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Background: Extreme panting under heat stress threatens dairy cattle milk production. Previous research has revealed that the gas exchange-mediated respiratory drive in critically ill dairy cattle with low O 2 saturation induces panting. Vascular endothelial growth factor (VEGF) signaling may play important roles in immunosuppression and oxidative stress during severe respiratory stress responses in heat-stressed cattle. The objectives of this study were to transcriptomically analyze mRNA expression mediating heat-induced respiratory stress-associated panting, evaluate gas exchange, screen hub genes, and verify the expression of proteins encoded by differentially expressed genes in lymphocyte pathways., Results: Jersey cattle were naturally heat-exposed. Physiological data were collected for response evaluation, and blood was collected for gas exchange and gene expression assays at 06:00, 10:00 and 14:00 continuously for 1 week. Lymphocytes were isolated from whole-blood samples for mRNA-seq and expression analysis of key pathway genes/proteins. The cattle respiration rates differed with time, averaging 51 bpm at 06:00, 76 bpm at 10:00, and 121 bpm at 14:00 (p < 0.05). Gas exchange analysis showed that both pH and pCO 2 differed with time: they were 7.41 and 41 mmHg at 06:00, 7.45 and 37.5 mmHg at 10:00, and 7.49 and 33 mmHg at 14:00, respectively (p < 0.01). Sixteen heat-related differentially expressed genes (DEGs; 13 upregulated and 3 downregulated) were screened between 212 DEGs and 1370 heat stress-affected genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) hub gene functional analysis annotated eleven genes to signal transduction, six genes to the immune response, and five genes to the endocrine response, including both prostaglandin-endoperoxide synthase 2 (PTGS2) and VEGF. Gene Ontology (GO) functional enrichment analysis revealed that oxygen regulation was associated with the phosphorus metabolic process, response to oxygen levels, response to decreased oxygen levels, response to hypoxia and cytokine activity terms. The main signaling pathways were the VEGF, hypoxia inducible factor-1(HIF-1), cytokine-cytokine receptor interaction and TNF pathways. Four genes involved Integrin beta 3 (ITBG3), PTGS2, VEGF, and myosin light chain 9 (MYL9) among the 16 genes related to immunosuppression, oxidative stress, and endocrine dysfunction were identified as participants in the VEGF signaling pathway and oxygenation., Conclusion: These findings help elucidate the underlying immune and oxygen regulation mechanisms associated with the VEGF signaling pathway in heat-stressed dairy cattle.

During the first trimester of pregnancy in dairy cows, the fetus is mainly recognized by the expression of major histocompatibility complex class I (MHC-I) in the maternal immune system. Before the embryo begins to implant in the maternal uterus, it requires a long time to remodel and develop vessels in the placenta. During this stage, the embryos are exposed to a hypoxic environment. However, the expression of bovine MHC-I has not been determined in hypoxic bovine endometrial epithelial cells (bEECs). Hypoxia-inducible factor-1α (HIF-1α) is a marker for hypoxic conditions in cells. In the present study, we used cobalt chloride (CoCl 2 ) to establish a hypoxic cell model and then determined the expression of the classical gene BoLA-A and the non-classical gene MICB. qRT-PCR and western blot assays were applied to determine the expression of HIF-1α. qRT-PCR was performed to detect the levels of BoLA-A and MICB mRNAs. The results showed that HIF-1α expression was increased in the hypoxic cell model. The expression of BoLA-A was increased, but MICB levels were decreased in bEECs. Our study provides a basis for exploring the cattle intrauterine environment during pregnancy., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: Numerous clinical abnormalities occur in cloned calves during the neonatal period., Objectives: Describe respiratory diseases affecting cloned calves., Animals: Twenty-five cloned Holstein calves., Methods: Retrospective clinical study of the cloned calves born at the Veterinary Teaching Hospital, Saint-Hyacinthe, QC., Results: Records of 31 cloned calves were reviewed. Twenty-five records were included. Four stillborn calves and 2 calves euthanized at birth were excluded. Twenty-two calves suffered from respiratory diseases. Nineteen calves received intranasal oxygen treatment (INO). They were tachypneic (78 breaths per minute) and 5 of them were hypoxemic (PaO₂ < 55 mmHg). Two of 19 calves remained hypoxemic despite INO. Thirteen calves were weaned from INO after a median of 70 hours and were discharged at a median of 5 days of age. Nine calves required ventilatory support: 3 from birth and 6 after INO. Five were successfully weaned from the ventilator after a median of 32 hours and were discharged at a median of 8 days of age. Three calves died and 1 was euthanized because of respiratory disease. Necropsy revealed atelectasis, pulmonary congestion, and alveolar damages., Conclusion and Clinical Importance: Respiratory disease occurs frequently in cloned calves. The most frequent abnormality is hypoxemia because of V/Q mismatch. It is possible to successfully support these calves by INO and mechanical ventilation., (Copyright © 2011 by the American College of Veterinary Internal Medicine.)

