ALS and 37 days for MS patients, but the later group was hospitalized 2-3 times more frequently than the former. Gastrostomy or tracheostomy and artificial respiration did not lenghten the lives of the patients.
A technique for producing graded spinal cord compression injuries in rats is described. A metal plate 2.2 x 5.0 mm in size is applied to the exposed spinal dura and loaded with weights. Neurological function is tested postoperatively on an inclined plane. Reading of the maximal angle of rat performance on this plane was found reproducible on comparison between different observers. Laminectomy per se had a minimal effect on the performance. Compression of 35 g for 5 min caused a pronounced but incomplete injury, with almost total recovery within 14 days and with no difference between animals on artificial respiration and those breathing spontaneously. Animals whose spine was fixed during the compression had a better outcome than those without such fixation.
Patients with chronic granulomatous disease (CGD), an uncommon inherited disorder of phagocytes resulting in the defective production of reactive oxygen intermediates, are prone to bacterial and fungal infections. In the case presented, therapeutic efforts including white cell transfusions, and amphotericin B and IFN gamma administration were undertaken to treat pneumonia caused by Aspergillus fumigatus. During a phase of artificial respiration, transfused white cells in peripheral blood and bronchoalveolar lavage fluid were monitored in order to examine their kinetics and functional activity. Using flowcytometrical methods, host-derived and transfused neutrophils could be distinguished by cytochrome b558 expression using the monoclonal antibody 7D5 for immunofluorescent staining as well as by production of reactive oxygen intermediates. Transfused PMN could be detected in both compartments and their kinetics could be followed up to 24 hours after transfusion. Using flowcytometry, even small numbers of transfused PMN could be measured during episodes of extreme leukocytosis. Since functionally intact transfused PMN were found in the bronchioalveolar lavage fluid, white cell transfusions in combination with antibiotic and immunomodulating therapy should be considered a part of the therapeutic regimens for life-threatening infections in CGD patients.
Cardiovascular and autonomic nervous responses to an injection of E. coli endotoxin were followed for up to 15 min. in cats anesthetized with chloralose and given artificial respiration. Within 60 seconds, endotoxin induced a drop of aortic pressure, with simultaneous cardiac acceleration and slight central venous hypertension. There was an associated, almost complete cessation of the aortic arch baroreceptor afferentation. The cardiac sympathetic efferentation increased up to 1.4 times the control level at its maximum. The splenic sympathetic efferentation increased up to 10.6 times the control level at the end of the 15 min period, when the other parameters studied showed a trend to control level. The sympathetic autonomic system seems to be activated through cardiovascular receptors sensing hemodynamic changes touched off by endotoxin-induced release of vasoactive substances.
We describe a patient who suffered respiratory arrest some minutes after retrobulbar block before cataract extraction. She was managed by artificial respiration for 20 min, and after the had recovered from this potentially fatal complication cataract extraction was performed without complications and without any neurological sequelae. Retrobulbar blocks, as well as other retrobulbar, injections, should be performed only in safe situations. Individuals trained in airway maintenance and ventilatory support should be immediately available, and the patient must be monitored for at least 10 min after the retrobulbar injection.
