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Biomedical subjects

M Manohar

Publications and source records attributed to M Manohar.

123 records · Page 7Linked to original sources
PubMed1976

Ventilatory control in peripheral chemoreceptor-denervated ponies during chronic hypoxemia.

The present study was designed to provide further insight into the role of the carotid and aortic chemoreceptors in ventilatory (VE) acclimatization during sojourn at altitude. Measurements were made: 1) on 10 ponies near sea level (SL, 740 Torr) under normal conditions, 2) on 6 of these at SL following chemoreceptor denervation (CD), and 3) subsequently on all 10 during 4 days of hypobaric hypoxia (PaO2 = 40-47 Torr). CD resulteo in hypoventilation at SL (deltaPaCO2 = d8 Torr, P less than 0.05), and it prevented hyperventilation normally observed with injection of NaCN and acute exposure to hypoxia (less than 1 h). In contrast, hyperventilation was evident in normal ponies during acute hypoxia (deltaPaCO2 = -6.7 Torr). Ventilation increased in both groups between the 2nd and 8th h of hypoxia (deltaPaCO2 from 1 h = -4 Torr, P less than 0.05). This change, a common characteristic of acclimatization, persisted throughout 4 days of hypoxia in the normal ponies. However, in the CD ponies this change was evident consistently only through the 12th h and after the 44 h hyperventilation was no longer evident. We conclude that the peripheral chemoreceptors are essential in ponies for normal VE acclimatization to this degree of hypoxemia. Two additional findings in CD ponies suggest the presence of a CNS inhibitory influence on the VE control center during chronic hypoxemia. First, acute hyperoxygenation on the 4th day of hypoxemia induced hyperventilation (deltaPaCO2 = -5 Torr, P less than 0.05). Second, again on the 4th day and during hyperoxygenation, VE responsiveness to CO2 and doxapram HCl was greater than at sea level.

Acclimatization↗
PubMed1976

Cardiopulmonary effects of the combination of neuroleptic azaperone and hypnotic metomidate in swine.

Cardiopulmonary measurements were made at given intervals up to 120 minutes on 6 awake, unanesthetized pigs given azaperone and metomidate. Decreases from control values occurred in arterial blood pressure (deltaBPart = 30 mm of Hg), heart rate (deltaHR = 30 to 35 beats/minute), and cardiac index (deltaCI = 1.5 L/minute/m2). Blood gas and pH measurements indicated no severe impairment of pulmonary function or arterial acidosis. Although the drugs led to decreases in the various functions, cardiopulmonary function remained stable and uncompromised.

Animals↗
PubMed1967

Platelet damaging factor, a fifth activity of staphylococcal alpha-toxin.

Crude and purified staphylococcal alpha-toxin were used to demonstrate that the platelet-damaging effect of crude alpha-toxin represents a fifth activity of the alpha-toxin molecule. The homogeneity of the purified toxin employed was demonstrated by ultracentrifugation, Ouchterlony, and immunoelectrophoretic methods. Continuous-flow electrophoretic migration studies demonstrated under a variety of conditions that the platelet-damaging and the alpha-hemolytic activities migrated as a unit. Fractionation studies with the use of Sephadex G-100, carboxymethyl cellulose, and diethylaminoethyl cellulose failed to separate these two activities. Further, when alpha-toxin of demonstrated purity and crude toxin were adjusted to the same hemolytic activity, they possessed the same platelet-damaging activity. In addition, heat-reactivation studies with crude alpha-toxin revealed that the platelet-damaging effect was inactivated and reactivated in parallel with alpha-hemolytic activity. Comparable studies with purified alpha-toxin showed parallel inactivation of both activities at 60 C. Additional heating at 100 C failed to reactivate either activity. Electron micrographs revealed that purified alpha-toxin produced distinct degenerative changes in rabbit platelets. These studies also provided definite evidence that purified alpha-toxin has a damaging effect on human platelets. Monovalent alpha-antisera prevented platelet damage.

Animals↗
PubMed1966

Heat reactivation of the alpha-hemolytic, dermonecrotic, lethal activities of crude and purified staphylococcal alpha-toxin.