Pulmonary arterial pressure (PAP) is an indicator of resistance to blood flow through the lungs and when measured at high altitude is a reliable predictor of susceptibility of an animal to brisket disease, a noninfectious cardiac pulmonary condition. (Co)-variance components for PAP, birth weight, and adjusted 205-d weaning weight were estimated from 2,305 spring-born, registered Angus cattle from a Colorado ranch at an elevation of 1,981 m. A single measure of PAP was collected after weaning on animals born from 1984 to 2003. The same licensed veterinarian measured every animal. Multitrait animal models with and without PAP maternal effects were fitted for a pedigree including 132 sires and 793 dams. The interaction of year x sex was a significant fixed effect (P <0.05) for PAP, but age of dam was not. Age at PAP testing was a significant (P <0.1) linear covariate for PAP, and scores increased 0.012 +/- 0.007 mmHg X d(-1) of age. Heritability of PAP direct was 0.34 +/- 0.05. Maternal heritability converged to a boundary at 0.0, and the model with maternal genetic effects for PAP was not significantly better than a model with only direct effects. Phenotypically, PAP was uncorrelated with birth or weaning weights. Genetically, PAP appeared to have positive, unfavorable relationships with direct effects for birth (0.49 +/- 0.12) and weaning weight (0.50 +/- 0.18). Positive correlations imply sires whose offspring exhibited resistance to brisket disease had lower weights and gains. A model that evaluated PAP in females and males as different traits had heritability estimates for each sex of 0.38 +/- 0.07 and 0.46 +/- 0.09, respectively, with a genetic correlation of 0.64 +/- 0.12 between the sexes and was not significantly better than the model assuming homogeneity by sex and a unit genetic correlation between sexes. The results suggest that PAP is moderately heritable in spring-born Angus cattle acclimatized and tested at high altitude, and selection for low PAP scores would be effective. Selection for growth at low altitude will produce cattle less suited to high altitude.

Some of the most valuable contributions to science have come about serendipitously, and, in 1913, when George Glover and Issac Newsom were commissioned by Colorado cattle ranchers to study high mountain disease, there was no way to anticipate the tremendous impact they would have on the study of high-altitude cardiopulmonary physiology. It was through the study of this agricultural malady that the correlation between chronic hypoxia, pulmonary hypertension, medial hypertrophy of the small pulmonary arteries, and right ventricular (RV) hypertrophy was recognized. The amount of vascular smooth muscle comprising the medial layer of pulmonary arteries varies significantly across species and can be used to predict the magnitude of pulmonary hypertension and RV hypertrophy elicited in response to chronic hypoxia. Within species, age and gender both significantly influence the severity of chronic hypoxic pulmonary hypertension and RV hypertrophy. However, despite all that we now know about hypoxic pulmonary hypertension, the specific mechanism(s) that differentiate the hypo- from the hyperresponder have yet to be elucidated. Adventitial fibroblast differentiation, circulating vascular progenitor cells, the presence or absence of specific vascular smooth muscle phenotypes, the upregulation or downregulation of vasoactive mediators, splice variants of oxygen-sensitive transcription factors, upregulation of growth factors, Ca(2+) sensitization, and/or the Rho/Rho-kinases signaling cascade could all potentially play a role in determining the extent of the vascular response to hypoxia within a species. Understanding the mechanisms that determine why some people, as well as some animals, exhibit a marked susceptibility to hypoxia is an important endeavor with far-reaching implications.