1. The responses of type J pulmonary receptors (identified according to existing criteria) were studied in anaesthetized cats by recording impulses in individual vagal afferent fibres whose conduction velocity ranged from 0.8 to 7 m/sec.2. Measurements of actual latencies between insufflation of halothane or ether into the lungs and the excitation of the endings, and the latencies before and after circulatory arrest have established that the endings are located in the interstitial tissues close to the pulmonary capillaries. Mainly for this reason, the term juxta-pulmonary capillary receptors (i.e. type J receptors) has been applied to these endings in preference to the term K deflation receptors used hitherto.3. The endings were stimulated by pulmonary congestion produced by occlusion of the aorta or left a-v junction for short periods. They were markedly stimulated during pulmonary congestion following injection of alloxan (150 mg/kg) or the addition of chlorine to the inspired air. This excitation was associated with a marked rise in pulmonary artery pressure and the occurrence of pulmonary oedema. However, the actual onset of excitation occurred some time after the rise in pressure and it was in fact more closely related to fall in pulmonary compliance. The frequency of discharge averaged over about 10-20 sec (in order to take the periods of relative inactivity into account) was 7.5 impulses/sec in 10 fibres (range 0.6-19 impulses/sec; S.D. 6.3). This is intense stimulation of the endings and the congestion so produced is therefore regarded as a severe stimulus for the endings.4. The pattern of excitation was variable. In some fibres the activity consisted of periodic bursts of impulses which seemed to be set off during the deflation phase of artificial respiration, sometimes during the inflation phase. This periodic activity was not due to contraction of smooth muscle as the endings are not stimulated following injection of histamine (into the right ventricle) which is known to stimulate smooth muscles in the alveolar ducts and respiratory bronchioles.5. It is postulated that the actual stimulus for the endings is a rise in interstitial pressure or volume produced by a rise in pulmonary capillary pressure. Evidence has been gathered to show that the latter rises during muscular exercise; this rise must stimulate the endings. It was therefore postulated that stimulation of the endings should cause reflex inhibition of limb muscles (for terminating exercise).
1. The possible role of acetylcholine (ACh) receptors in controlling neuromuscular synapse formation was studied by blocking the receptors with alpha-bungarotoxin during re-innervationf the rat diaphragm. Anaesthetized and artificially respirated rats were perfused with toxin throughout the 3-day period when most re-innervation was shown to take place (from day 4 to day 6 after a nerve crush). 2. The toxin treatment blocked about 99.9% of both junctional and extrajunctional ACh receptors, thereby eliminating virtually all end-plate potentials. However, a low level of ACh sensitivity returned to the muscle after several hours of washing, and small end-plate potentials were then recorded from the majority of fibres on the side that previously had been denervated. The degree of re-innervation was nearly as great as that seen in control denervated muscles that had not been treated with toxin. 3. The presence of bungarotoxin during re-innervation did not significantly affect either the appearance of newly formed synapses in the light microscope or the amount of transmitter they released during nerve stimulation. 4. Double innervation, which was not seen in normal muscles, was found in about 10-15% of re-innervated fibres in both the untreated and toxin-treated preparations. This suggests that some of the synapses formed during re-innervation may have been made over what previously had been extrajunctional membrane. 5. It is therefore unlikely that the ACh receptor, or at least that part of the receptor to which bungarotoxin binds, plays a direct role in controlling the process of synapse formation in mammalian skeletal muscle...
Action potentials were recorded from slips of the cervical vagi in anaesthetized cats. Single functional units with atrial patterns of discharge (type A, B and Intermediate) were first obtained and then attempts were made to alter (i.e. convert) their patterns of discharge. Finally the points of origin of their action potentials were located. The investigations were done in five stages. 2. In the first series, thirty unselected units were investigated in thirty cats. Twenty-five of these were located in the endocardium of vein-atrial system and consisted of two type A, fifteen type B and eight Intermediate type units. The remaining five units were located elsewhere in the chest Conversion of the pattern of discharge was achieved in sixteen of the twenty-five atrial units. Both atrial type A units were converted. 3. In the second series, eight type A units were selectively studied in twelve cats. Five were located in the atrial endocardium and all were converted. Of the other three units which were located at other sites in the chest, one could not be converted. 4. In the third series, four type A units which could not be converted were selectively studied in twenty cats. All were located outside the atria. 5. In the fourth series, three type B units which could not be converted were selectively studied in six cats. These units were located in the pulmonary veins and in the lateral walls of the atria. 6. In the fifth series, fifty-five units were investigated in three anaesthetized spontaneously breathing cats. The proportion of the types of units were similar to that obtained in the artificially respired cats (first series). 7. The present study has shown that atrial receptors with a type A pattern of discharge are relatively rare in the cat and that conversion of the patterns of discharge is a common phenomenon. Evidence is presented which suggests that there is one basic type of atrial receptor whose pattern of discharge is determined by their precise location in the vein-atrial system.