Manohar, M. (University of Minnesota, St. Paul), S. Kumar, and R. K. Lindorfer. Heat reactivation of the alpha-hemolytic, dermonecrotic, and lethal activities of crude and purified staphylococcal alpha-toxin. J. Bacteriol. 91:1681-1685. 1966.-Crude staphylococcal toxin loses its alpha-hemolytic activity more rapidly at 60 than at 100 C. This paradoxical behavior has been postulated to be due to the presence of a thermolabile inhibitor in crude toxin. This work provides experimental evidence for the presence of a thermolabile "protective inhibitor." This substance(s) protects the alpha-toxin against destruction at 60 C, yet simultaneously inhibits the hemolytic activity of alpha-toxin under the same conditions. Of greater importance, this work also demonstrates that the dermonecrotic and lethal activities of crude toxin are inactivated and reactivated in parallel with the alpha-hemolytic activity. Crude staphylococcal toxin possessing a high alpha-hemolytic titer when heated to 60 C for 30 min lost its alpha-hemolytic, dermonecrotic, and lethal activity. However, when this same toxin was immediately exposed to 100 C, a remarkable simultaneous reactivation of all three of these activities occurred. Contrariwise, electrophoretically purified alpha-hemolysin, which also possessed dermonecrotic and lethal activity, showed no reactivation under these conditions, thus demonstrating that reactivation is due to a substance(s) distinct from the alpha-toxin. The fact that alpha-hemolytic, dermonecrotic, and lethal activities were inactivated at 60 C and simultaneously reactivated at 100 C provides additional proof that these activities are all associated with one toxic component. The probability is remote that three separate entities would exhibit the same rate of inactivation and the same strange reactivation.

Animals↗
PubMedDate not supplied

Pulmonary haemodynamics in the exercising horse and their relationship to exercise-induced pulmonary haemorrhage.

Exercise-induced pulmonary haemorrhage (EIPH) is a common occurrence in race horses. Although blood in cases of EIPH has been suspected to originate from the bronchial circulation, which receives approximately 1% of the left ventricular output, physiological evidence has recently emerged to indicate that the pulmonary circulation, which receives the entire output of the right ventricle, is a more likely source. High transmural pulmonary capillary pressures have been shown to cause breaks in the capillary endothelium, basement membrane as well as in the alveolar epithelium. Blood constituents escape into the interstitium and alveoli through such breaks in the blood-gas barrier--a phenomenon referred to as stress failure of pulmonary capillaries. Concomitant measurement of pulmonary arterial and venous pressures in strenuously exercising horses have revealed that both of these variables increased dramatically such that the intravascular pulmonary capillary pressure during exertion at 14 m/s (heart rate of 214 beats/min) approached 105 cm H2O (79 mmHg). Alveolar pressure during peak inhalation is likely to be negative; therefore, it is probable that transmural (intravascular minus perivascular) pulmonary capillary pressure of maximally exercising horses may be greater than 105 cm of water. Thus, the pulmonary blood-gas barrier, which has to be thin to provide for adequate diffusion of O2, is exposed to very high transmural forces associated with high cardiac output during exercise. Recent evidence suggests that the alveolar-capillary membrane may not be able to withstand the high transmural forces during maximal exertion, and that stress failure of pulmonary capillaries occurs, leading to EIPH. Intravenous furosemide premedication 4 h before exercise attenuates the exercise-induced rise in pulmonary arterial, capillary and venous pressures and, therefore, may be efficacious in reducing or limiting the extent of EIPH in race horses.

Animals↗
PubMedDate not supplied

Impact of 70% nitrous oxide administration on regional distribution of brain blood flow in unmedicated healthy swine.

Regional distribution of brain blood flow was examined in 11 healthy, spontaneously breathing swine using 15 micron in diameter radionuclide-labeled microspheres that were injected into the left atrium. Measurements were made during inhalation of 30% O2/70% nitrogen (control) and at 15, 45, 75, and 120 min of 30% O2/70% nitrous oxide breathing. The animals were surgically prepared 10-12 days before the hemodynamic study. Arterial blood-gas tensions, arterial pH, mean aortic pressure, and cardiac output remained near their respective control values during exposure to 70% nitrous oxide. Control values of blood flow in the cerebrum, cerebellum, and the brain stem were 68.5 +/- 4.7, 75.6 +/- 4.2, and 54.2 +/- 4.0 ml . min-1 X 100 g-1, respectively. At 15 min of exposure to nitrous oxide, blood flow in the cerebrum, cerebellum, and the brain stem was 169, 127, and 145% of the control values, respectively. For the caudate nuclei and the corpus callosum, the corresponding figures were 141 and 131% of control, while that for remainder of the cerebrum was 178% of the control value. In the medulla, pons, and thalamus-midbrain, blood flow was 151, 157, and 141% of the respective control values. In all regions of the porcine brain, elevated levels of blood flow persisted throughout the 2 h of exposure to 70% nitrous oxide and no marked fluctuations occurred. It is concluded that administration of 70% nitrous oxide to healthy pigs caused pronounced cerebrovascular vasodilatation in all regions of the brain. This persisted throughout the 2 h of its administration.