Hypoxic pulmonary vasoconstriction (HPV) is a physiological phenomenon in healthy lungs and a regulatory mechanism in alveolar hypoventilation by which blood flow is diverted from poorly ventilated areas to better ventilated alveolar regions. Maintained alveolar hypoxia (related either to respiratory diseases or to high altitude) results in a persistent activation of HPV. The latter mechanism is involved in the development of pulmonary vasoconstriction and right heart failure (Cor pulmonale) in chronic airway diseases. Compared to other species, especially the bovine and the porcine lung is highly susceptible to develop pulmonary hypertension because of anatomical and physiological pecularities. Consequently, therapeutic support of the heart is indicated in cattle and pigs suffering from respiratory diseases. In contrast, non-selective vasodilators are not recommended because they override the compensatory effect of hypoxic vasoconstriction and impair pulmonary gas exchange.

Objective: Hypoxaemia accompanies dorsal recumbency in the horse and frequently complicates general anaesthesia. The physiology associated with this phenomenon is poorly understood. One possible cause of poor tolerance to dorsal recumbency is an absent or reduced response to hypoxic pulmonary vasoconstriction (HPV). This study compared the HPV response in isolated pulmonary artery vessels from equivalent regions of equine and bovine lung., Animals: Equine and bovine, in vitro study., Materials and Methods: Equine and bovine pulmonary arteries were removed from the lungs of euthanased horses and cattle. Measurements of isometric tension were made on isolated rings of pulmonary vessels at 37 degrees C in a Krebs' saline solution. Hypoxia was induced by bubbling with a nominally 0% O(2) gas mixture., Results: A significant HPV response was observed above a baseline tension induced by phenylephrine (PE; 0.3 microm) or 5-hydroxytryptamine (5-HT; 0.1 microm). The HPV response in equine pulmonary vessels was approximately 33% less than the response observed in equivalent bovine vessels (equine 196 +/- 20%versus bovine 290 +/- 32%; p < 0.05). Removal of the endothelium (by rubbing the luminal surface) significantly reduced but did not abolish the HPV response. Incubation with the nitric oxide (NO) synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME; 100 microm), or COX-1/COX-2 inhibitor indomethacin (10 microm) markedly attenuated the HPV response in equine vessels., Conclusions: These results suggest that a significant HPV response exists in isolated equine pulmonary vessels; a component of this response requires a functional endothelium. Inhibition of cyclooxygenase and NO synthase attenuated the response, suggesting the involvement of a COX product and/or NO in mediating this effect either directly or indirectly. Alternatively, a non-COX related action of the nonsteroidal anti-inflammatory drug, indomethacin, may be involved.

Blood oxygen transport and tissue oxygenation were studied in 28 calves from the Belgian White and Blue breed (20 healthy and 8 hypoxaemic ones). Hypoxaemic calves were selected according to their high respiratory frequency and to their low partial oxygen pressure (PaO2) in the arterial blood. Venous and arterial blood samples were collected, and 2,3-diphosphoglycerate, adenosine triphosphate, chloride, inorganic phosphate and hemoglobin concentrations, and pH, PCO, and PO2 were determined. An oxygen equilibrium curve (OEC) was measured in standard conditions, for each animal. The arterial and venous OEC were calculated, taking body temperature, pH and PCO2 values in arterial and venous blood into account. The oxygen exchange fraction (OEF%), corresponding to the degree of blood desaturation between the arterial and the venous compartments, and the amount of oxygen released at the tissue level by 100 mL of blood (OEF Vol%) were calculated from the arterial and venous OEC combined with the PO2 and hemoglobin concentration. In hypoxaemic calves investigated in this study, the hemoglobin oxygen affinity, measured under standard conditions, was not modified. On the contrary, in vivo acidosis and hypercapnia induced a decrease in the hemoglobin oxygen affinity in arterial blood, which combined to the decrease in PaO2 led to a reduced hemoglobin saturation degree in the arterial compartment. However, this did not impair the oxygen exchange fraction (OEF%), since the hemoglobin saturation degree in venous blood was also diminished.

Rapid deaths in confinement cattle caused by exposure to hydrogen sulfide (H2S) gas from manure pits has not been reported in the USA. In 1997, 158 cattle in 2 confinement pens were exposed to H2S gas as the manure in the pits under a slatted floor was agitated prior to pumping. Approximately 35 of the cattle were lying on the floor when the upper agitator was turned on. Within 5 minutes, many these cattle were down on their sides and paddling. Of these, 26 died within a few minutes. The survivors were treated and sent to slaughter. Cattle that did not show immediate signs of toxicosis remained clinically unaffected. Two steers that were near death were brought to the Purdue Animal Disease Diagnostic Laboratory for clinical evaluation, euthanasia, and necropsy. They were recumbent and unresponsive to visual and auditory stimuli. Necropsy examination yielded no significant gross lesions. No evidence of viral or bacterial infection was found. Ocular fluid nitrate concentrations were within normal limits, and no lead was detected in either animal. Microscopic examination revealed lesions consistent with H2S-induced central nervous system anoxia. Histologically, sections of brain demonstrated massive, diffuse cerebral cortical laminar necrosis and edema. Portions of the outer lamina contained hypereosinophilic and shrunken neurons. The subcortical white matter was vacuolated in some areas. The history, clinical signs, and histologic lesion of cerebral laminar necrosis led to a diagnosis of H2S toxicosis in these cattle.

The effects of an acute non-isocapnic hypoxia on ventilation and pulmonary mechanics were investigated in 6 healthy unsedated Holstein-Friesian (HF) calves and in 7 double-muscled calves of the Belgian White and Blue (BWB) breed known to develop more severe hypoxemia during exercise and respiratory diseases. Data were collected at 1 min intervals throughout the following protocol: breathing air (FIO2 = 21%), then breathing hypoxic gas mixture (FIO2 = 10%) for 5 min, and, finally, breathing air again for 5 min of recovery. Arterial blood was sampled at rest and at the 4th min of hypoxia for blood gas analysis. In HF and BWB calves, hypoxia induced a significant increase in tidal and minute volume, but did not change respiratory rate, dynamic lung compliance and total pulmonary resistance. However, with regard to their ventilation during normoxia at rest, BWB calves showed a comparatively greater rise in ventilation than HF calves during the first 4 min of hypoxia. On the contrary, by the 5th minute of hypoxia, ventilation of BWB calves declined to the normoxic level while HF calves largely sustained hyperventilation. This hypoxic ventilatory depression in BWB calves could be explained by the proportionately greater initial increase in ventilation. It was concluded that BWB calves supported this hypoxic challenge less easily than HF calves.

The erythrocyte density separation test (EDT) divides the red blood cells into two groups: younger (less dense) and older (more dense) erythrocytes. Using this test enables veterinarians to assess the erythropoiesis in calves on the basis of the percentage of less dense (younger) red blood cells. Anemic calves, as well as those with pneumonic infections show higher proportions of less dense red blood cells in the EDT than healthy ones. This testing procedure makes it possible to estimate the effects of an oxygen deficiency condition, such as hypoxemia, anemia, shock etc. on the peripheral tissues. So the EDT represents a valuable complement to existing hematological laboratory methods. Carrying out the EDT is very simple and suitable in routine clinical testing.

The erythrocyte density separation test (EDT) divides the red blood cells into two groups: younger (less dense) and older (more dense) erythrocytes. Using this test enables veterinarians to assess the erythropoiesis in calves on the basis of the percentage of less dense (younger) red blood cells. Anemic calves, as well as those with pneumonic infections show higher proportions of less dense red blood cells in the EDT than healthy ones. This testing procedure makes it possible to estimate the effects of an oxygen deficiency condition, such as hypoxemia, anemia, shock etc. on the peripheral tissues. So the EDT represents a valuable complement to existing hematological laboratory methods. Carrying out the EDT is very simple and suitable in routine clinical testing.