Animals↗
PubMedDate not supplied

Regional brain blood flow and cerebral cortical O2 consumption during sevoflurane anesthesia in healthy isocapnic swine.

Regional distribution of brain blood flow was examined in seven previously catheterized healthy isocapnic swine while awake (control), and during 1.0 and 1.5 minimum alveolar concentration (MAC--2.66 and 3.99% end-tidal, respectively) sevoflurane anesthesia using radionuclide-labeled 15-micron diameter microspheres that were injected into the left atrium. In six additional pigs, the superior sagittal sinus was also catheterized so that cerebral cortical O2 consumption could be ascertained during these conditions. Control values of blood flow in the cerebral cortical gray matter, white matter, and caudate nuclei were 117 +/- 9, 38 +/- 2 and 105 +/- 8 ml X min-1 X 100 g-1, respectively. At 1.0 MAC sevoflurane, blood flow in these regions decreased to 66, 76, and 75% of respective control values, and these values were not different from those recorded at 1.5 MAC anesthesia. Cerebral cortical O2 consumption decreased by 50 and 52% at 1.0 and 1.5 MAC sevoflurane anesthesia, but the hemoglobin-O2 saturation in the cerebral cortical venous drainage (57 +/- 3% and 69 +/- 3% at 1.0 and 1.5 MAC) consistently exceeded control value (42 +/- 1%), suggesting that cortical O2 supply during both levels of sevoflurane anesthesia remained adequate. In cerebellum, blood flow decreased from 86 +/- 5 (control) to 68 +/- 4 ml X min-1 X 100 g-1 with 1.0 MAC sevoflurane, but returned toward control value at 1.5 MAC anesthesia. The thalamohypothalamic perfusion decreased to 59 and 75% of the control value with 1.0 and 1.5 MAC sevoflurane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMedDate not supplied

Porcine brain and myocardial perfusion during enflurane anesthesia without and with nitrous oxide.

Brain and myocardial blood flow (MBF) were examined in 10 previously instrumented swine during isocapnic conditions using 15 micron in diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of enflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was 1.66%. In pigs, 50% nitrous oxide decreased enflurane requirement for 1.0 MAC anesthesia by 0.82%. Each animal was studied during the following conditions: (a) unanesthetized (control); (b) 1.0 MAC enflurane anesthesia (1.66% end-tidal concentration); (c) 1.5 MAC (2.49%) enflurane anesthesia; (d) the equivalent of 1.0 and 1.5 MAC anesthesia produced by enflurane (0.84 and 1.67%) plus 50% nitrous oxide. Cerebral and total brain blood flow values were the same as control values during both levels of enflurane anesthesia. However, blood flow in the brainstem and cerebellum exhibited a dose-related increase; the increment of 28% for each of these regions at 1.5 MAC achieved statistical significance. Vascular resistance in all regions of the brain decreased with enflurane anesthesia. Substitution of 50% nitrous oxide for enflurane to maintain the same level of anesthesia markedly increased cerebral blood flow. At 1.0 and 1.5 MAC anesthesia produced using enflurane plus 50% nitrous oxide, cerebral blood flow was 151 and 183% of the control value, respectively. During enflurane plus nitrous oxide anesthesia equivalent to 1.5 MAC, cerebellar and brain stem blood flow were 135 and 180% of respective control values. MBF in all regions decreased in a dose-related manner with enflurane anesthesia. At 1.5 MAC enflurane, perfusion values in the walls of the left and the right ventricles were 52 and 59% of respective control values. During both levels of enflurane plus 50% nitrous oxide anesthesia, transmural MBF in all regions remained close to awake values. Subendocardial/subepicardial perfusion ration in both ventricles exceeded 1.00 during all steps of the protocol, thereby suggesting that subendocardial O2 delivery kept pace with O2 demand. These experiments have demonstrated that usage of 50% N2O with enflurane to produce equipotent anesthesia resulted in a dramatic increase in cerebral blood flow while MBF remained near awake value.

Anesthesia, Inhalation↗