The peak time period for the average beef producer to experience the majority of calf losses has consistently been from the time of birth through the first seven days of life. Weakness is a principal clinical sign of diseases or conditions responsible for mortality including birth trauma, prematurity or dysmaturity, congenital malformations, metabolic defects, intrauterine infection, anoxia or hypoxia, hypothermia, starvation, extremes in birth weight, and post-natal infection. This article discusses anoxia/hypoxia and septicemia in greater detail because of their involvement as a common cause of weakness in the newborn calf.

In this review article the problem of perinatal mortality and the birth of weak calves is discussed. Two main causes can be distinguished: hypoxia and infections. It is emphasized that for a correct diagnosis a combination of a comprehensive anamnesis, a thorough examination of the calf and a laboratory investigation is necessary. Treatment of weak calves is in many cases disappointing. Preventive measures as an excellent management of periparturient cows are important.

Labor and delivery stimulate increased release of catecholamines and endogenous opioid peptides in neonates. Catecholamines promote adaptation to the extrauterine environment after birth. Enkephalins are stored together with catecholamines in the adrenal medulla and have an inhibitory effect on catecholamine release. We investigated the influence of labor and neonatal hypoxia on epinephrine, norepinephrine, and met-enkephalin release in calves. Blood samples were taken from the umbilical artery before rupture of the umbilical cord and from the jugular vein repeatedly after birth. Highest plasma norepinephrine concentration was found in calves delivered at the end of gestation (term calves) before umbilical cord rupture. In calves delivered before the physiologic end of gestation (preterm calves), norepinephrine values increased after cord rupture, but remained lower than values in term calves. Epinephrine release followed a similar pattern, but norepinephrine was clearly predominant. In term calves, met-enkephalin values were significantly higher than values in preterm calves. In calves of both groups, met-enkephalin release increased after cord rupture. During birth, the increase in catecholamine release seems to take place earlier than that of enkephalins. Norepinephrine-dominated stimulation during expulsion of the calf might be followed by increasing enkephalinergic inhibition after cord rupture and onset of respiration. Reduced release of catecholamines and enkephalins in preterm calves may be connected with delayed adaptation to the extrauterine environment.

Vascular medial thickening is a prominent finding in people and animals with refractory neonatal pulmonary hypertension. Smooth muscle cells are capable of 2 distinct growth responses in vivo: hypertrophy or hyperplasia. Hypertrophic smooth muscle cells may undergo DNA synthesis without cell division, leading to a polyploid state. To better understand the nature of smooth muscle cell growth in healthy and pulmonary hypertensive neonatal calves, we measured incorporation of the thymidine analog bromodeoxyuridine (BrdUrd) and total DNA content in medial cells from control (pulmonary arterial pressure = 32 +/- 2 mm of Hg) and hypobaric hypoxia-exposed (pulmonary arterial pressure = 120 +/- 7 mm of Hg) calves. Labeling of medial cells with BrdUrd measured by flow cytometry was increased (P < 0.02) in pulmonary arteries of hypoxia-exposed calves (n = 5), compared with control calves (n = 5). Immunohistochemical localization of BrdUrd indicated that BrdUrd labeling of large elastic pulmonary arteries from hypoxia-exposed calves was increased almost exclusively in the outer half of the medial wall. Increased BrdUrd labeling of muscular pulmonary arteries from hypoxia exposed calves was observed in the arterial media and adventitia, and tended to exit in clusters. Analysis of DNA content by flow cytometry indicated a decrease (P < 0.05) in percentage of tetraploid medial cells in pulmonary arteries from hypoxia-exposed calves, compared with control calves. Bivariate analysis for BrdUrd labeling and DNA content of cells from the pulmonary arteries of hypoxia-exposed calves indicated a subpopulation of diploid cells with positive BrdUrd labeling, suggestive of DNA synthesis and subsequent cell division.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxic-induced pulmonary hypertension is known to be intensive in the bovine species and sometimes leads to pathological cardiac repercussions. On the other hand, doubled-muscled cattle are predisposed to develop hypoxaemia during exercise and with respiratory diseases. Therefore the purpose of this study was to investigate the cardiovascular response to acute hypoxia in double-muscled calves compared with calves of standard conformation. Pulmonary arterial pressure, electrocardiogram and blood temperature were simultaneously recorded, arterial blood was sampled for blood gas analysis and cardiac output was determined in six Friesian calves and six double-muscled calves of the Belgian White and Blue breed(BWB) when breathing air (fractional inspiratory oxygen concentration [FIO2]: 21 per cent) and when breathing a hypoxic gas mixture (FIO2: 10 per cent). All the absolute values of the measured parameters were significantly (P less than or equal to 0.001) different between the two breeds, except heart rate and arterial blood gas values. The pattern of hypoxic-induced decrease in arterial PO2 was similar in the two breeds of calves, suggesting that the pulmonary exchange capacities during hypoxia are no less efficient in double-muscled calves than in calves of standard conformation. Similarly, the percentage of variation of the mean pulmonary arterial pressure from its normoxic to its hypoxic value was the same in the two breeds of calves, suggesting that double-muscled calves are not predisposed to develop a more precocious or more intense pulmonary hypertension for a given level of hypoxaemia. The significantly smaller normoxic and hypoxic cardiac index and stroke index found in BWB compared with Friesian calves was interpreted as a less efficient cardiac function in double-muscled subjects.

The effect of reduced oxygen tension in arterial blood (hypoxic hypoxia) for 24 h postpartum on the absorption of colostral Ig was studied in 12 neonatal calves. During this period, inspired air for hypoxic calves contained 10.5% O2, whereas that for normoxic calves contained 21% O2. After 24 h, inspired air for all calves contained 21% O2. Three dietary regimens also were imposed during the initial 24-h period: colostrum at 0 and 12 h, whole milk at 0 and 12 h, or fasting. Colostrum was fed to all calves at 24, 36, and 48 h. During the initial 24-h period, means for arterial partial pressure of oxygen were 26 and 73 mm Hg for hypoxic and normoxic calves, respectively. In those fed colostrum at 0 and 12 h, hypoxia extended the period of Ig absorption from 20 to 40.5 h. In calves fed whole milk or those that were fasted, no such effect was noted. These observations suggest that the effect of hypoxia on the cessation of Ig absorption by the small intestine is mediated through a secondary and as yet undetermined mechanism.

The effect of reduced oxygen tension in arterial blood (hypoxic hypoxia) for 24 h postpartum on selected metabolic parameters was studied in 12 neonatal calves. During this period, inspired air for hypoxic calves contained 10.5% O2, whereas that for normoxic calves contained 21% O2. After 24 h, inspired air for all calves contained 21% O2. Three dietary treatments also were imposed during the initial 24-h period: colostrum at 0 and 12 h, whole milk at 0 and 12 h, or fasting. All calves were fed colostrum at 24, 36, and 48 h and whole milk at 60 and 72 h. Parameters included plasma glucose, lactate, fructose, and IgG; arterial blood gases; and pH. Arterial partial pressure of oxygen was maintained near 25 mm Hg throughout the period of hypoxia. Arterial partial pressure of carbon dioxide was unchanged during the period of hypoxia (approximately 45 mm Hg) but was lower (39 mm Hg) in posthypoxic calves. Glucose tended to be lower in hypoxic calves; however, this difference was not statistically significant. Hypoxic calves had significantly higher plasma lactate concentrations contributing to a progressive primary metabolic acidosis.

All calves fed locoweed (green and dry Oxytropis sericea Nutt and dry Astragalus lentiginosus Dougl) at high elevation developed clinical signs, gross and microscopic lesions of congestive right heart failure. Clinical signs and microscopic lesions of locoweed intoxication were also evident. Control calves did not develop the clinical signs, gross or microscopic lesions demonstrated in the locoweed fed calves.

A severe degree of hyperplasia of the chief cells occurs in bovine carotid bodies at high altitudes, compared to sea level. As a result, the carotid body from an animal at high altitudes is significantly heavier and larger than the carotid body from an animal at sea level (P less than .001). In eight of 20 (40%) animals at high altitudes, the hyperplastic reaction had progressed to form chemodectomas. The findings suggest that neoplasia can result from chronic stimulation by a biologically essential environmental factor (atmospheric PO2) that acts pharmacologically on the target tissues (chief cells of the carotid body).

Hemodynamic responses to acute pneumonia and to hypoxia were investigated in 10 newborn calves. Experiments were performed on heparinized, anesthesized and ventilated calves. Control calves were inoculated intratracheally with bovine fetal serum. Pneumonia was induced in treated calves by intratracheal inoculation with P haemolytica suspended in bovine fetal serum. Before inoculation (base line), at the time of inoculation (T = 0), and at 30-minute intervals for 3 hours, pulmonary arterial pressure (Ppa), systemic arterial pressure, cardiac output (CO), arterial blood gases, pulmonary vascular resistance (PVR), and systemic vascular resistance were determined. At T = 0, calves in both groups became hypoxemic, alveolar-arterial O2 difference, PVR, and Ppa increased, and CO and systemic vascular resistance remained unchanged. At subsequent measurement intervals, all values returned to base-line in control calves, whereas treated calves had progressive hypoxemia associated with a decrease in Ppa and PVR, with no change in CO. Three hours after inoculation and after inhalation of 10% O2 in N2, PVR increased significantly in the control calves. In the treated group, hypoxia did not increase the resistance, compared with base-line and 3-hour values. The data indicate decreased Ppa during pneumonic pasteurellosis is because of a decrease in PVR and that pneumonia may attenuate the normal pulmonary hypoxic vasoconstrictor response.

During all of 1974, we surveyed, for illnesses and deaths, about 407,000 yearling feedlot cattle maintained at 1,600 m altitude. Of 1,988 cattle necropsied, 116 (5.8%) had brisket disease. The malady occurred during all seasons but was most common throughout fall and winter. The gross changes were hypertrophy and dilatation of the right ventricle and generalizaed passive congestion. The postulated causative factors were high genetic susceptibility, rapid growth rate, previous mountain grazing, and hypoventilation with airway hypoxia.

The cause of arterial hypoxia during natural infection with bovine respiratory syncytial virus was studied in seven calves (three to nine months of age) originating from five herds with respiratory tract disease and serological evidence of infection with the virus. Blood gas values were measured during ambient air breathing and during 100 per cent oxygen breathing. The percentages of contribution to the arterial hypoxia from alveolar hypoventilation, mismatching of ventilation and perfusion, and right-to-left shunting were calculated from the measured parameters. Calculated percentages of total venous admixture varied from 14 per cent of cardiac output in relatively mild cases to 48 per cent in the worst affected animal. This venous admixture had been caused mainly by right-to-left shunting of blood, while mismatching of ventilation and perfusion became important in the more severely affected animals. Alveolar hypoventilation was only important in the worst affected animal.

Observations in several species suggest that pulmonary vascular reactivity may be reduced during pregnancy. We tested this hypothesis in two groups of unanesthetized cows, one "susceptible" and one "resistant" to high mountain or brisket disease. At the altitude of residence (1,524 m), mean pulmonary arterial pressure was elevated during pregnancy by 18% and total pulmonary vascular resistance by 32% in susceptible but not in resistant cows. During acute exposure to simulated altitudes of 2,120--4,550 m, pulmonary arterial pressure was increased by 16% and total pulmonary resistance by 28% during pregnancy in susceptible cows. The pulmonary pressor response to a 5 microgram/kg bolus of prostaglandin FIalpha was not different during pregnancy in either group. Resistant cows hyperventilated while pregnant, raising arterial partial pressure of oxygen (PaO2) by 6 Torr both at 1,524 m and, on the average, by 7 Torr at altitudes of 2,120--4,550 m. Susceptible cows increased their PaO2 less than did the resistant cows during pregnancy. The results indicated that pregnancy was associated with a greater rise in pulmonary arterial pressure and total pulmonary vascular resistance during acute hypoxia and failed to elicit as great a ventilatory response in susceptible than in resistant cows.